How can some residues in the active site of enzymes be protonated with a pKa < 7? It is reported in many papers, that some residues in the active site of enzymes need to be protonated to get functional enzyme, where these residues have a low pKa (for let us say 5).

How can that happen in the physiological conditions (with pH=~7.4)?

It is mentioned that a raise in the pKa value is happening during the catalytic activity to get that protonation state. But how is that happening?

Here is a publication where this protonation and pKa raising is described.

https://www.ncbi.nlm.nih.gov/pubmed/7306491

  This conclusion is confirmed by the result that a group with a pK value of 6.7 must be protonated for the binding of methotrexate. It is proposed that the binding involves the formation with N-5 of dihydrofolate or N-1 of methotrexate of a hydrogen bond which has considerable ionic character and which lies within a hydrophobic environment. Further, it is suggested that the same hydrogen acts as an auxiliary catalyst which facilitates hydride transfer from NADPH to dihydrofolate for its conversion to tetrahydrofolate. Evidence to support this suggestion comes from the finding that the V profile is similar to the V/K profile except that the pK of the group which must be protonated for maximum enzyme activity is shifted upward by about 2 pH units. Such an increase in a pK value is consistent with the formation of a hydrogen ionic bond in the ternary enzyme-NADPH-dihydrofolate complex. The results of inactivation experiments with trinitrobenzenesulfonate appear to indicate that a lysine residue is necessary to maintain the enzyme in its active conformation.

Generally speaking, even though physiological pH is generally ~7.4, this is not necessarily the pH inside the enzyme active site. The enzyme's catalytic machinery may experience a completely different pH for one of two reasons: 1) because the enzyme is located in a place where the pH is simply not 7.4, and 2) The enzyme's amino acid composition shifts either the pH in the active site or the pKa of the active site residues relative to the surrounding environment such that the effective local pH in the catalytic site is lower or higher than 7.4.

For example, there are places in humans, such as the stomach or around muscle cells during anaerobic respiration where the pH is actually acidic relative to the standard physiological pH of 7.4, due to the presence of HCl or lactic acid respectively. Additionally, certain subcellular organelles, such as lysosomes, also are relatively acidic, since they are a site for breaking down proteins into amino acids.

However, the case presented in this paper seems to be an example of the second situation, where an enzyme that is in a pH neutral environment relies on one or more protonated amino acids to perform catalysis. This is relatively common. Basically, the enzyme's active site has an amino acid composition that when folded correctly, alters the local pH around the catalytic residues to favor catalysis. For example, in the enzyme acetylcholinesterase, the active site serine is rendered nucleophilic by being positioned next to a glutamate and a histidine, in an arrangement referred to as a catalytic triad. The glutamate is an acidic residue, and its close proximity to the histidine means that it will stabilize the protonated form of the histidine. Energetically, this makes protonation of the histidine very favorable. This causes the histidine to take a proton from the active site serine. Now that serine's oxygen is deprotonated, it can act as a strong nucleophile. After the serine forms a covalent interaction with the substrate, the histidine will facilitate a similar nucleophilic attack by a water molecule, regenerating the enzyme and completing the catalytic cycle.

Something similar is seen with the beta-lactamase TEM-1. In this case, TEM-1 uses a lysine (pKa ~11) instead of histidine (pKa ~6), so multiple acidic residues are in the active site to facilitate the deprotonation of the lysine during the catalytic cycle. In effect, the amino acid composition of the active site allows for the shuffling of protons needed for catalysis.

So to summarize, while physiological pH is widely regarded to be 7.4, an enzyme's catalytic machinery may experience a very different pH through either the cellular/physiological localization, or through the amino acid composition of the active site. In the latter case, the presence of acidic or basic residues can alter the protonation state of other acidic or basic residues, meaning the effective pKa of these residues or the effective pH around them is higher or lower than 7.4.


Did dinosaurs have more than one brain? If so, why? I once remember reading (15 years ago) that dinosaurs had two brains. One for their head and another one for their digestive functions. What is the current opinion on this theory? Has more evidence become available?

It would appear that at one time it was thought that a "gap" in the skeleton of a Stegosaurus was a space for another brain. This is now thought to be a storage space for extra food.
Googling your question brings up a number of answers along these lines:

https://en.wikipedia.org/wiki/Stegosaurus#%22Second_brain%22
https://dinosaurs.about.com/od/dinosaurdiscovery/tp/dinoblunders.htm
https://wiki.answers.com/Q/Did_a_dinosaur_have_two_brains


Transitivity of Species Definitions There are many definitions of "species" which usually take the form

Two individuals are of the same species if ...

An implied (rarely made explicit) property of any sensible species definition is that the relation "is the same species as" should be an equivalence relation (the reason why this is sensible is that only such a relation partitions the set of all individuals into equivalence classes, that is, separate species). In particular, it should be transitive, that is

If A and B are of the same species, and B and C are of the same
species, then it follows that A and C are also of the same species.

It appears to me that all species definitions in use violate that property.

Example
Are the Chihuahua  and the Great Dane  of the same species?
Not according to the "biological" species definition, which states:

Two individuals are of the same species if and only if they can produce fertile offspring.

Since that is (presumably) not true of Chihuahua and Great Dane, according to that definition, the two dog breeds are not of the same species.
However...
Let us say that the Chihuahua can produce fertile offspring with the Dachshund...

... and the Dachshund with the Golden Retriever...

... and that at last with the Great Dane as desired.
Then, if we assume transitivity, Chihuahua and Great Dane are of the same species - contradiction!

Another Example
Are the Chimpanzee  and the White Oak  of the same species?
Intuitively, they are of course not, the very idea seems ridiculous. Sure enough, with the definition (a variation of the "genetic" species definition)

Two individuals are of the same species if and only if their genome differs in less than 0.5% of base pairs.

the two are indeed not of the same species.
However, we can again construct a "chain" of intermediate individuals, each of which is similar enough to its predecessor to satisfy the definition, eventually connecting Ape and Tree and violating transitivity again.

My question to biologists: How is this problem resolved in practice? Are there any species definitions that preserve transitivity?

I am pretty sure you cannot jump from an oak tree to an ape with whatever common definition of species you're using. But this is some kind of practical implication of your question.

The concept of species was already being used by Aristotle and was kept up to now although the grouping of living things into species might not be a clever thing to do. I don't think there is any non-arbitrary, logical way of making groups out of living organisms. Here is a podcast (It is in French, sorry!) that is interesting for those wanting to learn about how the concept of species evolved.

The case you describe is called Ring species. There has been lots of discussion in philosophy about the concept of species. The concept of species is unclear and if accurately defined, then in practice we don't really follow this definition to improve efficiency in how we name lineages. The term lineage has a much more rigorous meaning and is often of greater usefulness.

Ensatina eschscholtzii (a salamander; see DeVitt et al. 2011 and other articles from the same group) is a classic example of ring species.

You should definitely have a look at the post How could humans have interbred with Neanderthals if we're a different species? which discuss the concept of species. Some other sources of info include:

Species problem wikipedia
Reduction of species
The evolutionist view of the species concept: ESU
Stanford dictionary


What is the mechanism behind ventilatory acclimatization? In my respiratory physiology lectures, my professor explained that hypoxia-induced hyperventilation occurs in 2 stages when people try to acclimate at high altitudes. My question is about the long-term 2nd stage, listed as #2 below:

there's an immediate increase in alveolar ventilation triggered by peripheral chemoreceptors, but this only leads to a small increase, and also decreases levels of $p_{CO_2}$.
over 8 hrs, there's a slow rise and 2 mechanisms are involved:
 a) bicarbonate ion ($HCO_3^-$) in cerebrospinal fluid is shuttled out and chemoreceptors increase their sensitivity to $p_{O_2}$
 b) kidneys excrete more $HCO_3^-$ to normalize blood pH

I get that the $HCO_3^-$ and $H^+$ comes from $H_2CO_3$ being broken down through carbonic anhydrase. But she never mentioned where the $HCO_3^-$ is shuttled to or which chemoreceptors are increasing their sensitivity to $p_{O_2}$ (I assume peripheral since it's mentioning sensitivity to $O_2$). She then says that because of this $H^+$ and $CO_2$ levels increase, stimulating central chemoreceptors to increase ventilation to help decrease the acidity/$CO_2$ levels. I don't understand how $H^+$ and $CO_2$ levels are even rising because I don't know where the $HCO_3^-$ is even going and what it's role is. This professor is terrible at explaining things, and I'm just so confused at this point! Any sort of direction would be so helpful! Thanks!

@Michael Kunh Carbonic anhydrase is used in the human body to tip the balance of the reaction  $H_2CO_3\rightleftharpoons H^++HCO_3^-$ to the right side, and is an important player in acidobasic homeostasis.

To answer the question:

$HCO_3^-$ is excreted through the kidneys. This represents the metabolic compensation to respiratory alkalosis that appears in altitude.

