Why do scary situations make our skin crawl? Why do we have goosebumps in such situations? I do not see why should scary situations make our skin "crawl". In scary situations, we supply less blood to our skin (which makes it paler), so shouldn't its activities reduce? Goosebumps should take up some energy to raise the hairs. Shouldn't that energy be conserved?

Goose bumps are based on a pilomotor reflex where tiny muscles at the base of hair follicles contract, which leads to the "bumps" and also raises the hair in the follicle.

It's often explained as a vestigal reflex, dating back when our ancestors had more hair than the modern human. The "puffing up" of fur has two effects, which today still both can be observed:

Raised hair traps air in the fur, thus minimizing heat loss in the cold.
Raised hair (often combined with certain postures) makes an animal appear larger, thus intimidating an opponent or predator. This is the scenario you mention in your question.


What are low-accumulating genotypes? What are low-accumulating genotypes? And how does it differ from high-accumulating genotypes?

Certain organisms and strains of organisms can accumulate certain substances, such as Cd (a toxic heavy metal). If they accumulate those compounds more rapidly and in higher amounts, the organisms can be said to be high-"substance" accumulating organisms, e.g high-Cd accumulating organisms. The genotype which causes being a high-Cd accumulating organism can be described as a high-"x" accumulating genotype, like in this paper. A high-accumulating genotype without reference to a certain substance doesn't make much sense. These genotypic predispositions to accumulation are often used with toxic heavy metals like cadmium and arsenic which persist in the body.

As another "substance" example, high-"x" accumulating organisms is also used in the description of high-plaque accumulating organisms, e.g in this paper.


Brain response frequencies while sleeping I'm not sure if this is the right place to ask this but Biology seemed to fit best.

I'm trying to find out what frequencies the brain responds to best while sleeping.

The reason for this is recently I attended a lecture where it was stated that the brain hears low frequencies/deep noises better, meaning fire alarms for example might not be as effective as we think.

However I remember there was an episode of The Big Bang Theory where they said high pitch noises are heard better while sleeping as a built in response to, for example, a baby crying. Now I know this is just a TV show but I presume they must have some basis for the remark since they do have science advisors, it also just seems to make more sense.

Does anyone know which is correct or better yet can point me in the direction of some research to help.

Sleep as you may know is divided into 2 broad categories which are the REM (Rapid Eye movement) and NREM (non rapid eye movement). NREM is further divided into 3 stages (reference). You never know which stage of sleep you are in when you are subjected to a particular frequency of sound. Your response to different sounds differ in your different sleep cycles.

The present 3 stages in NREM sleep is an update by The American Academy of Sleep Medicine (AASM) in 2007 (reference).The original 4 stages in the Rechtschaffen and Kales (R&K) standardization of 1968 (reference) has been used to explain the effect of disturbances in different sleep cycles

  Stage 1 is still the phase of sleep from which it is easiest to wake
  someone up.

  People in Stage 2 sleep are unlikely to react to a light or a noise,
  unless it is extremely bright or loud.

  During Stage 3, the muscles still have some tonus, and sleepers show
  very little response to external stimuli unless they are very strong
  or have a special personal meaning (for example, when someone calls
  your name, or when a baby cries within earshot of its mother).

  Stage 4 is the stage of sleep that accomplishes most of the body’s
  repair work and from which it is most difficult to wake someone up (reference).

A study conducted to measure brain activity while sleeping subjects were subjected to varying degrees of sound found that some people did you wake up after being hit with 70db of sound while others woke up even at sounds between 40 - 50 db (reference). This could lead to new behavioral or drug therapies for people with sleep disorders.

A review on the affect of low frequency sound on sleep could not reach any significant conclusions warranting that more search needs to be conducted in the field.(reference).

You will be interested to know that different sounds have been found to wake up men and women. A list is available here. Differences between the sleep of men and women are listed in this article.


Effect of nerve pills and relationship to Shingles Do nerve pills actually suppress the nervous system and how would that effect the Shingles virus which is known to activate under large amounts of stress?

I gather you are talking about anti-axiety drugs (anxiolytics). Benzodiazepines is one of the major groups of anxiolytics, and includes Xanax. Benzodiazepines are central nervous depressants, meaning that they reduce the activity of neurotransmitters in the brain. They do this by binding to the GABA-A receptor and enhancing the effect of the inhibitory neurotransmitter GABA when it binds to the same receptor. The binding of GABA to a GABA receptor on a neuron causes hyperpolarization of the neuron by ion flow through the cellular membrane and decreases the chance of an action potential. So yes, nerve pills act by supressing the nervous system.

As for your question about interaction with Shingles, I think that's considered off-topic under the personal medical questions policy.


How difficult is it for wild birds to find food? This question came to my mind when I was wondering if my parrots would have it better on the outside than with me. Also, is starvation a significant cause of death at different stages in a bird's life cycle? Obviously, this is an open ended question due to the many species and different habitats, but I wanted to know what the answer is in general.

If you live in the Costa Rica rainforest then your parrot may be better off living outside in the jungle.If you live in downtown New York City then your parrot is better off living inside with you.Starvation , predation and accidents(especially in urban areas) are three main causes of early death in many species.


Need help identifying this wasp/hornet I am currently on holiday in southern France and have noticed that the house we are staying in has somewhat of a hornet/wasp problem.

Is there anybody that can help in identifying it? My best guess is a European Hornet but I'm no expert so may be wrong.

Below are some pictures. Sorry they couldn't have been of any clearer quality, they were taken through a window, and I didn't particularly feel like going out to get any closer because I've heard that some hornets can be quite aggressive even if unprovoked.

From what I saw, it has visible fur, and is around 2cm in length. The feature that led me to it being a Hornet is that the waist gets smaller before the abdomen.

This looks like a European hornet Vespa crabro to me. Wasp-like appearance, red on head and thorax and base of the abdomen. And the legs are red/dark, not yellow.

Picture from wikipedia

Hornets can be aggressive, especially if you come near the nest. Usually, European hornets are actually not really interested in people (unlike other wasps). But if there are many around your house, it is likely the nest is near, so be careful and perhaps contact the owner of the house.


What's unique for vitamin B-12 group? I've been trying to figure out what makes the vitamin B group really big with 8 vitamins.
Chemically they have different structures.
Solubility: not only vitamins from this group are water soluble vitamins (also vitamin C).
Function: not only this group of vitamins are cofactors for metabolic processes.

So what's the reason for this grouping, or why we can't include other vitamins in this group?
Also, what does the letter B stands for?

The common scientific belief around 1900 was that the only dietary components needed to support life were protein, fats, carbohydrates, and salts.[1]  In 1912 Hopkins reported on experiments showing that "accessory factors" seemed to be needed.[1]  In 1916, some of the factors began to be characterized in the paper "The Relation of the Unidentified Dietary Factors, the Fat-Soluble A, and Water-Soluble B, of the Diet to the Growth Promoting Properties of Milk."[2]  The title itself designates two factors as A and B.  Lack of factor A seemed to be associated with various problems particularly with the eyes, and factor B with a condition similar to beriberi.  Before long, another factor was found that was associated with scurvy. In 1920, the literature had a confusion of terminology in use, and Drummond, using a variant of Funk's word, proposed:

  that the substances be spoken of as Vitamin A, B, C, etc. This simplified scheme should be quite sufficient until such time as the factors are isolated, and their true nature identified.[3]

It was only later that the factors became well characterized. Vitamin B came to be known to be a complex mixture, and its components took decades to be characterized.(Wikipedia)  As components of Vitamin B came to be known, subscripts were assigned.  Some of the subscripts were assigned to compounds that later turned out to not to be fundamental and essential, and so are no longer used. Vitamin B12 took a particularly long time to characterize.(Wikipedia)

The vitamins are now well understood, and each has a specific name unrelated to the vitamin naming scheme, yet the vitamin terminology continues to be used because it is well known and useful to people at many different levels of technical knowledge. The significance of the name of the B group of vitamins is that "B" follows "A" and precedes "C" in the alphabet, and the history of discovery is still embedded in the names we use.

[1]  Hopkins FG. Feeding experiments illustrating the importance of accessory factors in normal dietaries. J Physiol. 1912 Jul 15;44(5-6):425-60. doi: 10.1113/jphysiol.1912.sp001524. PMID: 16993143; PMCID: PMC1512834.

[2] EV McCollum, N Simmonds, W Pitz. The Relation of the Unidentified Dietary Factors, the Fat-Soluble A, and Water-Soluble B, of the Diet to the Growth Promoting Properties of Milk - Journal of Biological Chemistry, 1916

[3] Drummond JC. The Nomenclature of the so-called Accessory Food Factors (Vitamins). Biochem J. 1920 Oct;14(5):660. doi: 10.1042/bj0140660. PMID: 16742922; PMCID: PMC1258930.


The role of GC content in promoting or hindering transcription This is quite a specific question, and I'm hoping someone might be able to assist in a literature hunt I've been engaged in for ages.

I study some long bacterial operons, and have noticed that the GC% content at the 3' end drops significantly compared to the beginning of the operon.

I vaguely recall hearing (I can't remember if it was from a paper or a lecture or something), that lower GC (higher AT) content can promote transcription. This sounds plausible to me since it promotes strand separation (this is how replicon origins are often defined), but I've tried several times to find a paper that might demonstrate/attest to this. The hypothesis therefore, is that the distal ends of the operon might have lower GC in order to enhance transcription as the influence of the 5' UTR promotor sequences etc being to wane over a distance.

Has anyone ever come across such a paper or has any information to confirm or deny this? Information to the contrary (e.g. high GC reduces transcription) would also suffice.

This paper suggests the opposite in mammalian cells. Obviously, gene regulation is quite different in prokaryotes, so don't know how much confidence you want to put into that one.

This paper suggests more of the same, but includes some caveats related to prokaryotes that may pique your interest. They do a pretty in-depth dive of GC content near genes from many different species, but I haven't read it closely enough to give a good breakdown.


Nerve fiber responses to intense stimuli Can one instantaneous, high-intensity stimulus performed on a nerve fiber generate a series of action potentials? Or are nerve fibers limited to one response action potential, no matter how intense the stimulus?

Short answer
It depends on your definition of 'instantaneous' and on your definition of 'stimulus'. I can safely say that secondary neurons can fire multiple action potentials to a single, short physical stimulus delivered to the associated sensory neuron.