To summarize:

ascension leaves us in with a lower partial pressure of oxygen. This will stimulate the peripheral chemoreceptors of the carotid bodies and aortic arch to increase ventilation (hypoxic ventilatory response). In consequence, an acute respiratory alkalosis develops.
renal adaptation begins after more or less 8 hours, and reestablishes homeostasis after 24-48h. To do that, the kidney will excrete $HCO_3^-$, which will tend to acidify blood (metabolic acidosis to counterbalance respiratory alcalosis). To accelerate this phase, one could take some acetazolamide, a diuretic drug that causes $HCO_3^-$ excretion.


Which animals live in trees and make noises like rubber ducks at night? I was recently at night in a public park in Karlsruhe, Germany. I've heard many (at least 10, probably many more - it's hard to tell) animals in the trees making noises similar to that of a rubber duck which is pressed.

What could that be?

It is most likely a Tawny Owl (Strix aluco), or Waldkauz in German, one of the most common owl species in Central Europe. These owls have many different calls, and you can hear them often here in Karlsruhe at night. Particularly their "kewick" call sounds similar to squeezing a rubber duck. It is usally emitted by female individuals during the mating season, but also males can produce it. Juveniles have a similar call as well. But most of the time - as far as I have noticed - you only hear their more common "hoo-hoo" calls (listen here or here).

Photo of a Tawny Owl:

Image Source:

https://commons.wikimedia.org/wiki/File:Waldkauz-Strix_aluco.jpg


Hybrid vs introgression zone in natural populations In the book An Introduction to Molecular Ecology, the authors say that

  Introgression is the diffusion of alleles from one population or
  species into another as a result of interbreeding or hybridization
  between them.

And that hybridization is (roughly) the breeding of two distinct species.

I thought that when we were talking about introgression zone and hybrid zone, it was the same thing.

But here is my interpretation:

See the image below. Across an area, you would have 2 populations of 2 species (A-E). They could interbreed in the middle, this would be called the hybrid zone (in C). But the change of allele (or the transfer of allele) between two populations is not only done by hybridization (B vs C). It can be done by a new hybrid breeding with a non hybrid (backcross, in B). Then, B to D would be the introgression zone.

I don't really know what would happen in that case when 2 hybrids breed together for the colours!

So my question is: What is the difference between introgression zone and hybrid zone (is my interpretation correct?)?

I think you're correct. See Harrison, R.G. and E.L. Larson. 2014. Hybridization, introgression, and the nature of species. J. Hered. 105: 795–809. Also see https://www.differencebetween.com/difference-between-hybridization-and-vs-introgression/

Interesting that you're received no responses to this. It's an interesting (and I think important) question.


Difference between pulse and blood pressure I'm a very naive and biologically illiterate person, and from what I've read on the internet I'm not really sure I understand the difference between pulse and blood pressure. I'm guessing for most of you this is trivial so I'm hoping for something clear for someone of my "level".
On a side note, I speak french, and we have two words: pression / tension (artérielle). One of them must be wrong since they mean totally different things and makes things even more confusing.
But from what I could gather, are the next statements correct/accurate or am I completely off?

The blood pressure is the fluid's movement "strength" in the veins (or "arteries", please edit my post with the correct english word)
The "tension" is the force applied on the veins itself, kind of like when you're pulling a rubber band
The pulse is just the wave of blood moving, which creates different tensions over the vein and whose movement is created by the pressure.

The blood pressure is the fluid's movement "strength" in the
  arteries (or "artères", please edit my post with the correct english word)

Blood pressure is a measurement of the strength of flow through the arteries. (I.e., the force per unit area exerted by the blood on arterial walls.) So replace vein with artery and your definition is correct.

  The "tension" is the force applied on the veins itself, kind of like
  when you're pulling a rubber band

In cardiovascular terminology, hypertension and hypotension are used interchangeably with high and low blood pressure (even though technically tension uses force units and pressure uses force/unit area units). Your definition sounds more like arterial tensile strength, which is the ability of the artery to withstand pulling forces without breaking (which decreases with age).

  The pulse is just the wave of blood moving, which creates different
  tensions over the vein and whose movement is created by the pressure.

Pulse is an indirect measurement of heart rate. So, yes, it's the rate of the "wave of blood moving." It creates different "pressures" measured by systolic (the "wave" in your terms) and diastolic (the "trough") whose movement is created by the force (of the heart walls contracting).


Can you identify this fossil? I found this fossil near a beach in Victoria, Australia. Can anyone identify it?

It is roughly the size of an Australian 20 cent piece (~30 mm). I think it might have been washed down from an eroding cliff.

I found another similar sized but less detailed fossil near by, which might be the same thing.

That's an Echinoid, or Sea Urchin (Phylum Echinodermata). We can clearly see the five rows of ambulacral groves and the base of the spines.

Here is an image of a fossil Echinoid, from the Melbourne Museum, for comparison:

Fossil echinoid (sea urchin), Lovenia bagheerae; late Miocene (c. 8 my old), Portland, Victoria
Photographer: Frank Holmes / Source: Museum Victoria

According to the museum:

  Victoria contain fossils of many different kinds of echinoderms, including sea stars, brittle stars, crinoids, cystoids, blastoids, edrioasteroids and carpoids. They occur in the Heathcote, Kilmore, Kinglake, Melbourne and Lilydale districts. In much younger rocks of the Cainozoic Era (less than 65 my old), the most abundant echinoderms found in Victoria are the echinoids or sea urchins. They occur mainly in limestones exposed in coastal areas including the Portland, Port Campbell, Torquay, Geelong and Lakes Entrance districts. (emphasis mine)

Your second image, from below, really seems like this image of Lovenia bagheerae:

Source: Museums Victoria


Are human teeth only diphyodont or both diphyodont and monodont? Many books say human teeth are only diphyodont .But premolars appear only once and one molar appears later which should be considered monophyodont.
 Dental Formulae :

CHILD -
 1. Incissor -2/2
 2. Canine -1/1
 3. Premolar-0/0
 4. Molar-2/2
ADULT-
 1. Incissor-2/2
2.Canine-1/1
3.Premolar-2/2
4.Molar 3/3 .

Here the 3rd molar and two premolar appear only once. Therefore human teeth should be both diphyodont and monophyodont

The definitions from the Oxford Dictionary of Dentistry:

Diphyodont

  Describing the development of two successive dentitions, one primary
  and another secondary (permanent), as found in most mammals including
  humans.

Monophyodont

  Possessing only one generation of teeth. It is a characteristic of
  some mammals, including the manatee, seal, and walrus.

As you can see, the term diphyodont is generally not used to refer to the individual teeth, but rather to the whole animal (i.e. the sets of teeth). A monophyodont is an animal that has only one set of teeth.


What does this sentence about angina mean? I do not understand this sentence

  Angina can be treated ambulatory (in out-patient) in stable angina.

I think ambulatory refers to ambulatory ECG monitoring.
So I understand this that you can treat stable angina based on ambulatory ECG.
How do you understand this sentence about "ambulatory" angina?

Ambulatory means there is no emergency and refers to where the patient is and not to the disease itself (here the patient is out of hospital): for example there is no need to perform urgent PTCA or other procedures related to unstable CAD (coronary artery disease).

Another option is - to hospitalize the patient to perform urgent or planned procedures if the patient is unstable and there is deterioration in his/her status which may worsen and threaten the life.

The key word in this sentence "stable".


What would be required to evolve an animal (non-human) brain to obtain human-level cognition? Could any animal subject to the right conditions evolve human-level intelligence? Suppose that an artificial intelligence (AI) decided to artificially evolve a population of octopus (don't ask why, its for science) by restricting them to calculated environmental pressures, and over millions of years, the AI manages to produce a relative of the octopus that has a similar level of cognition to humans. Is this possible? If it is possible, what are some steps (in general) that might be required to evolve a complex animal brain (to human-level cognition or beyond)?

Answering the question what is needed for a human brain to evolve starting from a cephalopod brain is hard. However, I can expand on what is thought to have been the driving forces behind the evolution of the humanoid brain (Hawks, 2013):

The species of the famous Lucy fossil, Australopithecus afarensis (~3-4 mln yrs ago), had skulls with internal volumes of between 400 and 550 milliliters, which is comparable to chimpanzees and gorillas. Australopithecine brains started to show subtle changes in structure and shape as compared with apes. however. For instance, the neocortex was expanding, which is an indication that the evolutionary pressure on higher functions of the brain was important.

Homo habilis, the first of our genus Homo, who appeared 1.9 million years ago, saw a modest hop in brain size, including an expansion of a language-connected part of the frontal lobe called Broca's area. The first fossil skulls of Homo erectus, 1.8 million years ago, had brains averaging a bit larger than 600 ml. This shows that language development is a likely factor that has driven evolution of the human brain.

By 500,000 years ago, the humanoid brain reached a volume of about 1,000 ml. Early Homo sapiens had brains within the range of people today, averaging 1,200 ml or more. It is thought that cultural and linguistic complexity, dietary needs and technological prowess took a significant leap forward at this stage, and that our brains grew to accommodate the changes. The shape changes we see accentuate the regions related to depth of planning, communication, problem solving and other more advanced cognitive functions.

Interestingly, in the past 10,000 years of human existence the brain actually shrank. Limited nutrition in agricultural populations may have been an important driver of this trend. Industrial societies in the past 100 years, however, have seen brain size rebound as nutrition increased and disease declined (Hawks, 2013).

Indeed, one of the driving components behind the expansion of the human brain is increased availability of fatty fish to sustain the large amounts of fat needed in a brain - survival of the fattest (Cunnane, 2006).

Although the past does not predict future evolution, a greater integration with technology may lead to further expansion of the human brain (Hawks, 2013).

References
- Cunnane, Med Sci (Paris) (2006); 22(6-7):659-63
- Hawks, Sci Am (2013)


What is the highest competency possible for E coli? I am looking to find a highly competent E coli strain.  I am making a library of a ~6.6kb plasmid and I am not getting high enough efficiency.  Does anyone have a suggestion of a strain/protocol with ultrahigh efficiency (>1010).

This is a great question as I just made my own "homebrew" chemically competent cells.

There are a vast variety of E. coli strains that are commonly used for cloning. They may be transformed chemically by heat shock method, or electrically by electroporation (a brief summary may be found here). These can be made in the lab manually, or purchased commercially from reputable vendors (I recommend Invitrogen/Life Tech, NEB, Promega).

Chemically competency is achieved using Hanahan's method or some a variation thereof. The method involves washing the bacteria in a series of buffers containing various di-valent cation chloride salts (CaCl2, RbCl2, etc). Commercially available E. coli are sold as "regular" and "ultra" competent, ranging from 106 to 106 for regular, and the highest I've seen is 1010 cfu/µg DNA. For maximum efficiency, especially since a small plasmid such as yours will be easy to transform, electroporation is a more efficient technique, but requires specialized equpment. Electroporation can yield >1010 cfu/µg. For standard cloning practices, regular or high efficiency chemically competent E. coli are perfectly adequate. Since you mentioned you are creating a library, you certainly want to go with ultra high efficiency chemical transformation or, if you have the necessary equipment, electroporation. I have not seen electroporation efficiencies reported > 5x1010.

Transformation efficiencies are standardized by reporting a rate as the number of colony forming units (cfu) per µg of some control plasmid, typically pUC19. Transformation efficiency is very sensitive to many factors, including heat shock time, cooling times, thawing time, amount and size of plasmid DNA. All things being equal, the size and quantity of DNA are important for your purposes. Transformation efficiency generally increases with quantity of DNA, but there is a saturation point, and evenetually having too much DNA decreases the yield. Also, efficiency decreases linearly with plasmid size. For example, pUC19, the control vector, is ~2.7 kbp, and your library plasmid is ~6.6 kbp, so you should expect for the same mass of DNA you will have lost 60% transformation due to plasmid size. This loss is due to the physically larger size of DNA being more difficult to move into the bacteria.


Is 1 g/l living biomass for a Biogas fermenter plausible? A usual number for a healthy biogas fermenter is $10^9 - 10^{10}/mL$ Bacteria, 10-15% of which would be methanogenic archae. Exceptionally healthy fermenters have more total bacteria and up 25% archae.

The mass of E. coli is given with 670 femtograms. If E. coli is representative for fermenting bacteria that would put us on the order of magnitude of 1 g/L living biomass.

This seems like much to me, though this is just a gut feeling.
As additional information, such a fermenter will have a total solids content of about 10%. A typical loading rate will be 4-5 g VS/d l *, two thirds of which get metabolized to gas. To put it another way: The amount of digested biomass per day would be the same order of magnitude as the living biomass. However, as anaerobic digestion is a multistage process, with at least three steps, each population will have a higher rate of digestion to mass.

Are the numbers basically sound? Is E. coli an exceptional bacterium in terms of mass? Are archae generally as massive as bacteria? What are bacteria counts for other fermentation processes?

(*) g volatile solid per day and liter: for each liter fermenter volume, this many g potentially degradable matter are added per day

I've done experiments with yeast, and they can easily ferment glucose at the rate of 4g/L/d.  Probably faster, if one were to optimize it.  So your numbers don't seem crazy.


histones in the Hershey / Chase experiment When DNA is injected into the cell why aren't histones(protein) also injected and why wouldn't the radioactive sulfur therefore also be present in the infected cell

It's true that eukaryotic chromosomes have histones associated with them. But the DNA in the Hershey-Chase experiment was viral, no histones.


Can the characteristics of an offspring depend on the locality of its conception also? Transfer of characteristics from a parent to its offspring is explained in biology. When an adult male and female (of humans) who are displaced from their local environment to another (say, a different continent)for a considerable period of time, conceive and give birth to a baby, the newborn also shows some traits related to the people of the new locality . How is this explained?

Genetic makeup can not vary with the place of conception, but certainly the way genes are expressed can change with change in place of conception. Such changes are called epigenetical changes. Epigenetic change is switching on or off of genes which can be achieved by various method:-

1)  DNA methylation

2)  Histone modification and

3) RNA associated gene silencing

In theory, change in place of conception, can result in silencing or activation of differential genes in foetus. In fact there is this nice article which discusses how maternal nutrition switches on or off six genes in foetus 1 and [2]. Even stress can cause such epigenetic changes [3]. These environment triggered changes may also result in change of phenotype. For example in mice, the agouti viable yellow (Avy) gene which is a retrotransposon and is found in upstream of the agouti gene. The Avy elements are generally methylated and hence are shut off but in Agouti mouse, they are unmethylated and therefore switched on, which leads to a yellow coat.Though this methylation or unmethylation in agouti mice has not been proved to be a result of environmental factor, but in a strict theoretical sense this can happen (with some or other phenotypic trait)

1] Painter R.C., Roseboom T.J., Bleker O.P. Prenatal exposure to the Dutch famine and disease in later life: an overview. Reproductive Toxicology 20, 345-52 (2005).

2] Maternal nutrition at conception modulate DNA methylation of human metastatic epialleles(NCBI)

3] Exposure to stress even before conception cause genetic changes to offspring(science daily)


How does Vibrio cholerae benefit from infecting its host? As far as I know, V. cholerae secretes a toxin called choleragen into the intestinal lumen which affects the intestinal epithelial cells causing release of Na+ and Cl- ions into the lumen and reducing the lumen's water potential which causes water to flow into the intestinal lumen resulting in diarrhea. How does this benefit V. cholera in any way?

After V.cholerae gets into the human intestine it starts to multiply its numbers, and then becomes virulent after sufficiently expanding its numbers. This virulence drives the diarrhea which in part causes the bacteria to slough off into the intestinal lumen, and then into the external environment again.

So in short it uses the human intestine to increase cell numbers.

See work by Bonnie Bassler for a really fascinating understanding of the complexity of this infection.


What is the difference between disruptive, divergent and diversifying selection? In our lab meeting we were chatting about divergent selection. I was confused at some point because I wasn't sure what was the meaning of this work in comparison to diversifying/disruptive and other types of selection.

Diversifying selection was coined by J. T. Gulick and I haven't found an interesting answer to compare with our contemporary definition of these terms.

The way I understand this is that, divergent selection is broader and include directional selection as well as disruptive selection. Is that correct?

I think you are conflating selection and evolution. Diversifying selection is when the variance of a trait in the population increases and even potentially becomes bimodal. This may lead to divergent evolution, i.e. a speciation event. Whereas directional selection still leads to evolution but not necessarily a the formation of a new species.


Will neurons die if they are inactive for a long time? We know that when muscles are not used they atrophy. Does something similar also happen in neurons if they do not receive any stimulus?

Short answer
Yes.

Background
Postsynaptic neuronal degeneration after deafferentation are notorious in the peripheral sensory systems. There, marked degenerative processes are present when input to the secondary neurons is lost due to degeneration of the primary sensory neurons. In other words

When the hair cells are lost in the cochlea, the auditory nerve degenerates (e.g., Kuyama, 2010);
When the retinal photoreceptors are lost, for example due to degenerative diseases like retinitis pigmentosa, bipolar and horizontal cells in the retina degenerate due to a loss of efferent input (Mazzoni et al., 2008). For more information see the works of Marc & Jones, e.g.., Jones & Marc (2005).

Note that in the central nervous system these effects play less of a role, as neurons have ample opportunity to reconnect to other neurons, for the better or worse; e.g., in the hearing impaired and visually impaired, spontaneous sensations of sound and visuals may develop and lead to tinnitus and photopsias, respectively. These symptoms are caused by cortical sensory neurons desperately and randomly looking for sensory input after being deafferented due to peripheral loss of hearing or vision. When they cannot obtain useful input any longer, they gather irrelevant, non-useful input and start generating spontaneous 'illusionary' perceptions instead.