Background
Physiologically, external stimuli are processed by sensory neurons. Sensory neurons generally work with graded potentials, not action potentials. Sensory neurons typically convey their graded response onto a secondary neuron that translates it into a frequency-modulated pulse train.

Hence, I interpret your question as "can a single, short stimulus delivered to a receptor generate multiple action potentials in the associated secondary neuron".

If sensory neurons were restricted to one action potential per stimulus, then a stimulus could only be detected in terms of its onset or offset. We can, however, sense prolonged stimuli. For example, we can perceive a continuous auditory tone and we can look at an image for extended periods without it fading away.

However, it all depends on the sensory system. A great example is the tactile system, where some receptors mediate prolonged sensations, whereas others only mediate onset or offset responses. Their associated secondary neurons are therefore classified as rapidly adapting and slowly adapting fibers.

Figure 1 shows the response profiles of various secondary neurons connected to different mechanoreceptors in the skin.

Fig. 1. Responses of various secondary neurons to tactile stimulation. Source: Mann (1997)

For example, the Pacinian corpuscle is a rapidly adapting mechanoreceptor. If it receives a static pressure difference, its associated neuron fires only a single action potential (or very few action potentials) at the start and end of the stimulus. Slowly adapting receptors causes their associated neurons to continue firing even after prolonged stimulation. Slowly adapting mechanoreceptors are Merkel's disks and Ruffini endings (fig. 2)

Fig. 2. Skin receptors. Source: Purves et al. (2001).

If you, however, mean with an 'instantaneous' stimulus a nearly infinitesimal short stimulus, then this question becomes a search for the shortest possible stimulus still capable of evoking a response in the secondary nerve fiber. In the auditory field, the shortest acoustic stimulus possible is probably the click stimulus, which is akin to a pulse stimulus. An acoustic click is hence about the shortest possible stimulus known to activate a sensory neuron. An acoustic click can be as short as 30 microseconds. A short stimulus like that, however, still evokes multiple action potentials in auditory nerve fibers (Parham et al., 1996). Admittedly, due to the mechanics of the inner ear, most notably the basilar membrane and the travelling wave the click evokes, the factual physiological stimulus may be longer, but in the auditory field at least, tens of microseconds is about as short as it gets.

Hence, I would answer "yes, instantaneous stimuli can evoke multiple action potentials in a given nerve fiber'.

References
- Mann. The nervous sytem in action (1997)
- Parham et al., J Neurophysiol; 76(1): 17-29
- Purves et al., Neuroscience. 2nd ed. Sunderland (MA): Sinauer Associates (2001)


Why does ant queen keep the eggs out of her hive? I have captured an ant queen and now I'm trying to create an artificial ant nest.

I have noticed that though she has dug a hole to hide in, she keeps the eggs out of it unless she feels that they are in danger.

I have two theories explaining why she does that:

Ants naturally put eggs in sunlight to keep them warm. In her situation, they are not gonna be any warmer of course - the jar is whole about the same temperature.
She is digging a nest and she needs some space. If this is true, where is all the dirt?

According to various websites and literature I found,

Starting a new colony

During the mating season, Queen Ant grows wings and mate with male (flying) ant. In most of the species the queen will fly away to a new place where, she will loose her wings and dig a tunnel. She may lay eggs inside or outside because of the humidity and temperature, mostly they wait till spring, so that the humidity is high as well as warm temperature.

For laying eggs she will dig a tunnel inside and close the gates. She won't eat or move and completely avoid light, if the eggs are unhatched or some other problem occurs she will eats her own eggs. After around 8-10 weeks eggs will pop and you will get new worker ant babies. They will form the hive and feed the queen ant.

More info: http://antnest.co.uk/colony.html


Anomaly in growth of fungus in Potato dextrose broth.. turbidity is not seen in one flask I have inoculated six flasks of 200 ml potato dextrose broth, one of which does not show any turbidity and the medium is clear with a fungal disc in it.

All were inoculated at the same time and from the same pure fungus culture.

What might be the reason for this anomaly?

Several explanations are conceivable. Knowing what type of fungus you are working with and how exactly you proceeded to inoculate the cultures could help narrowing down the possibilities.

Here are some possible explanations:

Since you inoculated six liquid cultures from the same stock culture, the process might have been too long. Let me explain. Most fungi are strictly aerobes and do not tolerate well even short lack of oxygen. So, as I can guess, while you were inoculating the dextrose broths one after the other, the stock culture just remained unaerated on your bench. Since it can take a few tens of minutes to prepare everything and to proceed to the inoculations, it is possible that while you were doing so, the physiological state of the fungi just kept deteriorating, to such a point that one of the last inoculations did not contain enough viable cells to initiate a growth in the broth.
You might have forgotten to shake the stock culture just before taking the sample used in order to inoculate the broth. So it is possible that all the biomass in the stock culture was sedimented and you just inoculated your broth with the supernatent.
Also, a classic mistake is to mix up some of your broths. You think that you have inoculated all six broths with the stock culture, but maybe you unintentionally skiped one, or maybe you inoculated the same broth twice.


How does soap affect membrane permeability? Which component of the membrane does it affect? In a lab we used distilled water + 3 drops of soap to examine how beetroot would be affected by it. I believe the beetroots membrane denatured and a red pigment leaked from it. However, I cannot explain why this has happened. Can anyone explain the topic question to me?

@mdperry answered well. If you need some diagrams to help with understanding, this article Should be helpful.

As you surmised, when you add detergent, it is lysing some cells of the beetroot that contain pigment.  That pigment then gets released into solution.  I've annotated the image below for the micelles that gets formed, except I spelled it wrong :/


Did cyanobacteria commit evolutionary suicide by producing oxygen? I heard this story from one of my friends:

  Cyanobacteria can convert carbon dioxide into oxygen through
  photosynthesis, so the concentration of oxygen in the atmosphere kept
  going up over a long period after their appearance. Finally, those
  oxygen poisoned cyanobacteria through some mechanism, which
  effectively killed many of them. As a side effect, the oxygen produced
  lead to the evolution of fishes and other fantastic creatures,
  including human beings.

I wonder whether it is true. After some searching, I found that cyanobacteria can perform photosynthesis. However, I can't tell whether oxygen is poisonous to them.

Oxygen is, indeed, highly toxic to cells, due to its oxidizing power, i.e., the ability to remove electrons from another substances. Since the first carbon-reducing organisms started to increase the amount of molecular oxygen in the atmosphere, more than 2 billion years ago, life on earth has been dramatically changed by this compound: you can even consider that aerobic respiration appeared originally as a mechanism of reducing the toxic molecular oxygen to the innocuous water.

Today, organisms that use water to reduce carbon dioxide, releasing oxygen as a by-product, have molecular mechanisms (as aerobic respiration, for instance) to protect them from the very oxygen they produce.

But your question is quite interesting: how did the first photosynthetic organisms protected themselves against the oxygen they started producing?

This is a catch 22. An interesting solution was proposed by a team of geobiologists from Caltech: There was a little amount of molecular oxygen in the ocean's water before the appearance of photosynthesis. This small amount of oxygen was able to promote the evolution of biochemical mechanisms protecting organisms from its toxicity. Some of those organisms, then, were capable to develop photosynthesis and protect themselves against the huge amount of oxygen that they started releasing. According to the team:

  Low levels of peroxides and molecular oxygen generated during Archean and earliest Proterozoic non-Snowball glacial intervals could have driven the evolution of oxygen-mediating and -using enzymes and thereby paved the way for the eventual appearance of oxygenic photosynthesis.

Source: Liang, M., Hartman, H., Kopp, R.E., Kirschvink, J.L. and Yung, Y.L. (2006) "Production of hydrogen peroxide in the atmosphere of a snowball earth and the origin of oxygenic photosynthesis", Proceedings of the National Academy of Sciences, 103(50), pp. 18896–18899. doi: 10.1073/pnas.0608839103.

EDIT: according to your comment, all you want to know is "whether cyanobacteria is able to survive oxygen". Well, that's even easier to answer:

Cyanobacteria can perform aerobic respiration. That means that they can easily use protons and electrons obtained from organic matter to reduce molecular oxygen to H2O:

  Cyanobacteria... are among the very few groups that can perform oxygenic photosynthesis and respiration simultaneously in the same compartment,and many cyanobacterial species are able to fix nitrogen. Therefore, they can survive and prosper under a wide range of environmental conditions.

Source: Photosynthesis and Respiration in Cyanobacteria


Are restriction enzymes active at −20 °C? I have digested my DNA with NotI enzyme and put it in the −20 °C freezer without heat inactivating it. Can restriction enzymes work at −20 °C? Should I expect STAR activity?

Enzymes have temperature optima based on the organism they were isolated from. So I would predict the there is virtually no activity at −20 °C. Another consideration is that the reactions are likely to be frozen solid, so that would limit diffusion, and also slow it down. But the real question is: what are you afraid of? Just the star activity? Even if there were star activity, would that adversely affect your experiments?


How do neurons inverse an action potential? See the following figure (source):

The pathway on the right (SN $\rightarrow$ interneuron $\rightarrow$ F Neuron $ \rightarrow $ flexor muscle), is explained as follows:

  The action potential in the sensory neuron invades the synaptic terminal of the sensory neuron causing the release of transmitter, and subsequent excitation of the postsynaptic interneuron colored black.  This neuron is called an interneuron because it is interposed between one neuron (here the SN) and another neuron (here the MN).  The excitation of the interneuron leads to the initiation of an action potential and the subsequent release of transmitter from the presynaptic terminal of the interneuron (black triangle), but for this branch of the circuit, the transmitter leads to an IPSP in the postsynaptic flexor (F) motor neuron (colored red).  The functional consequences of this feedforward inhibition it is to decrease the probability of the flexor motor neuron becoming active and producing an inappropriate flexion of the leg.

Specifically, it states that but for this branch of the circuit, the transmitter leads to an IPSP in the postsynaptic flexor (F) motor neuron. But it doesn't give an explanation of how this works.

How can a neuron generate an inhibitory postsynaptic potential when it is given an action potential? Can this specific neuron inverse the signal? How does that work?