References
- Jones & Marc, Exp Eye Res (2005); 81(2): 123-37
- Kuyama, J Neurosci (2009); 29(45): 14077–085)
- Mazzoni et al., J Neurosci (2008); 28(52): 14282–92


Brainbow fluorescence labeling technique I have this picture describing the Brainbow system here:

The paper I am reading says it uses Cre-lox recombination to express a certain color. If the cell in question was expressing a yellow fluorescence then what would the construct in that cell look like in terms of the picture given? Would it just be a single line with the UAS, EGFP, and mKO2 in that order or would it be two lines, wone with the UAS and EGFP and on with the UAS and mKO2?

Yellow would need the expression of red and green so that would mean the excision of the blue fluorophore. It would be one line with egfp and the other line with mKO2--- the order doesn't matter-- these represent chromosomes.


Why does a housecat (or other predator) play with it's food before killing and eating it? Does it make the food taste better? I've read a couple people theorize that a cat playing with a mouse causes the mouse's body to be flushed with adrenaline before the final kill and that this adrenaline makes the meat more tender/easier to digest/more nutritious etc.

Is there any evidence to support the idea that by playing with it's prey the cat is making it taste better or easier to eat?

Animal Planet is quoting researcher Dennis C. Turner who claims this is an instinct which is supposed to tire the prey:

  Cats, rather, wear down prey to avoid sustaining injuries. They're motivated by self-preservation, just like most other animals, and they know what could happen if they aren't careful. Mice and rats, for example, can deliver nasty bites that can cause injury or spread disease. Birds, for their part, are able to scratch and peck. So, what's a cat to do? Rather than playing with their prey for amusement, cats tire out their victims to the point where they're too worn down to fight back. And after that, the cats will feel better, and safer, about finishing them off, according to researcher Dennis C. Turner. So while it might look like a display of cruelty, a cat playing with its prey is just an (admittedly harsh) example of animal instinct in action [1].

Karen B. London (animal behaviorist) agrees:

  Actually, the way that cats let go of and then recapture their prey is not a way for them to have fun, but rather a way for the cats to protect themselves from serious injury. Cats kill their prey by breaking the spinal cord with a strong bite to the neck. If a cat must let go of the animal in order to grab it on the neck, that cat is risking escape or retaliation by their prey [2].

Playing (not only with prey) also gives cats experience and improves their ability to make judgments [3].

References:

Animal Planet. Why do cats play with their prey? Available from http://curiosity.discovery.com/question/why-cats-play-with-prey (accessed 27.07.2014)
Karen B. London, Ph.D.. London Zoo: Why do cats play with their food? Available from http://azdailysun.com/lifestyles/pets/london-zoo-why-do-cats-play-with-their-food/article_46a97775-232d-5e56-b0ea-dd1c8782b062.html (acessed 27.07.2014)
Perfect Paws. Predatory Behavior of Cats. Available from http://www.perfectpaws.com/help3.html#.U9TLpON_tJk (accessed 27.07.2014)


Bug larvae identification anybody know what this might be, found in my bed. Pennsylvania, USA . Thanks

That's a silverfish (order Zygentoma) https://bugguide.net/node/view/79 This individual is not in great shape, and probably got crushed, however you can see it had the cerci in its tail. The individual is lacking antennae, which are usually long, but the eyes  are also very characteristic. You can see a similar picture on this thread (https://bedbugger.com/forum/topic/here-we-go-againcame-home-now-and-found-this-id-please-silverfish. They are fairly common in homes and are harmless. They feed on fibers and detritus in your home.


Does the entire surface of the earth contain organisms? Does the entire surface of the earth contain organisms?
My teacher mentioned that in some parts of the earth, there aren't any organism. Is this true?

Thanks in advance.

That will depend on many things. How do you define surface? Is one meter underground still "surface"? How about a kilometer?

Also, how large an area are we talking about? You could probably find a square millimeter in, for example, Antarctica that has no organisms. I don't think you would find a square kilometer with no organisms though.

There are organisms (called extremophiles) that thrive in the most hostile environments we know, they can survive extreme heat, cold, acidity, salinity etc. I found this very nice list:

  Cold – The McMurdo Dry Valleys in Antarctica are some of the coldest, driest deserts on Earth, with average annual temperatures of
  -20oC (-4oF) and less than 10 centimeters (4 inches) of precipitation a year. Scientists have found bacteria in liquid water pockets
  embedded about twelve feet deep in “solid” lake ice. Some of these
  bacteria use chemical nutrients from particles of dirt in the ice and
  use energy from sunlight for photosynthesis.
  Hot – Large concentrations of microbes thrive in Yellowstone National Park’s Grand Prismatic Springs, a hot spring with water
  temperatures up to 90oC (188oF). Other hot springs in Yellowstone are
  extremely acidic, yet are home to many different kinds of bacteria and
  microbes. Many of these microbes use chemical nutrients in the waters
  and energy from sunlight for photosynthesis. Deep underground –
  Scientists have discovered bacteria living in ground- water 5
  kilometers below the surface in deep gold mines of the Witwatersrand
  Basin in South Africa. These microbes thrive in cavities and cracks in
  rocks. Scientists are also are investigating life within and below
  permafrost in north- ern Canada.
  Bottom of the sea – Scientists have found abundant life clustered around hydro- thermal vents on the ocean floor, including bacteria,
  mussels, clams, shrimp, and giant tubeworms that can reach ten feet in
  length. Water pouring out of the vents in the complete darkness
  thousands of feet under the surface of the sea can reach temperatures
  of 113-120oC (235-248oF). The high pressures keep the water from
  boiling. Bacteria use chemicals in the vent’s water, primarily
  hydrogen sulfide, as their energy source instead of sunlight. Other
  creatures survive by eating the bacte- ria or each other.
  High Acidity – The water in the Rio Tinto in southwestern Spain is very acidic, a result of chemical reactions between the water, and
  iron and sulfur minerals in the ground. The river has a deep red
  color, like wine, because of iron dissolved in the water. Microbes
  living in the water use chemical reac- tions with iron and sulfur
  minerals to generate the energy they need. Products from these
  metabolic reactions contribute to the low pH in the environment. Many
  algae and fungi also live in the acidic waters.

As far as I know, there is no evidence of life in molten lava. Apart from that though, just about every habitat you can find on the earth has been colonized by life. Ask your teacher what parts of the earth she is talking about, and report back here.

UPDATE:

MCM's very interesting answer prompted me to do some more research. It seems that life has now been found even in the Atacama (taken from Azua-Bustos
et al):

  For a long time it was thought that regions of the Atacama could not
  uphold any type of life forms. However, recent culture-independent
  methods (metagenomics, transcriptomics, in situ hybridization, etc.)
  have improved the sensitivity for life detection. Thus, microorganisms
  have been found even in the driest areas of this desert, which makes
  scientists wonder about the true limit of water availability needed to
  sustain life as we know it. In this review, we summarize the efforts
  devoted to the characterization of microbial life in the Atacama
  Desert.

So, it seems that life can exist even in the Atacama. That leaves only molten lava...

Reference

Azua-Bustos et al, Life at the dry edge: microorganisms of the Atacama Desert, FEBS Lett. 2012 Aug 31;586(18):2939-45


What is the difference between the usages of bis-tris methane and bis-tris propane? I came across "bis-tris" buffer in Rodney Boyer's Biochemistry Laboratory book and tried looking it up. Then I found that there's bis-tris methane and bis-tris propane that are both buffers. What exactly are they used for and are the usages different?

They have different acid dissociation equilibria and so buffer at different pH.

                    pKa1    pKa2
Bis-Tris methane    6.5     -
Bis-Tris propane    6.8     9

[source]

The two titratable secondary amines of Bis-Tris propane make it usable over a wider pH range.


How can I calculate alpha helix content from molar ellipticity? How can I calculate the alpha helix content (i.e. percent) in a protein from a given molar ellipticity of 222 nm, without using any software. I have tried the Greenfield-Fasman equation, but the answer doesn't seems to be correct.

You can use the information at this site, especially section 3. (https://www.photophysics.com/resources/tutorials/circular-dichroism-cd-spectroscopy)

Notice the different CD spectra for alpha-helix, beta-sheets and random coil. If your protein is measured at 222nm you need to compare your measured values to the the spectra at 222nm, this will allow you to guestimate the secondary structure of the protein, but if you want to be accurate, you will need to measure at several wavelengths to determine the distribution of alpha helix, beta-sheet and random coil. This is because all three contribute to the measure spectra and as such you need several measurements to figure out the relative contributions of each secondary structure.


Can you do better than "Sock-Wasp"? I met this beautiful fellow when I was choosing my socks this morning. It seems I had found her cozy place. A stowaway, supposedly sneaked into my bag while camping, and me taking her all the way home. She just sat there for about a minute (probably just as tired as me, thinking "Duuuuuude, why did you wake me?"), then stretched her neck and and set off, searching for a calm spot to get her 5 more minutes.

Ca. 3 cm long. At home in Austria/Southern Germany.

I searched the internet a bit, and I think it's a female wasp, possibly Dolichovespula because of the pointy snout(?). I don't think it's a commom wasp, due to its size. Also no median wasp queen, because there's no red.
Maybe a tree wasp?

TL;DR: Can you help me identify this buzzer?