The University of Texas site where you obtained this picture states in section 6.7:

  What about the transmitter substance that is released by the inhibitory interneuron in the spinal cord? The transmitter substance is glycine, an amino acid which is used frequently in the central nervous system as a transmitter that produces inhibitory actions. It is not the most common, however. The most common transmitter with inhibitory actions is gamma amino butyric acid (GABA).

Glycine receptors activate a chloride-selective transmembrane channel, which is predominantly expressed in the spinal cord and brain stem (Rajendra et al, 1997). Chloride hyperpolarizes the neuron, thereby inhibiting the motorneuron controlling the flexor muscle, and thereby facilitating the extensor muscle to contract. If the opposing flexor muscle would not be inhibited, the extensor muscle would be counteracted and the knee jerk reflex would be less efficient, if present at all.

Typically, an inhibitory interneuron will only release inhibitory neurotransmitter. In the example here, the opposite circuit to bend the knee would activate the flexor muscle. This would be accompanied by opposite events. However, the inhibitory F neuron above in your figure would not reverse its action though, it will simply be silent, thereby allowing the acetylcholine from the E neuron do its job. In more general terms, neurons cannot reverse their action from inhibitory to excitatory. Their outputs are typically simply the release of a pre-defined vesicle pool, which is a yes/no event without further qualities. In other words, an inhibitory neuron will be inhibitory and it cannot change the nature of the neurotransmitters released (excitatory versus inhibitory) based on different inputs.

Reference
- Rajendra et al, Pharmacology & Therapeutics (1997), 73(2): 121–46


Are there species that occupy several roles in the food hierarchy? Are there species that occupy several roles in the food hierarchy?

By role, I am referring to producer, primary consumer, secondary consumer, tertiary consumer, quaternary consumer and so on.

Examples of more specific questions

Are there species that are both primary and secondary consumer?
Are there species that are primary consumer, secondary consumer and a tertiary consumer?
Are there species that are both producer and primary consumer?

Food hierarchy and food web

Ecological trophic interactions are better represented by food webs rather than simple hierarchical relationships. As a consequence, the concepts of primary/secondary/tertiary/... consumers sometimes poorly apply to reality.

Obligate and Optional

Many species are able to feed on a various source of nutrients. As a consequence, a species can be a primary consumer under one environmental condition and be a secondary consumer under another. Such species might eventually almost never be both a primary and a secondary consumer at the same time and it renders the classification of species into one or another category a little more arbitrary.

How much does one need to eat to belong to a given category?

Note also that species like the cat, for example, are generally considered as being just carnivorous while in reality they often eat a very small amount of plant material. They also indirectly consume plant materials that are present within the gut of their preys. Such cases make the categorization more arbitrary again

Examples

Primary, secondary and tertiary consumer

This one is pretty easy. Humans, pigs, bears, corvids and catfish are all examples of species that are primary, secondary and tertiary consumer all in the same time. In other words, humans are omnivorous.

I am currently preparing a stew for tonight $\ddot \smile$. There are a number of vegetables and a little bit of pork (which itself is omnivorous). Tomorrow, I'll make some salmon (which is a secondary consumer as it mainly feeds on zooplankton).

Producer and secondary consumer

Carnivorous plants are able to photosynthesize and to capture animals. Most animals they capture are often best described as a primary consumer but some carnivorous plants small fish that feed on phytoplankton or even mice and frogs according to this video.

Producer and primary consumer

Parasitic plants (such as the common holly) are able to both photosynthesize and parasitize other primary consumers (it therefore also is a primary consumer if we equate parasitism to consumerism).

The eastern emerald elysia (a sea slug) feed on algae and is able to photosynthesize (using the chloroplasts of its preys).

Producer, primary consumer and secondary consumer

I cannot think of any examples right now but I would bet that it exists (eventually in a chemoautotroph species and eventually in a species that has a various life cycle).


Why the length constant of passive current flow isn't depend on the membrane capacitance? I read that the equation for the length constant for passive conductance along a neuron depend on the resistance of the plasma membrane, the intracellular axoplasm and the extracellular medium. My question is why it's not dependent also on the membrane capacitance, since it can also affect how far the current can propagate (if for example the capacitance of the membrane is large, more negative charge will be on it's intracellular side, and will cause to the positive current to attract to the sides of the membrane).
Thanks!

Length constants are defined in the 'steady state' regime of constant voltage; capacitance is important for time-dependent electrical functions but disappears in the steady state.

In a real neuron, where you have other time-dependent (dynamic) features like ion channel opening, time constants and length constants interact to determine how current flows in a length of neurite, as you intuit, but these passive properties by themselves are insufficient to describe that behavior: you need to also consider ion channel gating and conductances.

See also https://en.wikipedia.org/wiki/Cable_theory - note how the capacitance is always multiplied by a changing voltage dV/dt in the differential equations.


By just looking at an unlabeled picture, how do you know it is a protein? I'm learning about proteins and need to understand this concept. What makes this colourful ball of squiggles identifiable? Why is it a protein, and not any other biomolecule (like DNA for example)? What are the colours showing? What are the variations in the shape of the image?

Basically, the question is: What is this image trying to tell me about this protein?

Shapes
This is a common way of illustrating a protein and is often called a "protein cartoon". There are other common ways of illustrating proteins.
This cartoon shows you where α helices are (spirals) and where β sheets are (arrows) which are important structural elements. The strings connecting those structural elements are flexible "loop" regions.
If you want to query this against other structures and see which protein it is, check out PhyreStorm. You'll need the PDB file, not just an image.
Colour
The colouring is also common. The N-terminus (the first amino acid) is coloured blue, and the colours go through the rainbow to red, the C-terminus (the last amino acid in the polypeptide chain).


Is Zymase, A Complex of Enzymes? Which ones? Some websites state that the enzyme zymase (which I understand to be a complex of several enzymes) is responsible for catalyzing glycolysis in order to produce pyruvate.
On the other hand, some other websites state that zymase is responsible for catalyzing the conversion of pyruvate to acetaldehyde, and acetaldehyde to ethanol and carbon dioxide.

Which one of the above is correct? And, what are the names of the enzymes that are collectively called zymase.

I thank you for your time and consideration. Good day!

This is all correct it seems, but maybe the term is more of historical interest rather than current science.

Zymase is a term which is no longer in use in the scientific literature.  It seems to have disappeared in the 1950s.   The latest reference I can see is 1970s.

The reason seems to be that Zymase was purifiable from yeast with 19th century techniques.  The term was coined in 1897.  This is probably because in brewers yeast the Zymase components are either in a protein complex or contained within a compartment in the cell that could be separated from the rest of the organism.  Here's an early reference - german isn't so great.

The Zymase activity was shown to vary from one strain of yeast to another, which makes the discovery seem more a manifestation of the physiology of that one strain of yeast.

Later work showed that Zymase activity was organizable into a more universal set of genes which are conserved in all living things and called the 'citric acid cycle' or the Krebs Cycle. Krebs performed his work without reference to Zymase, where biochemicals were added to a culture and their transformation tracked. So, Zymase seems more like a historical footnote...

Wikipedias' entry sounds as if the extraction was not very pure - its called a 'press juice' so I think it would be difficult to describe exactly which specific enzymes were in Zymase.  I'd naively assume that nearly all the citric acid cycle enzymes would be involved in Zymase activity, where observed.

Many of the enzymes in the citric acid cycle form large complexes with themselves and other of the enzymes, which might be responsible for the original discovery of Zymase.


How were genes located before the development of bioinformatics? I would like to know the detailed procedure of how scientists in earlier time were able to locate genes like how we were able to locate Huntington gene in 1983?

The earliest genome maps were constructed from Escherichia coli by abusing conjugation of special Hfr-mutants. I'm assuming you are somewhat familiar with bacterial conjugation - the process of transferring genetic material between bacterial cells.

Usually, only mobile plasmids are transferred. They carry the necessary tra-genes for the construction of the sex-pilus, replication and transfer system. They also need the oriT-site (origin of transfer), at which transfer is initiated. A famous mobile plasmid is the F-plasmid.

Some mutant cells integrated the F-plasmid into their main chromosome via recombination. Thus, they are able to transfer their whole genome to a recipient cell. These strains are called Hfr-strains (high frequency of recombination) and they were used intensely in early genome mapping.

They discovered, that it takes roughly 100 minutes for a Hfr strain to transfer its entire genome to another cell. By interrupting conjugation (e.g. by vigorous shaking) the transfer was interruped and the genome could be divided into sections by transfer time (10min, 20min, 30min and so on).

The function of the genes (or genome sections) was revealed by mating Hfr strains with defective mutants. If the mutant was unable to grow on saccharose for example, several conjugation experiments with different mating times were conducted. When a mutant was able to grow on saccharose again after mating, the transfer time was checked. If the strain was able to grow again after 30 minutes of conjugation, but not after 20, they knew the genes necessary for saccharose growth lay in the 20 - 30 min region.

It took a painstaking amount of experiments with a wide range of mutants to construct the first map of E. coli genes, but it was achieved before even the nucleotide sequences were known.


How do mutations actually occur? DNA replication seems so mechanical- the DNA polymerase just running along the template strand. I just don't understand how mutations can arise. When it comes to substitutions, I get that a wrong nucleotide may just bind and it won't be as strong a binding as with the complementary base, but I suppose it can happen. However when it comes to mutations such as insertions or deletions, I dont understand how the DNA polymerase could just skip a section of the DNA or add in extra bases. Chromosome translocation also seems like a mystery to me- almost as if the cell believes it should undergo meiosis but with the wrong chromosomes paired up and it only occurs with one pair...

I realise that this is quite a broad question, but any information on the mechanism of how mutations occur would be much appreciated :)

Mutation of DNA can be caused by an exogenous or endogenous source. Many external factors like irradiation or chemicals induce mutations. Some endogenous mutations arise from oxidative stress, insufficient DNA repair or spontaneous mutations on the molecular level.

There are many mechanisms for DNA repair like base excision repair, nucleotide excision repair, homologous end-joining or nonhomologous end-joining (Löffler, Biochemistry and Pathobiochemistry).
But it is more difficult for the cell to repair the mutation if it is present in both DNA strands.
According to your second question:

  DNA polymerase could just skip a section of the DNA or add in extra bases

DNA polymerase cannot reconstruct what was the original strand or the orientation of the strand. To prevent cell death, some DNA repair mechanisms include alteration in the genome. The DNA polymerase can reads through and the mutation will be replicated when the cell divides. Consequently, the key question is how the effects of the mutation influence the ability of the cell to survive.