End of story:
After a lot of buzzing on her side, me chasing her with glass and cardboard in hand, and she dozing off two times in very uncomfy places (I was a bit embarassed about how un-hospitably dusty everything was), she settled for a box of clothing and snuggled her way into my shirts. I praised her sense of Cozyness, but then carefully emptied the box piece by piece outside and found her inbetween a flowery garment. She slowly stuck her head out from the folds ("DUUUUUUDE, again?!") and flew around the terrace for a while. I hope she's found a snug place out there.

I presume it is a female Dolichovespula adulterina living in the Palearctic (Austria and Germany) and Nearctic regions.


Why does ESR have to be waited for one hour? It is said that the length of the column of clear plasma in a narrow tube left by erythrocytes which gradually sediments after one hour is the measure of ESR(erythrocyte sedimentation rate). Its normal values are found to be 3-5 mm after 1st hour for male and 4-7mm after 1st hour for female. What I want to know is why "1 hour" has been chosen. Why not 30min, 2hr, 3hr etc?

Does it really make a difference how long they settle, or why they chose that amount of time? At one extreme, you haven't really given them adequate time, at the other, there's no more useful information to gather.

The tubes in which Sed Rates (or ESR) are measured are 200 mm in height. Why wait three hours for the result (which is still expressed as a rate, i.e. mm/hr)? In three hours, they may (depending on how quickly they settle) have all settled an hour and a half ago. (If an ESR is 100mm/hr, it will hit the settled cells at the bottom before it finishes settling if two hours is the length of the test.

The test is simple, cheap, easy, with good sensitivity and specificity. And the results come back in a little over an hour. The sooner the diagnostician gets the results back, the sooner the answer helps in the decision tree needed for the treatment of the patient. Longer wait times aren't helpful and may not be accurate with very elevated ESRs.

Acute Phase Proteins Molecular Biology, Biochemistry, and Clinical Applications By Andrzej Mackiewicz, Irving Kushner, Heinz Baumann, 1993


Understanding intra and extracelullar concentrations (membrane potential) I have 4 question (not homework)

What happens to the cells membrane potential if:

a) Na+ outside rises by 40mM

b) K+ inside rises by 10mM

c) K+ outside rises by 10mM

d) A- (impermeable ion) inside rises by 100mM

e) Na+ outside decline by 50mM

So my answers are:

a – hyperpolarisering (more negative)

b – Depolarisering (more positive)

c – Hyperpolarisering

d – Depolarisering

e - Depolarisering

I think it like this:

Membrane potential is the DIFFERENCE in electrical potential inside and outside the cell. When we say a cell has a resting potential of -60mV we mean that the cell has 60mV LESS than the extracellular space.

So when I am asked what happens if all of a sudden, the extracellular space increases in mV (first question) then I can say that the difference is now GREATER than 60 mV, it is now in fact 100 mV, as the extracellular space has increased by 40 mV, then plussing the already established 60 mV.

Is this the correct way to think about these problems?

Afaik you can describe the potentials between the two sides of the cell membrane using the Nernst-equation. Yepp wikipedia writes the same here.

Membrane potential is a very important thing, because human cells require stable internal concentrations of Na+, K+, Ca2+, etc... in order to work properly. These concentration can depend on species, for example plants cells work completely different than animal cells, they have higher Na+ than K+ in their cytoplasm. So every human cell has to maintain a membrane potential if they don't want to die. It requires a lot of ATP (energy) to do so... Human cells typically maintain this potential against the blood plasma. Cytoplasm has around 120mM K+ and 15mM Na+, while the blood plasma has about 5mM K+ and 140mM Na+. You can count the membrane potential from these concentrations using the Nernst equation (a short presentation about how). I don't remember the exact mV value, does not matter. So human cells are working hardly on keeping the Na+ outside and K+ inside, and they can possibly die because of membrane potential changes (e.g. when they require too much energy to maintain the internal concentrations and/or osmolarity).

Excitable cells, e.g. nerve cells or muscle cells are very special because they can change their membrane potential rapidly by sending out K+, Ca+ or sending in Na+. This can create small electric discharges, which can be used to send electric signals or contract muscles, etc... Different cells have different discharge diagrams, e.g. axons have something like this:

Figure 1 - axon electric discharge diagram - source

and muscles have something like this:

Figure 2 - muscle electric discharge diagrams - source

Summa summarum it can depend on the cell type what happens, but basicly you can count the new potential using the Nernst equation by the concentration changes you mentioned...


Is the sun's damage to skin sufficient to warrant protection anytime the average person goes outside or just for extended periods? According to the American Academy of Dermatology website,

Everyone needs sunscreen
Sunscreen should be used every day if you will be outside. The sun emits harmful ultraviolet (UV) rays year round.
Even on cloudy days, up to 80% of the sun’s harmful UV rays can penetrate your skin.

I also saw this video a while ago.

The two of these make it sound like we should be wearing sunscreen even if I step outside to get my mail.

Is the sun's damage to skin sufficient to warrant protection anytime I go outside or just for extended periods? What is the general criteria this kind of organization uses to determine what is "sufficiently" damaging to warrant sunscreen protection?

Because the website you link speaks of cancer, they probably go by the rule that a single exposure and even a single photon of UV may be sufficient to cause that one mutation in that one skin cell that will eventually lead to cancer.

In the end, they are right, because mutagens (UV, cigarettes, radiation) do not follow typical toxicological rules. There is no threshold dose of UV that does not cause cancer, as even a single short exposure may do the trick. Obviously, multiple exposures and longer exposures increase the chance. This, as opposed to toxic substances that generally feature a threshold dose. Below this threshold dose they are considered harmless.


What causes the colors we see in eyes? Genetics aside, what are the biochemical reasons for the different colours of human irises?

Also, related, how does eye colour change, particularly in childhood?  (example:  my eyes used to be blue, but are now greenish-hazel).

The colour of human eyes is determined by the pigmentation present and the scattering of light. Variance in the colour and density of the pigments affects how light is absorbed and reflected causing the different iris colours we see. Wiki has a fairly comprehensive coverage on the topic so,I'll use a few of the wikipedia examples to explain how the pigmentation and scattering of light interact to give colours:

Blue eye colour is the result of pigment in low concentration and Rayleigh scattering (or Tyndall effect) of the short light wavelengths (blue is short, red is long).

  "There is no blue pigmentation either in the iris or in the ocular
  fluid. Dissection reveals that the iris pigment epithelium is brownish
  black due to the presence of melanin. Unlike brown eyes, blue eyes
  have low concentrations of melanin in the stroma of the iris, which
  lies in front of the dark epithelium. Longer wavelengths of light tend
  to be absorbed by the dark underlying epithelium, while shorter
  wavelengths are reflected and undergo Rayleigh scattering in the
  turbid medium of the stroma. This is the same frequency-dependence
  of scattering that accounts for the blue appearance of the sky.
  The result is a "Tyndall blue" structural color that varies with
  external lighting conditions.

Brown eyes are the result of higher melanin concentrations which absorbs more of the light, reducing the amount of light being reflected.

  "In humans, brown eyes result from a relatively high concentration of
  melanin in the stroma of the iris, which causes light of both shorter
  and longer wavelengths to be absorbed."

Green eyes appear to be mid-ground between blue and brown, they have more pigment than blue but less than brown.

  "As in the case of blue eyes, the color of green eyes does not result
  simply from the pigmentation of the iris. Rather, its appearance is
  caused by the combination of an amber or light brown pigmentation of
  the stroma, given by a low or moderate concentration of melanin, with
  the blue tone imparted by the Rayleigh scattering of the reflected
  light."

More can be read on this in these two studies: study 1 & study 2

What is Rayleigh scattering / the Tyndall effect and why do they turn eyes blue?

I shall refer to this as the Tyndall effect but in the literature both Rayleigh and Tyndall are used because they are apparently very similar though Tyndall occurs with much larger particles. The Tyndall effect is caused by the variable scattering of light by particles depending on the wavelength of the light and relative size of the particles. Shorter wavelength lights are scattered more than the longer ones (so more red light is absorb than blue) which means more blue light is reflected. When more melanin is present in the iris it will better absorb the short wavelength light than when there is little melanin, therefore, people with low melanin levels appear to have blue eyes.

  "An analogy to this wavelength dependency is that longwave electromagnetic waves such as radio waves are able to pass through the walls of buildings, while shortwave electromagnetic waves such as light waves are stopped and reflected by the walls."

Why do eye colours change?