Do animals have different taste preferences within the same species? Humans (especially children...) seem to dislike certain foods or drinks, that other humans seem to like. Common examples are coffee, french cheeses, olives, milk, fish and cabbage. Are there examples of animals either wild or in captivity that show the same behaviour? For example a group of primates that eat something except one or two members of the group? And if so, any clues to the evolutionary aspects of such preferences?

Yes. Intra-species variation in food preferences has been observed in

Rabbits (Bilko et al. 1994)
Copepods (Rieber 1982; Berghe and Bergmans 1981)
C. elegans (Abada et al. 2009)
Earthworms (Bonkowski 2000)
Butterflies (Jermy et al. 1968)
Beetles (Sarker et al. 2013)

I am sure most pet owners will find the existence of this variation quite intuitive. No too cats have the same food preferences.

Why such variation exist?

I can think of several possible (non-exclusive and non-exhaustive) reasons for why such variation exist?

Individuals compete. If preferences vary, it allow specialisation (inspired from @John's comment)
Phenotypic variance (whether genetic, environmental or other) is not necessarily maintained by some kind of balancing selection. You may observe purely neutral variation in preferences.
Genetic variance can explain variance in food needs and therefore it is good that preference can be plastic
Same as above but for environmental reason. Say, an individual may have different need based on its environment.
One must learn to recognize good food. There might be a tradition among family of liking specific types of food.


Why is thymine not incorporated into mRNA? I am aware that in transcription uracil bonds to adenine and not thymine. But what is it that actually prevents thymine from bonding to adenine in transcription, that is not present in replication?

Nice question! But sadly, it comes under the category of questions about which we don't know everything yet. We don't yet know how RNA Polymerase differentiates between uracil and thymine while adding nucleotides to growing mRNA chain (at least, I was unable to find research papers online), most probably because it has proved difficult to know the exact mechanism of RNA synthesis which RNA polymerase undergoes. But we do know what factors it could use to do so. For general introduction, these factors are:

mRNA chains contain NTPs instead of dNTPs. Now, TTP is very (very) rarely found in cells. So, RNA Polymerase can look for 2'-OH in nucleotide for adding base (pay attention that RNA polymerase is not known to have proofreading mechanisms, but there is growing evidence that RNA polymerase can correct a faulty base pair matching, see Thomas et al). RNA polymerases are known to be able to distinguish between NTPs and dNTPs (Svetlov et al), although the precise mechanisms in multi-subunit RNA polymerase remain elusive. Yet, this property certainly plays a role (refer to EDIT 1 for details about this).
UTP and dTTP have another basic structural difference: of a methyl group. This difference is crucial for differentiating the two, especially for DNA repair machinery. It is so because cytosine can spontaneously convert to uracil (by deamination). So, there has to be something for repair enzymes to look for while repairing mutated cytosine, and a methyl group saves thymine from repair. See the following image for comparison:

source

Just for information, we know the flip side i.e. how DNA polymerases prevent dUTP from adding in DNA chains, because dUTP is much more common than TTP. Simply saying, they don't. Mutations can (and do) occur, leading to faulty addition of dUTP in DNA. But, this is where repair machinery helps. Cells contain an enzyme, uracil DNA glycosylase, which replaces uracil by thymine in DNA (Longo et al). So, until we find the exact mechanism for RNA polymerase, you can assume that it uses much similar mechanism for proofreading (along with the first one of course).

EDIT 1: I will add some details about the mechanism of base pair matching by RNA polymerase as just leaving the point at yet, this property certainly plays a role makes the answer misleading to some people. But, because putting the whole mechanism here would make the answer too long and also out-of-scope (keeping in mind you asked 'why', not 'how'), I'll try to keep this part as small as possible. Giving a diagram for better understanding:

Pay attention at the Tyr639 and His784 (sugar discriminators), this is how the RNA polymerase distinguishes NTP from dNTP. It has also been shown that removing Tyr639 will convert the RNA polymerase to DNA polymerase(!), though removing His784 would just decrease its activity, suggesting its role to be minor w.r.t. Tyr639. For more information, have a look at this page from Brooklyn college website.

EDIT 2: In another answer, the answerer says RNA synthesis requires rNTPs instead of dNTPS as precursors, but does not explain why it is so (which is indeed an important part). So I'll add that part in my answer. It can be explained by following points:

The sugar discriminators of RNA polymerase (describe above) do not allow dNTPs to add to the growing chain. Thus dNTPs cannot act as substrates for RNA synthesis.
The enzyme for synthesis of thymine (dTTP) is thymidylate synthase, which requires dUMP as substrate. Thus, it is not possible to create rTTP instead of dTTP.
Conversion of uracil to thymine requires energy, meaning uracil is energetically less expensive than thymine. This also directly explains (partly) why mRNA doesn't incorporate thymine into the chain.
Degradation of mRNA requires an enzyme ribonuclease which cannot degrade dNTPs. Also, in the mechanism of degradation of mRNA, 2' -OH plays a role. This can be explained by diagram below:

As is visible, 2' -OH is an important part for RNA degradation. Thus, it wouldn't be possible to degrade mRNA in this way if it contained dNTPs.

References:

Matthew J Thomas, Angelina A Platas, Diane K Hawley, Transcriptional Fidelity and Proofreading by RNA Polymerase II, Cell, Volume 93, Issue 4, 15 May 1998, Pages 627-637, ISSN 0092-8674, http://dx.doi.org/10.1016/S0092-8674(00)81191-5.
Svetlov V. Vassylyev D.G. Artsimovitch I. Discrimination against deoxyribonucleotide substrates by bacterial RNA polymerase J. Biol. Chem.  2004 279 3808738090
Mary C. Longo, Mark S. Berninger, James L. Hartley, Use of uracil DNA glycosylase to control carry-over contamination in polymerase chain reactions, Gene, Volume 93, Issue 1, 1 September 1990, Pages 125-128, ISSN 0378-1119, http://dx.doi.org/10.1016/0378-1119(90)90145-H.
Dziuda, D.M. (2010). Data Mining for Genomics and Proteomics: Analysis of Gene and Protein Expression Data. Wiley
Roberts, Gordon C. K. et al. “THE MECHANISM OF ACTION OF RIBONUCLEASE.” Proceedings of the National Academy of Sciences of the United States of America 62.4 (1969): 1151–1158.


Why do the feet of the Gecko Lizard not stick to Teflon surfaces? I have noticed that lizards feet can stick to walls but not to Teflon surfaces?

Why is that?

Gecko feet have been the focus of a lot of research over the past 10 years.

Their ability to walk up vertical or even hanging from ceilings is attributed to tiny branching hairs growing from the pads of their feet.  The hairs branch down to the size of 100s of nanometers and its believed that this gives them large surfaces at the molecular scale, giving them a strong van der Waals adhesion force.

Teflon, being hydrocarbon chains covered with 'hard' electronegative flourine atoms doesn't provide the same attraction to the hairs, as van der Waals forces rely on mutual polarizability of atoms in close contact. That is to say, electronically fluffy atoms can stick together more readily.


Tree Identification - California Bay Area I've seen these trees in the Bay Area in Mountain View and Fremont, and have been searching for different pine tree varieties that have wider canopies. Does anyone here know what trees these are, they are very beautiful.

Here is the link to the exact location where I saw them recently:
https://goo.gl/maps/NSfAXZSgzypWXKqj9

For California trees, my go-to is A Californian's Guide to the Trees Among Us by Matt Ritter (Heyday, 2011).  California trees can be challenging due to the extremely varied habitat and many introductions over the years.
Your trees appear to be younger specimens of Pinus pinea or the Italian Stone Pine, based on the description on page 14 in Ritter. No other conifer in the book matches better.  Going to Wikipedia the description also seems to fit, in particular they mention "...in youth it is a bushy globe..."  There is also good information at Kew where I found this image, which looks to be very similar to what you observed.
Of course, if you can visit the location again you can check for needles in pairs, and orange-brown scaly bark.


What is the minimal focal length of the human eye? What is the minimum length to which the focal length of our eye can go, even when  considering the blurred images too.

Short answer
The focal length of the average, healthy, adult human eye at near-point is about 18.5 mm. Young individuals can accommodate their lenses further to a focal length of around 15.4 mm.

Background
The focal length of the human eye is the distance between the lens and the retina when an object is in focus (Fig. 1). Therefore, the ...even when considering blurred images too part in the question doesn't make much sense. So, I will focus my answer on sharp images only (pun intended).

The lenses of the eye are thicker in the center than at the edges, and hence positive and converging lenses. They form an inverted image on the photosensitive layer in the back of the eye - the retina (Fig. 1) The retinal image is shaped by two lenses: 1) the cornea with a fixed focal length and 2) the eye-lens, which is a lens with variable focal length through shape changes (Fig. 1) called accommodation and is mediated by the ciliary muscles (Kolb, 2012).

When the ciliary muscles are relaxed, the focal length of the eye-lens is maximal and the distant objects are in focus (infinity). When the ciliary muscles contract they shorten the focal length of the eye-lens to bring nearer objects into focus. The two limits of this range are called the far-point, (ciliary muscles relaxed), and the near-point (maximal accommodation) (source: University of Colorado, Boulder).

The distance between the eye-lens and the retina is about 20 mm. When an object is far away from the eye (infinity), the image is located essentially at the focal point. Therefore the focal length of the cornea and the eye-lens should be about 20 mm when the muscles of the eye are relaxed. The lens strength is the reciprocal of its focal length in meters. Hence, the strength of the cornea and the eye-lens at the far-point is about 1/0.020 = 50 diopters (source: University of Colorado, Boulder)..

When an object is located at the near-point (the closest point at which an object can be brought into clear focus on the retina), the focal length of the cornea and the eye-lens must be changed so that the image is formed on the retina, which is still 20 mm away. The typical near-point in an adult is 25 cm, corresponding to a focal length of the cornea and the eye-lens of 18.52 mm using the standard ray-tracing rules of lenses. Hence the strength of the cornea and the eye-lens must now be about 1/0.01852 = 54 diopters. In other words, the muscles of the eye can provide an accommodation range of 4 diopters (source: University of Colorado, Boulder).

Kids can, however focus to points as close as 6.5 cm away, i.e., 15 diopters worth of optical power, i.e., a minimal focal length of 15.39 mm.

Fig. 1. Human eye. Upper panel: non-accomodated relaxed eye. Lower panel: accomodated eye. source: Khan Academy

Reference
- Kolb, Gross Anatomy of the Eye. In: Webvision. The Organization of the Retina and Visual System, Moran Eye Center (2012)


Does the MS2 RNA binding protein have any translational repression effects? Reposted from Quora: http://www.quora.com/Does-the-MS2-RNA-binding-protein-have-any-translational-repression-effects

I'm thinking of the MS2 protein binding to its RNA hairpin target. Would the interaction of the MS2 protein to the hairpin placed upstream of a ORF cause any translational repression?

I assume you are talking about the mTAG visualization technique for mRNAs (1). You are probably familiar with it, but the OFR of interest is tagged with MS2L sequence downstream of it and upstream of the 3'UTR. There is also a modified version, in which you can visualize both the mRNA of interest, and the protein that is translated, see the figure below (2). Haim and colleagues found that yeast expressing mCherry and MS2L tagged ATP2 grew on glycerol-containing media, which would require efficient translation of ATP2.

So I would assume that there is no translational repression if you tag the mRNA downstream of the ORF. Unless you have a very good reason to tag the ORF of interest with MS2 upstream of the start codon, I wouldn't do it, because these stem-loop structures would most probably stall translation, as mRNA secondary structure has been implicated in translation initiation efficiency.


What is the name of this tree with yellow flowers? Location is South India,

Tree is very large, but leaves are very small.

Image: http://imgur.com/fgtFzVD

Looks like this one: https://en.wikipedia.org/wiki/Peltophorum_pterocarpum
Peltophorum pterocarpum or the Copperpod


Can life forms exist from simple structures not made of the four bases? I understand that all life forms on the planet are made from adenine, gauatine, cytosine and thymine, which chemically joined together to form RNA or DNA (correct me if I'm wrong). This goes on to form all complex life as we know it.

I was wondering if it was possible- even studied theoretically- that other life forms could exist made of different elements and compounds, perhaps let's say iron, cobalt or tungsten? Or are the 4 bases the only possible way of life as we currently know it?

So this question is difficult to answer because it has some errors in it, in that lifeforms being dependent on rarely used elements is a different question than lifeforms using different DNA bases, but I will answer both.

So for the question about whether or not organisms could exist that use DNA bases not found in organisms on earth, the answer is certainly yes.[1,2]

The above reference shows a very elegant example of completely synthetic DNA bases being incorporated into E Coli and propagated in culture without providing any noticeable negative effects. This provides strong support that life on Earth developed around the same 5 bases (CTGAU) by chance.

As for whether or not organisms could rely heavily on elements other than H,C,N,O, and P, this is certainly possible and evident already here on Earth. Extremophiles are a general class of organisms that have some pretty interesting properties to them. Some metabolize sulfur or metals, others live in really extreme temperatures or in areas of high radiation.

So really yes in both cases, life can really take numerous shapes and forms even when it seems completely impossible for them to do so.


calculate the number of heterozygotes The ability to taste PTC is due to a single dominant allele "T". You sampled 215 evolution students, and determined that 150 could detect the bitter taste of PTC and 65 could not. Assuming this trait is in Hardy-Weinberg equilibrium in this population and that there are only two alleles, calculate the number of heterozygotes for this trait there are in the population.

Hardy-Weinberg law gives the frequencies of genotypes from allele frequencies: $p^2 + 2pq + q^2$

Because the allele "T" is dominant, the frequency you're directly measuring through the experiment is the addition of $p^2$ and $2pq$.

$$p^2 + 2pq = 150/215 ≈ 0.6976$$

solving for $p$ (and replacing $q$ by $1-p$) gives:

$$p = 1 - \sqrt{\frac{13}{42}} ≈ 0.45 $$

The frequency of heterozygotes is given by:

$$2p(1-p) ≈ 0.4950 $$

And the number of heterozygotes in a population of 215 individuals is given by:

$$215 \cdot 0.4950 = 106.43$$

That sounds very alike what you wrote in the comments!


A few questions regarding immunology I know that there is a variable region on antibodies which can recognize a wide variety of antigens, and that germinal centers create more "fit" antibodies to respond to an infection.

So I was just wondering:

Does this process itself evolve? Only vertebrates have this type of immune system if I understand correctly, do we actually get better (faster/more efficient) at responding to disease?
Is there any antigen which antibodies don't recognize?
Can an organism be so efficient at this process of immune response, that it essentially never gets sick or dies of disease?
There are cases where organisms contain viruses which do not harm them. Could an organism have this relationship with all viruses? As in, no virus is actually a disease to them?

This is a pretty broad question, but I will try to give an answer:

This process will undergo further evolution over time, no question. It has evolved into the current state and there is no reason to assume that this ended. When there are mutations which prove advantageous, they will evolve. This may also involve a faster response time for example, but we can of course make not definite claims about it.

There are antigens which are not recognized by the immune system, the process is called molecular mimicry. In it, microorganisms mimic molecules or structures which are found inside the body of the infected person and which are therefore not recognized by the immune system (if the immune system recognized self-antigens, this leads to autoimmune diseases). Have a look at the references 1 and 2 for more details.

This is a rather theoretical question. Our immune system is really efficient in clearing potential threats before you get a real infection. You can see the difference when you compare healthy individuals with persons which are immuno suppressed because of a transplantation. These persons need to be very careful about their environment in avoiding the exposure to potential pathogens. And they easily get infections. Additionally microbes evolve to evade our immune system. So I think the answer here is no.

These are viruses which co-evolved with the organism, an example would be the ebola virus in certain fruit bats. Here it does no harm, while it is a big problem for humans. As there is a really, really big number of viruses available in nature, it is quite unlikely that we learn to tolerate all of them. Additionally viruses mutate and change over time, so we would have to learn again to live with them.

References:

Molecular mimicry
Molecular mimicry and immune-mediated diseases.


Convergent evolution of fruits Many fruits are not homologous, originating from different parts of a plant. Yet they all have similar properties:

Ripe fruits all have yellow to dark red color
They all have a lot of water and sugars, even in dry climate where water is in shortage.
Besides sugars they usually have acids making them sour to sweet in taste

I understand that these possibly developed as a contract between the plants and the animals in that the plant would provide beneficial fruit tissue so that the animal to swallow the seed so to propagate it for longer distances.

But I wonder, why there are no fruits that would imitate the taste of meat, nuts, seeds,  foliage, grass, mushrooms, roots, milk and other food sources, common for the animals?

Why there are no salty fruits for instance or those rich in proteins rather than sugar and water, or having the smell of carrion?

Howe and Smallwood (1982) provide a nice review of the many methods of seed dispersal that have evolved in plants. The review is broad but they do have a section on frugivory.  They highlight hypotheses developed by McKey, and Howe and Estabrook (see Howe and Smallwood for citations) that suggest plants may use one of two strategies.

One strategy is the "high investment model." Plants invest lots of resources to produce large seeds and nutrient rich fruits. THe hypothesis is that these types of fruits tend to attract relatively few but specialized frugivores that are will to invest the energy necessary to find these types of fruits and their associated nutritional reward.

The second strategy is called the "low investment model." In this model, plants invest little in individuals seeds and fruits but produce an abundance of them. The hypothesis is that these types of fruits will be eaten by as many different potential seed dispersers as possible. These tend to be very small or starchy although they can still be colored as you describe.

Other factors also come into play. For example, tropical fruits tend to have large seeds and nutrient rich pulp while temperate fruits tend to be smaller and offer less nutritional reward.  All of this is placed in the context of the community diversity of frugivores. The Howe and Smallwood paper was an interesting read.

A paper by Gatier-Hion et al. (1985) looked at the characters of fruit choice and seed dispersal mechanisms by tropical forest vertebrates. The showed the relationships between fruit characteristics and the corresponding frugivores. They looked at 122 different fruit species and the frugivores that consumed them.  Their results showed that fruits tended to separate along one of three axes:

Heavy, indehiscent fruits with fibrous flesh and well protected
seeds vs light, dehiscent fruits with unprotected seeds. Many of
small fruits are red,
Lots of seeds produced (typically the the large indehiscent) vs few
seeds produced, and
Juicy and brightly colored fruits vs dry and dull-colored fruits.

Figure 2 from Gautier-Hion et al., shown here, shows the relationship between different frugivores and the fruit types.  Notice that small granivores, which are frugivores, don't eat large, juicy fruits. They consume lots of small green or brown grains that are easy to manipulate and produced in high quantities.  Squirrels are similar.

Thus, as you suspected, fruits and seeds have evolved in response to their frugivores but the fruits do not always have the traits you listed. I think, but do not know for certain, that the fruit traits you list are the result of selection being driving by the frugivores. The sugars provide lots of quick energy, which is necessary for active animals. The carbs probably provide a much greater nutritional reward than salts or proteins (which are present anyway). The colors may help the fruits to stand out against the green foliage (for organisms that are not red-green colorblind). These traits probably provide the greatest reward (lots of energy) with the lowest energy investment by the frugivore (easy to find).

Throughout, I've assumed natural conditions and not fruits modified by artificial selection for human consumption.

Literature Cited

Gautier-Hion, A., et al. 1985. Fruit characters as a basis of fruit choice and seed dispersal in a tropical forest vertebrate community. Oecologia 65: 324-337.

Howe, H.F. and J. Smallwood. 1982. Ecology of seed dispersal. Annual Reviews in Ecology and Systematics 13: 201-228.


How many people in the world have bad eyesight? I was watching this ted.ed episode and heard it was around 500,000 but that didn't sound right-- does anyone know?

I do know that the TED Ed episode linked (at 3:50) actually says that 500 million people have myopia or hyperopia, which is 1000 times what the question says, and which seems more reasonable for a world of 7.4 billion people (skewed towards the young).


Why there is no vaccine against Human Immunodeficiency Virus (HIV)? I was informed by my teacher that this retrovirus changes its RNA, so there is not a drug which can recognize the RNA and somehow inactivates it. Are there any other reasons explaining why there isn't a vaccine for the HIV?