Again, wikipedia has a fairly thorough section on this and I will just summarise and directly quote it. Eye colour can change because the melanocytes responsible for the pigments have to continually produce pigment and, just like those causing colour in hair, they can become less productive (which is why we have grey hair) and this happens more with age. Infants often have blue eyes that turn dark, just like yours did, because the melanin is gradually accumulated - it just takes time for enough pigment to build up and allow the eye colour to match it's genetic determinants:

  "Most babies who have European ancestry have light-colored eyes before the age of one. As the child develops, melanocytes (cells found within the iris of human eyes, as well as skin and hair follicles) slowly begin to produce melanin. Because melanocyte cells continually produce pigment, in theory eye color can be changed. Most eye changes happen when the infant is around one year old, although it can happen up to three years of age. Observing the iris of an infant from the side using only transmitted light with no reflection from the back of the iris, it is possible to detect the presence or absence of low levels of melanin. An iris that appears blue under this method of observation is more likely to remain blue as the infant ages. An iris that appears golden contains some melanin even at this early age and is likely to turn green or brown as the infant ages.
  Changes (lightening or darkening) of eye colors during puberty, early childhood, pregnancy, and sometimes after serious trauma (like heterochromia) do represent cause for plausible argument to state that some eyes can or do change, based on chemical reactions and hormonal changes within the body.
  ... eye color over time can be subject to change, and major demelanization of the iris may also be genetically determined."

In this study 10-15% of those studied had changes in eye colour beyond childhood so, al though colour is generally stable past childhood, it is not uncommon for eyes to change, and this is likely due to changes in melanin composition. This study is an example of clour change in birds too.

A side note: Animals with other colours

It is common for animals to have other eye colours, for example Blackbirds (Turdus merula) have an Orange eye, which is caused by Carotenoid pigments, rather than melanin as in humans. The reason they have this could be as an indicator of quality in courtship - carotenoids are hard to get, males with bright orange eyes therefore have access to good food resources, and female blackbirds find that attractive. (This section is all from my memory after a talk with a tutor on my undergrad field course in the Isles of Scilly).


Why do flies fly in circles? Lying on my bed, doing nothing I recently noticed flies usually fly in small circles, right under my ceiling lamp. Worth noting - the lamp was off as it was middle of a day. And those flies kept flying like this for hours, not moving anywhere else! Later I noticed it repeated every day, pretty much the same pattern. Why is that?

Flies use any object they can find as a landmark.

  The flies patrol well-defined airspaces underneath landmarks like lampshades. ... Male flies approach a landmark from below and, in the absence of other flies, settle to patrol an airspace close to the landmark. A second male approaching the same landmark chases, or is chased away by, the patrolling fly when it comes too close and may eventually settle to patrol 10–30 cm below the airspace occupied by the first fly. ... The position of male patrolling stations relative to the landmark suggests that females might arrive at landmarks from the side (and not from below, as males do), thus crossing the dorsal visual field of patrolling males.

Source: Jochen Zeil. The territorial flight of male houseflies (Fannia canicularis L.) Behavioral Ecology and Sociobiology. August 1986, Volume 19, Issue 3, pp 213-219


Small yellow bug with black head and three black stripes on the back Can anyone help me to find the name of this small yellow bug with black head and three black stripes on the back. It was found in Jura, France:

It looks like a yellower version of the brown marmorated stink bug (halyomorpha halys) nymphs I've seen in my garden in the US (west Texas). They change colors throughout their life span, so perhaps that's an older nymph that's begun changing to brown. They're prevalent in the US, Europe, and Asia, according to Wikipedia (https://en.wikipedia.org/wiki/Brown_marmorated_stink_bug).

I have no research experience with this insect, and I am not a biologist -- all of my research on this consisted of google searches for variations on "small red beetle three black lines."


What is the best way to clean plastic flasks that have been used for cell cultures - is virkon a good idea? When you use cultures e.g. insect cells, which are infected with virus one way to clean the (plastics) shake flasks is with virkon. Which is the most effective way to clean your flasks in order to extinguish the virus?
Also, is it effective to use SDS in order to denatured the virus proteins?

I use virkon for cell cultures, but for viruses I tended to use standard bleach during the time I worked in a virology lab.


Will dissolved proteins pass through a 0.2 micron filter? Given that there may be exceptions, can you usually expect protein to pass through?

Many proteins will pass through a 0.2 micron filter. If the proteins aggregate or if they stick to the filter material because it is charged, they may not.

Barring the above, a 0.2 micron filter will allow proteins up to 200kd to pass through.  There are some proteins that are larger.

Editing with some source material.

Nice Presentation on Pore Sizes and Membranes Here

Graphic from that presentation:


How do fish tolerate pH changes in water? I want to know how aquatic animals behave as a natural indicator of the acidity in lakes and rivers.

How do they tolerate these pH change?

Often, in terms of a water body becoming acidified, it depends on the rate of acidification.  Fish and other aquatic species, such as invertebrates, are fairly resilient to miniscule changes, but they also have a threshold at which not a lot of them, adapted or no, can survive.

From the U.S. Environmental Protection Agency (http://www.epa.gov/acidrain/effects/surface_water.html):

  Acid rain causes a cascade of effects that harm or kill individual fish, reduce fish population numbers, completely eliminate fish species from a waterbody, and decrease biodiversity.  Low pH [...] is directly toxic to fish. In addition, low pH and increased aluminum levels cause chronic stress that may not kill individual fish, but leads to lower body weight and smaller size and makes fish less able to compete for food and habitat.

  Some types of plants and animals are able to tolerate acidic waters. Others, however, are acid-sensitive and will be lost as the pH declines.

Commonly, benthic invertebrates (including insects, crustacean and molluscs) are used as indicators for ecosystem health.  Invertebrates that need a high amount of calcium, such as crayfish (for their exoskeleton), are typically not found even in slightly acidified lakes.  Other invertebrates can be used as indicator species because they respond to changes in water conditions, such as pH.

A good example of this is the acid rain that occurred in Sudbury, Ontario, Canada as a result of sulfur dioxide emissions from mining activities, which were especially high in the 1970s.  This affected the lakes in the area not only from acid rain, but the runoff as well as there were no trees left.  The pH was so low that it effectively made all lakes in the area sterile. Since then, a lot of effort has been put into bringing back the native aquatic species, such as liming the lakes and restocking them with species such as Brook Trout (Salvelinus fontinalis).  More information can be found here:

http://link.springer.com/article/10.1007%2FBF00160348

Therefore, I do not know that aquatic animals necessarily behave a certain way as a natural indicator of acidity, however it is more of their presence or absence that biologists use to determine acidity and the overall ecosystem health in lakes and rivers.


What happens to blood after a person dies? After a human dies, what happens to their blood?  I know that it tends to accumulate in the lower areas of the body, whichever parts are closest to the ground, but I am wondering about coagulation.  Does the blood always coagulate?  How long does this take?  Does it ever "de-coagulate"?  If so, how long does that take?  If it coagulates, then "de-coagulates", does it "re-coagulate"?  How long does that take?

Note:  I'm asking this question because I am a fan of The Walking Dead, but I have always been a bit puzzled by the fact that on that show, the blood of zombies (who are dead) is consistently depicted as being fluid, dark red, and not coagulated at all.  I'm obviously not asking about the particulars of zombie blood, because zombies don't exist (yet).  I'm just curious as to whether it is possible for blood to remain liquid, and similar in appearance to the blood of living people, after death has occurred.  You can see my related question, on SF&F.SE, by clicking here.

After death, blood normally coagulates unless the deceased has ingested certain medications or chemicals (e.g. anti-coagulants).

According to this article, normal clotting time is 3-15 minutes: http://www.angelfire.com/sc3/cjrp/forensicsofdeath.html

However, this probably applies to external wounds, like cuts. When a person dies, the blood pooled internally would probably take longer to coagulate. You might find the answer by typing blood + coagulate + forensics into Google.


Immunoprecipitation compared to western blotting Immunoprecipitation and western blotting are both used to locate a specific protein within a sample and to isolate it.  In immunoprecipitation, a specific antibody and agarose beads ( or other insoluble beads) are used to precipitate the protein. In western blotting, SDS-PAGE is carried out and primary and secondary antibodies are used to locate and isolate the proteins on the nylon membrane.

My question is: which technique should be used when? what is the difference between the two? is one of them "better" / does one of them have advantages over the other?

The two techniques serve different purposes:

IP: purifies a protein

WB: visualizes or quantifies a protein

Most often when I have done IPs (in the hazy past) I have turned around and run the protein out on a WB, so one will frequently combine both techniques. Sometimes a protein is very low abundance so you will not see it in a small volume of crude cell lysate on a WB, and you have to IP it from a large number of cells to get enough protein to visualize on a WB.

Note that IPs will also co-purify associated proteins, so a good way to know whether two proteins stick together is to IP one of them and probe for the other on a WB. This "co-IP" analysis is a very common use case for both techniques.

Hope that helps.


DNA test to prove that two grand-grand-children descend from same grand-grandparents Can DNA test prove that two persons descend from same great-grandparents (or test where one great-grandchild and grand-child are tested)?

Yes testing for relatedness of grand-grand children is possible. (Ignoring some very unlikely, but theoretically possible cases.)

Grand-grand children are still highly related genetically, and this degree of relation is also shown in standard consumer grade commercial DNA testing kits (such as 23andme, where you could link to other people and see their degree of relatedness to you – even further beyond grand-grand children - or where you could even search for relatives, whom you may not know personally).


Why are the bacteria that cause hospital-acquired infections resistant to many antibiotics? Why are the bacteria that cause hospital-acquired infections resistant to many antibiotics, and why don't hospital acquired infections exist elsewhere ?