One of the reasons we don't have an HIV vaccine yet is we've only been trying to make one for a little over 30 years. It can take a long time to develop a vaccine. Beyond that, there are a number of specific challenges.

One of them is that, yes as your teacher said, the virus is highly variable. Specifically, the parts of the viral proteins involved in binding and infecting a host cell are highly variable. There are a number of other challenges. One important and related challenge is that, unlike with many vaccine preventable diseases (e.g., measles), an successful HIV vaccine will have to entirely prevent infection  rather than just control and clear infection without developing disease. Once a reservoir of infected cells is established, the opportunity for clearance is gone. This makes the production and maintenance of high titers of neutralizing antibodies that much more important.

There is a very good review of the challenges and current directions of HIV vaccine development here


Optogenetics - How do microbial opsins work? I'm just introduced to the optogenetics method and am having some trouble grasping the genetics (of the optogenteics) part of things.

So we have Retinal and Opsin that form Rhodopsin molecule that serves as a light-gated ion channel (which is, needless to say, very cool).

What is the process in which a cell population is targeted and implanted with these Rhodopsins?

And where does the microbial opsin gets into picture?

My main resource, so far, was - Optogenetics - Method of the year/Nature.

Thanks!

There is nothing special about the use of rhodopsin when compared to making a cell express any transgene. This question can then be read as:

  What is the process in which a cell population is targeted and implanted with a gene of interest?

There are many ways, which depend on the specific cell type and on whether you want to do it in vitro, in vivo and in which species, and it would be very complex to explain them all in detail here, so I will limit myself to two approaches that are popular when doing optogenetics in rodents: viral infection and transgenesis.

Viral infection uses an inactivated virus to deliver the transgene. Essentially you engineer a piece of DNA with the gene for the bacterial opsin of interest and you put it in a viral envelope, that is a series of proteins that form the "body" of the virus and that contain its genetic material.
You then inject the virus in the desired zone (e.g. in a specific brain nucleus) and wait for it to infect the cells around the injection site. A week later those cells will express the transgene.

For (at least, I think) historical reasons the first type of viruses used for this approach were lentiviruses. These, however, are a tad more complex to handle (especially as they require specialised rooms where they can be handled safely) so adeno-associated viruses (AAV) are becoming more and more popular.

Note that the virus is inactivated, that is, it cannot replicate, just infect the cells around the infection site, but it will not be able to spread around. This is both for safety reasons and because you want the infection to be confined to the specific region where you injected the virus.

As I was saying before, instead of putting a bacterial opsin you can put whatever gene of interest, the procedure is the same. As for the opsins, the first two that were used were the channelrhodopsin-2 (ChR2), a channel sensitive to blue light and that can be used to depolarize (=excite) the cells and the halorhodopsin (NpHR), a chloride pump sensitive to yellow light that will, conversely, hyperpolarize (=inhibit) the cells.
There are nowadays tens of variants of these and other opsins that can be used to drive cell activity with lights. Many of these are described in this (beware! Quite technical) review:

Optogenetics in neural systems - Yizhar et al., Neuron 2011

Transgenesis works instead by generating an animal that carries the opsin (or any other gene) in its DNA. This can be done in various way, such as by microinjection of embryonic stem cells carrying the transgene.

You can find a fairly detailed explanation of the process here: Transgenic Cells and Gene Knock-outs, well summed up by this figure (taken by the same page):

Transgenic mice generation http://9e.devbio.com/images/ch02/wt020302-2.jpg

But how do you get cell-type selectivity?
In front of the gene for the opsin you also will have to put another sequence, called promoter. The promoter is a sequence that is specific to each gene and that is used to determine which genes a cell will or will not transcribe. For instance, the promoter for the gene coding for a protein only present in muscles will be used by muscle cells but not by neurons. You can even get more specific, for instance by using promoters that are typical of a subset of cells and not other (e.g. glutamatergic neurons use a different set of promoters than GABAergic neurons, although these two sets will -at least in part- overlap). However, this means that if you want to change the cell type you are working on you will have to change the DNA vector you are using.
A commonly used approach to avoid this is that of using Cre-dependent vectors (note that this can be used both for viral infections or for transgenic animals).
Essentially you will have a mouse line which expresses a protein derived from the P1 phage, called Cre recombinase, only in the cell type of interest (again, using a specific promoter). Cre has the property of cutting DNA next to specific 34 base-pair-long sequences called loxP (with sequence ATAACTTCGTATAGCATACATTATACGAAGTTAT). Essentially, if you have loxP-[some sequence in the middle]-loxP and Cre recombinase is around, it will cut away the sequence in the middle, leaving only a loxP sequence.
Hundreds of different Cre-expressing mouse lines are commercially available nowadays, to target many different cell types in different organs.

Now, you just need a construct that allows you to express the opsin in a Cre-dependent manner. This is what was done by the group of Hongkui Zeng, and reported in this paper:
A toolbox of Cre-dependent optogenetic transgenic mice for light-induced activation and silencing. - Madisen et al., Nat. Neurosci. 2012

Without going into too much details, the idea is to flank a STOP sequence with two loxP sites. This will block transcription (that is what a STOP sequence does) unless Cre-recombinase is present.

Essentially:

Source: myself, CC-by-sa licensed, feel free to reuse it

Note that in the scheme, ROSA26 is an ubiquitous promoter, that is, a promoter used by all cells, so in this case the specificity is given by expression of Cre recombinase and not by the promoter of this construct. Also, a fluorescent reporter (e.g. GFP) is inserted to be able to visualize where the opsin is expressed.

By breeding these mice with the Cre-line(s) of your choice you can then express the opsins in the cell type of your interest.


If a non-mammal is starved of oxygen for some time, how long would it take the animal's neurons to die? This is a follow-up question to Why do neurons die so quickly (relative to other cells) when deprived of oxygen?.

I'm particularly interested in the case of reptiles, octopuses, and other invertebrates. Could it be that mammalian neurons are especially oxygen-demanding compared with the neurons of other animals?

Medically, recovery of brain function after 3 minutes of oxygen deprivation at body temperature is rare.

Further down here in 1 it indicates that at lower temperatures the time can be much longer.  At 13C, the record is 80 minutes for people.  Animals cooled to 0C have a record of recovery of three hours!  Not sure how much like themselves they feel after that though...


Have humans evolved to live longer? Do people live longer only because of better hygiene, medicine, society etc or also because they're slowly evolving to live longer under same circumstances?

Yes and no.

According to this paper, great apes and our ancestors had a life expectancy at birth of about 13 years (chimpanzees). Over a few million years of evolution, human life expectancy rose to >30 years in the 18th century. Industrialization and improved nutrition, hygiene and medicine resulted in a jump to >60 and now around 80 years in developed countries in just 200 years. The paper compares data from Sweden, but if you look at the data from gapminder.org, you see that this trend holds true for all nations (especially developing countries like India and China, who doubled their life expectancy in just 50 years).

So, while humans have evolved to live longer (as you asked in the title), due to a lower mortality and resulting increase in the age of maturity as well as the likely benefit of "grandmothers" (older, infertile females helping to feed their grandchildren) (discussed in this source), the recent increase in life expectancy in just a few generations is unlikely due to evolution.

While humans are still evolving, we have reduced the selective pressure. There is no benefit to the survival of the offspring when we live past 80-100 years. And comparing countries with lower standards in hygiene and medicine (I totally recommend playing with the gapminder tools), their life expectancy was still pretty low in recent years, only increasing with access to clean water, food and medicine. Comments on extending the lifespan usually refer to medical interventions to cope with the effects of aging.


What is Environmental Robustness? Is it different from plasticity? Hansen (2006) in his review uses the concept of environmental robustness independently of the other concepts of robustness (at pages 139 and 140) without defining it.

How is the term environmental robustness usually defined?

The concept of robustness (aka genetic robustness) can be further decoupled into mutational robustness, developmental robustness and maybe some others. I think envirnmental robustness is one of these sub-categories of (genetic) robustness.

Intuitively, I understand environmental robustness as something that is very close to plasticity in the broad sense. What I call plasticity in the broad sense is any phenotypic response to an environment whether or not the response is adaptive or not. Therefore, plasticity in the broad sense is adaptive plasticity + non-adaptive plasticity. I would intuitively think that a genotype is environmentally robust if the phenotype it produces varies little with environment, that is if this genotype has low plasticity (in the broad sense). Am I using a more or less standard definition of environmental robustness?

I think robustness and plasticity are different concepts, although related to each other.

I would define plasticity as the property of a system to adapt to external changes. As defined in the wikipedia page for phenotypic plasticity:

  Phenotypic plasticity is the ability of an organism to change its phenotype in response to changes in the environment.

I think this definition agrees with the one in your question.

Robustness in biological systems, however, is defined as (wikipedia article):

  Robustness of a biological system (also called biological or genetic robustness) is the persistence of a certain characteristic or trait in a system under perturbations or conditions of uncertainty.

From this article three references are cited, all of which give some definition of robustness in their introductions/abstracts:

Felix and Wagner (Heredity 2008):

  Robustness, the persistence of an organismal trait under perturbations, is a ubiquitous property of complex living systems.

Kitano (Nature Reviews Genetics 2004):

  Robustness is a property that allows a system to maintain its functions despite external and internal perturbations.

Stelling et al. (Cell 2004):

  Robustness, the ability to maintain performance in the face of perturbations and uncertainty, is a long-recognized key property of living systems.

All these definitions imply that robustness is the ability to remain unperturbed under external or environmental perturbations. In a sense this looks like the opposite to plasticity, which is the ability to change under external perturbations. Personally, I think that robustness is accomplished because biological plasticity allows organisms to compensate (with some limits) the external perturbation in order to maintain their state.


A new species of small bird? This picture is take from my village in Gujarat, India. I think it is a small bird which I have never seen before. It is smaller than an Indian hummingbird and even smaller than a neem tree leaf. You can see the leaf and the flowers. That flower's diameter is maybe a half inch so you can see how small the bird is. This bird has a very little trunk like a butterfly. You can't see this in the picture, but I saw it. This bird sucks liquid from flowers by that trunk.

Great picture and great find.  But unfortunately I don't think that is a new species of bird...or even a bird at all!

It looks like a hummingbird hawk-moth, Macroglossum stellatarum.

Here you can really see the 'little trunk' (as you described it) known as a proboscis, which it uses to feed on flowers.