The infections that are caused in hospitals are usually a result of bacteria that are resistant to multiple antibiotics making them difficult to treat, but why are the bacteria resistant to all these antibiotics?
I realize that a lot of antibiotics are used in hospitals but the question that comes to my head whenever I read this is "So?".
To make my misconception clearer, I will use MRSA as an example .
I mean , for the Staphylococcus aureus bacterium to become resistant , the antibiotic has to be used on it , so how can the antibiotics used to treat different infections in difference people act as a selection pressure for  Staphylococcus aureus ( the Bacteria that causes MRSA )?

Hospitals have certain features:

They are full of people immunocompromised in some way (old, exposed tissue, on steriods etc.)
They are full of people with pathogens
They are full of doctors who will give antibiotics to people with pathogenic infections

This is a perfect breeding ground for drug resistance in pathogens, with lots of pathogens, lots of places for them to grow (patients) and quite a lot of exposure to antibiotics.  You use Staphylococcus aureus as an example, and it is a good one.  We all have some of it on us, but it is not generally exposed to antibiotics so it does not develop resistance, and we do not generally have large areas of exposed flesh that would cause it to be pathogenic.  In hospital this is not the case, so we get it causing trouble and developing resistance.

These things do occur outside of hospitals, but it does not tend to be as common or frequent.


What is this thing that is growing in my yard? And should I get rid ot if? I live in Wilmington, Delaware (Mid-Atlantic USA).  The north side of my yard is largely shaded by my house and grass is spotty.

Periodically when I go into the yard I will find as many as four pod-like things have opened on the ground.  I almost never notice them before this stage, the one time I did it looked like a patch of dirt until I stepped on it and it sort of shattered.

I'm baffled by it and my wife thinks it's some form of fungus.

We have two children under 4 and we are concerned it could be poisonous.  It certainly doesn't enhance our yard's attractiveness.

With that in mind, I have a handful of related questions:

What is it?
Is it dangerous?
How can I get rid of it, if I so choose?

Addendum:

I believe we have found an unopened example of what we've been seeing:

Myriostoma is a fungal genus in the family Geastraceae. The genus is monotypic, containing the single species Myriostoma coliforme. It is an earthstar, so named because the spore-bearing sac's outer wall splits open into the shape of a star. Source: Wikipedia.

But this recent article shows otherwise https://pdfs.semanticscholar.org/08ea/2ee6be93787f2e0034b85222b751a5281167.pdf


Formation of disulfide bonds in protein expressed after transduction Say I transduce a nucleic acid sequence using a viral vector that encodes a protein having at least one disulfide linkage. For simplicity, let’s assume that there are only two cysteines in the protein and the side chains of these cysteines are close together when the protein is folded with the cysteines unlinked (reduced/thiol). Also assume that the cell being transduced is a eukaryotic cell (mouse or human). What is the chance that this disulfide will be linked (oxidized) when expressed by the cell? Does this happen pretty reliably? What might it depend on?

I am not an expert on expression of genes from viral vectors, but as I requested the poster to clarify his question I feel an obligation to provide at least a partial answer.

The first question to address is whether the mRNA for the protein of interest is expressed in the same way as normal cell proteins. In the case of the lentovirus vectors which are integrated into the genome there is no reason to think otherwise.

In this case the factors determining the formation of disulphide bonds would be the same as for any similar normal cell protein translated from mRNA.

In summary:

Only secreted proteins have disulphide bonds.
In eukaryotes these protein are synthesised on ribosomes on the endoplasmic reticulum, which obviously must be present in the cell in which one is trying to express the protein (i.e. it must be capable of secreting proteins). One assumes that if one is restoring a function found in normal cells this will be so.
Oxidation of sulphydryl groups occurs in the intercisternal space before secretion. It involves a number of proteins and there are reduction and chaperone systems to deal with inappropriate oxidation, which occurs to a greater or lesser extent. A recent freely-accessible account of this topic can be found in a Cold Spring Harbor perspective by Neil Bulleid in 2012.
The (small?) proportion of incorrectly oxidised proteins that are not recycled are presumably removed by the cellular mechanisms that degrade aberrant proteins.

It would not seem possible to answer in a literal manner the question what the numerical ‘chance’ is of correct oxidation, but this would not seem to be pertinent. The question of interest is whether the protein would be oxidised to the correct native structure with the same efficiency as in normal circumstances. There seems no reason to think it would not.


Why don't carrier proteins require energy to change shape? I know that carrier proteins can be used for both passive and active transport, but I am referring to the facilitated diffusion aspect. Even though facilitated diffusion via carrier protein goes along the concentration gradient, the protein still must change its shape, from what I understand. Why does this process still not require ATP, and why does it require ATP to go against the concentration gradient in the same manner?

The carrier proteins that participate in passive transport do not require energy in the form of ATP molecules, which is the primary form of metabolic energy of the cell, but this does not mean that the transport process is energetically 'neutral'. Many proteins bind their ligands via hydrogen bonds, partial or full ionic bonds, van der Waals interactions, etc. These interactions build up a type of energy known as 'binding energy', which can be enough to induce a conformational change in the transporter. In addition, consider that a chemical gradient in itself is a form of energy, which effectively drives the movement of many solutes across the membrane. In fact, the gradient of a molecule can be used to transport another type of molecule, without using ATP. For instance, consider the Lactose permease. Its mechanism is, I quote:

  Hydronium ions from the outside of the cell bind to a carboxyl group
  on the enzyme that allows it to undergo a conformational change. This
  form of lactose permease can bind lactose from outside the cell. The
  enzyme then everts and lactose is transported inward.

Below a diagram of this protein, with its ligands in the center:

That being said, some proteins that are involved in passive transport do not require conformational changes like these I described, because they are simply 'open' (like a tunnel), and the solutes can freely diffuse across the channel. This is the case, for instance, of aquaporines. The advantage of the carriers that need to change conformation is that the binding to their transported molecule implies a recognition mechanism, which gives high specificity, whereas the proteins that are simply 'open' are less selective and thus transport many different solutes. See, for instance, the central pore of an aquaporine:

Regarding your last question, the hydrolysis of ATP can release enough energy that (similarly to the binding energy described above) can induce a conformation change in the transporter protein (active transport). This is often used when going 'against' the gradient because, as I mentioned, the gradient in itself contains energy that if not used passively (as in passive transport) then it is not favorable to transport something against the gradient. Thus, an external source of energy is needed (ATP!).


Crispr-Cas9 method and nobel Since i had my first cell class at university i have heard about Cripsr Cas9 method. But I am quite surprised about one fact.  Why actually wasnt rewarded by Nobel price? Is it something like Einsteins relativity (to early to reward it)?

My guess is that some people (likely Jennifer Doudna, Emmanuelle Charpentier and Feng Zhang) will eventually be awarded a Nobel Prize for the discovery of CRISPR and the development of its applications for genome editing, because it really is a major advance. But for now, the University of California Berkeley and the Broad Institute are still legally fighting over patent conflicts, and the patent situation worldwide is generally complicated. I think this is a possible reason why the Nobel committee decided to wait.


What's the difference between diuretic veggies and alcohol that make the latter bad? So I'm reading this article to Treat Fluid Retention and it suggests

Eat foods with diuretic properties.

But also

Avoid drinks that will dehydrate the body such as tea, coffee and alcohol.

As I understand, tea, coffee and alcohol are plenty diuretic. So what makes those veggies's diuretic nature better than alcohol's?

I know alcohol is more harmful than veggies, but I mainly wanted to know how do diuretic veggies help you when infact the diuretic alcohol actually makes you dehyderated? How's veggies' diuretic nature more helpful than the alcohol's (disregarding other side-effects of it)?

Firstly I would suggest if you have concerns about suffering from symptoms fluid overload you should consult your doctor. Self diagnosis and self treatment is not a good option.

In terms of alcohol being used as a diuretic, you have to bear in mind that there are many deleterious effects of excess alcohol. By consuming alcohol as a diuretic you would most likely cause more health problems than you solve.


Can two hammerhead ribozymes simultaneously cleave each other? I am working on a project in which an XOR gate is being built by having two hammerhead ribozymes simultaneously cleave each other when both are expressed, but have these ribozymes cleave a target transcript when expressed alone. Has it ever been shown in the literature that a hammerhead ribozyme was able to cleave the flanking arms of another ribozyme?

[ For the sake of answering a question that is long unanswered ]

  Can two hammerhead ribozymes simultaneously cleave each other?

Yes, in principle they can.

  two hammerhead ribozymes simultaneously cleave each other when both
  are expressed, but have these ribozymes cleave a target transcript
  when expressed alone.

This may be realized only when ribosomes have higher affinity for each other than for the target. As you said in the comment, inserting few mismatches in the ribozyme-target interaction may work. You may need to notice that since the two ribozymes are complementary to each other but cleave the same target, the target sequences will form a set of two mutually complementary regions. If separated well enough, there may not be much of a problem. From your design strategy I guess that UTRs are the best place to keep the ribozyme target sequence. If you keep both the target sequences in the 3'UTR (lets say), then they may form a hairpin structure, which may interfere in the targeting. So you can insert mismatches that also destabilize the possible hairpin.