Fun fact: It's believed not to be a mimic of the hummingbird, but rather an example of convergent evolution.


What is it called when an animal only has one type/variation of dentition? An example would be alligators that only have one type/shape of tooth. Not the variation in function and shape like seen in humans, which have canines, molars, incisors, etc

Homodont

You can find the term "homodont" used in Lambert et al. (2014) or on wikipedia > dentition for examples. The opposite of homodont is heterodont (wikipedia > heterodont). In mammals, a classical example of homodonts is the dolphin.


Are grasshoppers monogamous? Noticed two grasshoppers jumping together on the porch, and started wondering if they are monogamous? I am aware they have males and females.

Male grasshoppers often mate several times with multiple female, and some females will mate again after, and perhaps even before they lay their eggs. So no, they are not monogamous.

Rufous grasshoppers for example have a very special mating cycle, the male will attract other females, possibly more than one with "pursuit sounds". After copulation, he keeps her close to prevent other males from mating with her, and the females enter a defensive mode where they refuse intercourse from other males. After laying eggs however, she enters a "relaxed" mode where she is open to others for mating.

Sources:

jrank

Rufous grasshopper: inaturalist


How do I download entire human genome for local blast formatting and searching? I'm trying to make a copy of the entire human genome for local blast queries on my machine.  I understand that I need to download it from the NCBI FTP server here...

ftp://ftp.ncbi.nih.gov/genomes/Homo_sapiens

After downloading it I need to format it into a database that blast can search.  I do this using NCBI's makeformatdb command.  It is run like this...

makeblastdb -in entire_human_genome.fasta -dbtype nucl -title human_genome -out human_genome.db

My question is...  Where do I get the fasta file containing the entire human genome?  Do I download the fasta files for all 22 chromosomes, the X chromosome, and then the Y chromosome and concatenate them?  Is there a fasta file on the site containing the entire genome?  A fasta file that is not partitioned by chromosome?

You can either download and concatenate the individual chromosomes from NCBI or make your life easier and download a single fasta file from Gencode (note that that's the primary assembly, if you want the one with haplotypes then it's here).

Having written all of that, the "human_genomic" files on the NCBI FTP server are the prebuilt blast databases for humans.


Are redundant codons used in translation? I am learning about redundancy in genetics and I came across this statement in my textbook:

  more than one codon for an amino acid means that some codons are redundant - the process of protein synthesis could function without them.

I understand that codons are used to make specific amino acids. Does the statement from my textbook mean that if there are two codons which code for the same amino acid that only one of the codons code for an amino acid and not both? I know the term reduntant means that in some cases - more than one codon can code for the same amino acid - but does it also mean that some codons are not used because another codon codes for the same amino acid?

Thanks

The textbook is asserting that translation could function without redundant codons, not that it does. In reality, all possible codons are used.

See this answer on the interchangeability of codons.


mFOLD prediction result interpretation I am trying to predict the secondary structure of certain predicted pre-miRNAs through mFOLD which is the generally accepted technique for structure prediction in most studies. I am finding it hard to interpret the result and accept if the pre-miRNA which I have picked and the miRNA I have can be accepted and included in my result.

This is one predicted pre-miRNA structure with the predicted miRNA position shown in green.

Is this a good/bad structure and if so, can anyone give me a reason why. Thank you.

edit: I understand that energy levels are also something that is looked for in the prediction. In this particular figure, ΔG = -75.00 kcal/mol which I think is fine.

Sequence used for folding is

AAAAATAAAAAACAGAACCATGAGGCAGCGCACCAAGAGCGTCGTGAACGTCCGCGAATA CTTCCGCATGGACGGCAGTGGCGCCCCCGAGCAGGAGGACGACGATGACAACGATGACTG GATGGCCATCGCCATGCAGGGCGCACCGCGTAAGGTCAGCGTGGAAGTCGTTAAGCCTGG CAAGAAGGCACGCGCTCGTACGTCGACGTGTGACTCAC

and the highlighted match area is

ACGATGACAACGATGAC

So this structure should be fine because the sequence lies along a stem-loop structure.

I am worried about that bulge on the left top corner though. That doesn't affect the predictability of this structure does it?

The green region will definitely not make an miRNA: It is not a part of a stem loop. See typical miRNA structures from miRbase.

EDIT

Bulges can sometimes determine which strand is chosen as mature miRNA. However, this green region is also is unlikely to form miRNA because the stem is just 15bp.


Why is Turner syndrome rarer than Klinefelter syndrome? Turner syndrome occurs in 1-1000 to 1-5000 females, and Klinefelter syndrome occurs in 1-500 to 1-1000 males.

Why is Turner so rare even though they both are caused basically by the same mechanism?

First of all, they are not caused by the same mechanism. They are both aneuploidies, but the mechanism is different.

Turner syndrome happens when one of the gametes (most commonly father's) lacks a copy of X chromosome, or the X chromosome is heavily damaged. This means that while normal women have two X chromosomes, Turner women have only one, and nothing else.

Klinefelter syndrome happens when one of the gametes retains an extra copy of the X chromosome. This way a Klinefelter man has two X chromosomes and Y chromosome instead of one X and one Y.

As you can see - the Turner woman is lacking some genetic information, while the Klinefelter man has too much of it. Generally, having too much genetic information is much easier to survive than not having enough of it, so this explains the relative difference on the most basic level.

But, you might say, what about Barr's bodies? Don't the women use only one X chromosome in each cell? And wasn't Y chromosome almost empty?

Yes, these are an important consideration for these two syndromes. In each cell of a women's body one of the X chromosomes is inactivated and folded into a Barr's body. This inactivation is random, so part of the cells keep mother's and part of the cells keep father's X chromosome active. The trick is that the Barr body is not entirely inactive (Genes That Escape From X Inactivation). Only about 15% of the genes are active, but just the lack of them is mostly lethal (Turner fetuses are usually aborted, Wikipedia quotes olny 1% surviving until birth), and accounts for the health problems and deformations in Turner women.

A Klinefelter man has two X chromosomes in addition to his Y chromosome, so one of the chromosomes inactivates into a Barr body. The presence of Y chromosome directs his body to develop into a male pattern, but at the same time, the existence of Barr's body with those still active genes, causes his body to develop also feminine features. There is little to cause spontaneous abortion.


What can thrombosis lead to? I am thinking this question.
Thrombosis can result in

organisation of thrombus,
sepsis
thromboembolism,
fibrinoid swelling
adiposity.

I fibrinoid swelling (edema) (4) can occur.
Also, I think (3) thromboembolism can occur and also (1) organisation of thrombus.

What can thrombosis result in?

Fibrinoid swelling involves necrosis and swelling so no.
Organisation of thrombus refers to some very large space of organising thrombus in different ways - so no, since there is an exact mechanism under.
Based on my interpretation of Robbins -book.

The correct answer is 3. thromboembolism.
Thromboembolism is a combination of thrombosis and its main complication, embolism.


Why is it that cats can jump so high for their size, compared with humans? My cat is about 1' high at the shoulder, and I am a little over 6', but my cat can easily jump onto something as high as I am. That is 6x it's height. If a cat can do this, then Why can't I jump up onto my barn roof? That is a little less than 36' up. I have a hard time jumping onto even a 4' platform. Now if my cat had trouble jumping onto an 8" platform, I would think that pathetic. Do cats have muscles 20x stronger than humans, for their mass?
Is it just their skeleton providing leverage?

There is not a linear relationship between the size of a muscle and its power. The cat weighs significantly less, but the decline in muscle power is not identical. If he weighs 20x less than you, but his muscle generate 1/5 as much force, he will still be able to jump way higher than you.


What makes us all different and similar to some extent? It is said that genes define how we look physically and psychologically; so for example if a male human sperm carries a certain number of genes, say x, and a female carries y, then mathematically there would be m genes from the male and n from the female, and a finite total available. Could there be people identical in appearance if the same genetic combinations recur?

Also we find similar-looking people with perhaps similar behaviour accross diferent geographic locations; does this means that they have similar genetic make-up, up to some percentage?

Please correct my biology and share the possiblity of having genetically identical people across different geographic locations.

For ease of explanation let me first tell you that the "genetic makeup" is called "genotype" and that "how we look physically and psychologically" is known as "phenotype". These are not complete definitions of the terms but this should help you understand what we're talking about. I also apologise for the lack of detail or inaccuracies which many fellow contributors may find aggravating, but the question calls for keeping things down to the most important aspects :)

Do genes define how we look?

Genotype defines to some extent the human phenotype, but we don't know exactly to what extent regarding most aspects of the phenotype. This is called the "nature vs. nurture" debate and is concerned with the effects of genotype itself on phenotype vs. the effects of non-genetic influences after fertilisation (such as chemical surroundings during embryonal growth, experiences at young age etc).

Numbers of genes from males and females

Another misunderstanding is that a sperm carries a certain number of genes which it combines with a number of genes from the egg. While this is strictly true, the number isn't what matters because we all carry the same number of genes (*). The genotype doesn't depend on the number of genes, but rather, almost all genes exist in several variants within the human population. So the genotype is actually about which variants an individual carries, not about the number of genes. In biology, we use the term "allele" to refer to variants in this context. So in other words, each gene can have different alleles.

People with identical appearance

If two people have identical alleles for all genes (i.e. identical genotype), then they can indeed look almost identical. However, because of the vast number of genes and alleles present in the human population, it is practically impossible for the same alleles to come together in two humans. With only one exception: if two individuals result from the same combination of sperm and egg cell, they will be identical, and this is exactly what happens in monozygotic twins.

Similarities by geographical region

However, the total number of genes and alleles is limited (**). This concept is what people call the "gene pool" and is the reason why humans are still always humans and share certain similarities. In particular, for most of human history our geographical movement has been limited (most of the time), creating geographical "sub-gene pools" (to keep it simple). This is why people from the same geographical region are more likely to look similar; they have a higher chance to share the same alleles of genes that determine appearance. In terms of behaviour - to whatever degree genotype influences behaviour, peopel from the same geographical region will be more likely to be similar in these regards than people from different geographical regions. However, you can now hopefully understand why this "degree of similarity" is next to impossible to quantify (lack of knowledge: which genes determine what, how many alleles exist of them, how many people have which allele, how much and how far do people travel,...).

(*) Ok, not quite - it is possible for an individual to have the odd gene actually completely missing, but for the sake of simplicity we all have the same number.

(**) Again, not strictly, because new alleles and possibly even entire genes can result from mutation, but this is relatively rare and on the large scale you can work on the assumption that they are limited in number.


Chance of child inheriting at least one copy of an allele - heterozygote mother, unknown father Our genetics professor has posted up working for previous examination answers, but I am not convinced that his answer is correct. My answer is close but may just be due to co-incidence.

Question: There is a dominant "risk" allele with a frequency of 5%; what is the chance that a woman with one copy of this allele, and her husband will have a child with at least one copy of the allele.

Heterozygote frequency: 0.095
Non-risk allele homozygote frequency: 0.9025
Risk allele homozygote frequencyy: 0.0025

Professor's answer:  0.50 (woman's chance of passing allele) + 0.095/2 (heterozygote frequency in population divided by chance of passing allele) = 0.5475

My answer:  There are three possible situations, that the husband is homozygous recessive, homozygous dominant and heterozygous. The probability that any child will have the allele in each situation is 50%, 75% and 100% respectively.
Hence my answer = (50% x 0.9025) + (75% x 0.095) + (100% x 0.0025) = 0.525

It seems that what you are trying to do is calculate the probability of the child having at least one copy of the "risk allele" which I will denote as "A" (and it's counterpart "a").

First of all you know that the mother is Aa, and the child will get one allele at random. The probability that the mother passes on the A allele is then 0.5.

The tricky bit is the seemingly unknown genotype of the father. However, you do know genotype frequencies, which are the probability for the fathers three possible genotypes.

If the father is AA then it is certain the child will get the risk allele, and the probability of the father being AA is 0.0025.
If the father is heterozygous then there is a probability of 0.5 he will pass on the A allele, and the probability of the father being Aa is 0.095.
If the father is aa there is a probability if 0 that he will pass on the A allele.

Combined these give the probability that the father carries at least one A and will pass it to his child.

$$(1 \times 0.0025) + (0.5 \times 0.095) + (0 \times 0.9025) = 0.05$$

The probability of the child getting at least one A is then the probability of getting it from the mother plus the probability of getting it from the father.

$$0.5 + 0.05 = 0.55$$


How to derive rate of product formation for an allosterically inhibited enzyme? I'm working through Mathematical Modelling in Systems Biology: An Introduction by Brian Ingalls, and in Chapter 3 there's an example of a simple allosterically inhibited enzyme with reaction scheme shown here:

$$\ce{S + E<=>[k_1][k_{-1}] ES->[k_2] E + P}\\[2em]
\ce{I + E<=>[k_3][k_{-3}] EI}\\[2em]
\ce{I + ES<=>[k_3][k_{-3}] ESI}\\[2em]
\ce{S + EI<=>[k_1][k_{-1}] ESI}
$$

where E is the free enzyme, I is the allosteric inhibitor, S is the substrate, P is the product, and ES, ESI, EI etc. are the various complexes between them. The book goes on to state that the rate of formation of P is

$$\frac{V_{max}}{1+I/K_I}\frac{S}{K_M +S}$$

where

$V_\text{max}$ is the maximal rate of reaction ($k_2$ * Total enzyme concentration), $K_I$ is the dissociation constant of the inhibitor $k_{-3}/k_3$ and $K_M$ is $(k_{-1}+k_2)/k_1$

No proof for this is shown, although the book says the solution is assuming a quasi-steady state of the complexes ES, EI and ESI. I've attempted to work it out, and arrived at almost, the same equation, except I have I/Ki * (k-1+k3)/k1 instead of I/Ki * KM. I have no idea how to get to the equation present by the book. Can someone explain how their equation was derived?

If you apply quasi-steady state approximation for the complexes then you will get three equations for each of the complexes. Then you have to use the conservation law for enzyme to obtain the equation with respect to just substrate and inhibitor. If you try solving these algebraic equations, it gets very complex and difficult to solve by hand. However, in this system of chemical reactions, you can notice one thing: the binding of the inhibitor is not affected by the binding of substrate. In other words, the amount of enzyme inhibited will not depend on the amount of substrate present. So, in the absence of substrate:
$$\frac{d}{dt}(EI)=k_3I.E - k_{-3}EI = 0$$

So the total uninhibited enzyme ($E_u$) would be:
$$E_u=\frac{E_0}{1+\frac{I}{K_I}}$$

When the substrate is present, the amount of total enzyme available for catalysis would be $E_u$. Now, apply the Michaelis-Menten equation for uninhibited enzyme but substitute total enzyme ($E_0$) with total available enzyme ($E_u$):

$$V=\frac{k_2S\left(\frac{E_0}{1+\frac{I}{K_I}}\right)}{K_M+S}$$

From here you can get the equation given in the book.

The above logic works only if the rate of inhibitor binding is much faster than that of substrate binding. If not, the dynamics of product formation will depend on the different reaction rates and this simplistic equation would not be valid.


Do pigeons have the smallest legs-to-body ratio of any bird? Proportional to their size, do pigeons have the smallest legs of any bird?

That achievement probably belongs to the Swifts, specifically known for their short legs. Their name Apodidae derives from the word for "footless" in Greek.


Notation for repetitive nucleic acids With regard to nucleic acids with repeating residues, could anyone provide a description of what the following sequences are, and the key differences between them:

Poly(dA)
Oligo(dA)
Poly(A)

dN denotes deoxyribonucleoside (where N can be A, T, G or C). If there is no d prefix, then it denotes a ribonucleoside.

Regarding the difference between poly and oligo:

The former refers to having a large number of monomeric units whereas the latter means having a few monomeric units. There is no strict definition of the boundary between poly and oligo. Poly-A tails are typically about 70-80nt long in yeast (Eckmann et al. 2010). So it logically follows that anything shorter than that should be called an oligo-A. Chemically synthesized stretches of DNA are often referred to as oligos even though nowadays one can synthesize more than 80nt long DNA/RNA. Moreover, a stretch of As in some mammalian mRNAs smaller than the usual length of ~150-250 is still referred to as a short poly-A tail instead of an oligo-A tail (Jalkanen et al. 2014; there are many more examples).

Additionally, even if the cutoff is, let's say, 100 units, it doesn't apply to proteins. A protein with 100 amino acids is still considered a polypeptide and not an oligopeptide. For peptides, the cutoff is generally around ~30.

So, I would conclude that the usage of these prefixes is quite contextual.


How does water buffer a sudden drop in temperature? A property of water is that it is slow to heat and cool. According to my biology book, some energy from an increase in temperature would spent breaking hydrogen bonds, so that temperature does not rise too fast - helping a cell to maintain homeostasis.

As far as I can tell, this answer does not explain how a drop in temperature would be slowed down by water in a cell. How does water slow down heat loss? Is it just because it is difficult for the heat that is already inside the cell to leave?

From pure biophysical viewpoint the question

"Why does water buffer sudden temperature changes?" can be answered in the following way:

Water has relatively high specific heat capacity. This is the measure of the energy required to raise the temperature of one kilogram of a substance by one kelvin without a change of state occurring. "Relatively high" means that water can absorb more energy without noticeable (for the cell) increase in temperature.

Here are some heat capacity values from the above-linked Wikipedia article:

  Animal (incl. human) tissue   3500 Jkg-1
  Water at 25 °C    liquid  4181.3 Jkg-1
  Methanol  liquid  2597 Jkg-1
  Ethanol       liquid  2440 Jkg-1
  Paraffin  wax solid   2500 Jkg-1
  Graphite  solid   710 Jkg-1

Water has relatively high thermal conductivity. This means that the absorbed heat is quickly distributed over the complete cell volume, leveling down the focal temperature increases in cell. Here are again some values for comparison:

  Water 0.6 Wm-1K-1
  Wood 0.2  Wm-1K-1
  Paper 0.05  Wm-1K-1
  Glycerol 0.3 Wm-1K-1

The follow-up questions:

"Why does water have relatively high heat capacity?" and "Why does water have relatively high thermal conductances?" are not within the scope of this site. However, here exactly comes your explanation with hydrogen bonds in play (from Wikipedia):

  Hydrogen-containing polar molecules like ethanol, ammonia, and water
  have powerful, intermolecular hydrogen bonds when in their liquid
  phase. These bonds provide another place where heat may be stored as
  potential energy of vibration, even at comparatively low temperatures.
  Hydrogen bonds account for the fact that liquid water stores nearly
  the theoretical limit of 3 R per mole of atoms, even at relatively low
  temperatures (i.e. near the freezing point of water).


Why do type 1 diabetics experience hypoglycemia? I know that type 1 diabetics do not produce enough (possibly none) insulin since beta cells of pancreas are damaged and as far as I know glucagon is produced by alpha cells (which are healthy in diabetic body, I suppose). So, my question is that since glucagon is released when the blood glucose is low, why do the diabetics experience hypoglycemia? Shouldn't the glucagon be released and increase the blood sugar?

Note that in Role of Alpha Cells in Diabetes1, the following is stated:

  Glucagon responses to hypoglycemia have been known to be blunted in
  type 1 diabetes of long duration, and this may be a result of a loss
  of alpha- and beta-cell communication secondary to insulin deficiency.

Rudy W Bilous. Role of Alpha Cells in Diabetes - Medscape - Apr 11, 2003.

Key to this question is that untreated, type 1 diabetics would never have hypoglycemia.  It is insulin treatment that causes the hypoglycemia.  Insulin brings sugar down and without insulin (as the case with type 1 diabetics) sugar just goes up.    Exogenous insulin will bring sugar down in anyone, diabetic or no.  Since Type 1 diabetics use insulin all the time, there is more chance for an accident (hypoglycemia).

Also, some Type 1 diabetics might not compensate against hypoglycemia or correctly perceive that they are hypoglycemic.  Reasons for this are laid out in the following article:

From Hypoglycemia in Type 1 Diabetes

  Three major defects in this homeostatic response contribute to the
  high frequency of hypoglycemia in type 1 diabetes.

The article summarizes what those are - basically a blunting of normal reactions to hypoglycemia stemming from the disease itself.  It then summarizes:

  Thus, the glucose counterregulatory defense against hypoglycemia in
  individuals with diabetes becomes impaired at almost every level and
  rendered even more defective through intensive insulin therapy