  Has it ever been shown in the literature that a hammerhead ribozyme
  was able to cleave the flanking arms of another ribozyme?

Not yet. Self cleaving examples are there but not mutually cleaving ones.


Unknown mite species in plant pots Does anybody know what kind of mite this is?

It is living in my pepper plants' pots.
My region is south of Germany. (Baden-Württemberg)

I will try to take another picture including some size measurement today.

Update:

As suggested by @theforestecologist, I added pictures including a size bar.

Thanks to @tyersome, I managed to merge my two accounts now.

These look a lot like dust mites, a collective term to describe cosmopolitan house-dwelling mites in the Pyroglyphidae family.

The most common species in temperate regions belong to the Dermatophagoides genus, including D. pteronyssinus (the European house dust mite) and D. farinae (the American house dust mite).

 source: Wikipedia

See here for a closeup of D. pteronyssinus

Alternatively, they may be "storage mites" belonging to the Acaridae family, which are another group of common dwelling-inhabiting mites that are more often found in stored foods vs dust, upholstery, or carpeting.

Lepidoglyphus destructor is one such example but that is also found to be present in dust [Source: Juliá et al.(1995)]. Another common storage mite, Tyrophagus putrescentiae typically eats mold, and could be found outside a food setting if the mold density was prevalent enough.

 L destructor (according to M. Deml on biolib.cz)

I'll note that there are hundreds of mites in these two families of mites alone, so someone may be able to get to a more specific species for you. Knowing more about where you found them (species of plants, etc.) may or may not help narrow down more specifically. For example, the person in this forum post found a very similar looking mite on their pots as well (see here).

Description:

Both male and female adult house dust mites are globular in shape, creamy white and have a striated cuticle. The female measures approximately 420 microns in length and 320 microns in width. The male is approximately 420 microns long and 245 microns wide.  [Source: UFL.edu]

Human impact:
The genus name Dermatophagoides means "skin eater," but these mites are not parasitic. Their diet mainly consists of eating dead skin flakes from mammals (and some birds).  Human detritus is one of the primary food sources for these mites, and so it's no surprise that they are often associated with dust in human dwellings.
So these mites don't bite humans or burrow into their skin. However, they do tend to have a negative impact on humans. Specifically their digestive enzymes remain in their feces, and these dried fecal enzymes (along with their dried dead exoskeletons) cause allergic reactions in people. In fact, according to Raulf et al. (2015), 20 allergens are known from just the two species of hdust mites mentioned above!
From UF IAFS

Mite allergens are mainly present in feces of house dust mites and may become airborne and inhaled by patients, giving rise to asthma, rhinitis, or atopic dermatitis

In fact, the family name, Pyroglyphidae, which literally means "fire + carve", seems to be related to the "burning itchy" eczema that some people develop that results in lots of scratching (carving :p).

Multiple sources suggest that storage mites often have similar allergic impacts as dust mites. Fro example, this site suggests:

In Europe, Lepidoglyphus destructor has been reported to be a major source of mite allergy in rural and urban environments

The question is, how many people are impacted?

Well, according to studies cited again by Raulf et al. (2015) that examined 7000 Germans found that  ~16% had a sensitization to D. pteronyssinus. Other studies (discussed in Hossny et al. (2014)) seem to suggest much higher prevalence in certain populations -- with sensitivities found in up to 90% of people tested from certain populations.

What can you do??
According to UF IFAS:

To manage mite populations, reduce the humidity below 70% and thoroughly vacuum mattresses, carpets, sofas, and chairs. Very sensitive individuals should encase their mattresses in plastic. Use drapes that can be washed and change bed clothing frequently. Vacuuming does not always remove all the live mites and Korsgaard (1982) stresses reducing humidity over sanitation. No one method has been found for reducing mites and relieving allergy suffering. Immunotherapy, i.e., injections of mite extracts into the patients to increase antibody level, has had variable success (Munro-Ashman et al. 1976).

Final word(s):

I'll just mention that there is a ton of literature about these mites and their impacts on humans, so if you're interested, DIG IN!

The [Major Mite Taxa] key by D. E.  walter (find at idtools.org](http://idtools.org/) is an excellent online resource for digging into mite identification further!

Citations:
Hossny, E., El-Sayed, S. and Abdul-Rahman, N., 2014. Sensitivity to five types of house dust mite in a group of allergic Egyptian children. Pediatric allergy, immunology, and pulmonology, 27(3), pp.133-137.
Julia, J.C., Martorell, A., Ventas, P., Cerda, J.C., Torro, I., Carreira, J., Guinot, E., Sanz, J. and Alvarez, V., 1995. Lepidoglyphus destructor acarus in the urban house environment. Journal of investigational allergology & clinical immunology, 5(6), pp.318-321.
 Raulf, M., Bergmann, K.C., Kull, S., Sander, I., Hilger, C., Brüning, T., Jappe, U., Müsken, H., Sperl, A., Vrtala, S. and Zahradnik, E., 2015. Mites and other indoor allergens—from exposure to sensitization and treatment. Allergo journal international, 24(3), pp.68-80.


What virus transforms full grown plants? I read an article by a gardener describing how a virus had transmitted a negative trait to his plants. It rather shocked me, because I hadn't realized that a virus could transform an adult plant. I was aware of dipping arabadopsis flowers in agrobacterium tumefaciens, but the concept of non-reproductive structures being transformed seems fascinating. What kind of virus is capable of that?

Viruses can infect just about any living thing, so that it could infect a plant is no surprise.

Your article describes how a small virus-infected part of a plant had been cloned and consequently the entire cloned plant was infected, and it infected plants grown hydroponically in the same water. No surprise there either.

Plant viruses have been known for centuries. One of the earliest recorded descriptions of a virus-infected plant can be found in a poem written by the Japanese Empress Kōken (718–770), in which she describes a plant with yellowing leaves in summer. The plant (a Eupatorium) was described as "autumnal".

The top 10 plant viruses (in one paper) in molecular plant pathology were listed as:

  (1) Tobacco mosaic virus, (2) Tomato spotted wilt virus, (3) Tomato yellow leaf curl virus, (4) Cucumber mosaic virus, (5) Potato virus Y, (6) Cauliflower mosaic virus, (7) African cassava mosaic virus, (8) Plum pox virus, (9) Brome mosaic virus and (10) Potato virus X, with honourable mentions for viruses just missing out on the Top 10, including Citrus tristeza virus, Barley yellow dwarf virus, Potato leafroll virus and Tomato bushy stunt virus.

Some plant virologists even care enough to argue about it.

One paper describes how a plant was improved by a viral infection:

  In all cases, virus infection delayed the appearance of drought symptoms. Beet
  plants infected with CMV* also exhibited significantly improved tolerance to freezing. Metabolite profiling analysis showed an increase in several osmoprotectants and antioxidants in BMV**-infected rice and CMV-infected beet plants before and after drought stress.

*Cucumber mosaic virus
**Brome mosaic virus

Aetiology: The earliest recorded plant virus disease
Top 10 plant viruses in molecular plant pathology
The REAL Top 10 for Plant Viruses

Introduction to Plant Viruses, the Invisible Foe

Virus infection improves drought tolerance


Scrotal temperature and vascularization The testes (at least in human males) are vascular organs, the vascularization extending even o the interstitial spaces of the seminiferous tubules. The function of the scrotal sac, is to isolate the testes from the abdominal cavity, and provide a lower temperature ($1-2^\circ \text C$ lower than normal body temperature of $37^\circ \text C$).

  But since the blood is the main temperature-buffer maintaining the
  normal body temperature and the scrotal (testicular) tissues are
  considerably vascularized, why doesn't the blood flow raise the
  scrotal temperature to normal body temperature?

If the reason is the location of scrotum external to the abdomen, then all limbs and limb-extremities are located in the similar way (and in those cases, heat dissipation would be faster than in case of scrotum due to less surrounding insulation by thighs and clothes), and hence the temperature of all parts except the interior of the head and abdomen must be at considerably lower temperature? Is this the case?

The fingers and toes (for example) ARE at lower temperatures than the interior of the torso.  It's why it's so easy to get frostbite on the extremities. As for temperature regulation of the testes, you have to also consider that humans evolved without clothes...i.e. The testes just "hang out" and get lots of airflow, as opposed to modern times, when they are typically under (usually) more than one layer of clothing.

Also, for reference, I took some quick IR temp readings on myself:

Room temp: 19.9C

Fingertip: 27.0C

Palm: 31.8C

Axilla: 34.6C


How are lysosomes formed? Lysosomes are irregularly shaped membrane bound organelles containing 50 different types of enzymes.

But how are they formed? How are they produced??

Cells take up external material in the process pf phagocytosis. This involves creating a vesicle from plasma membrane that will contain the external material. The vesicle enters the cytoplasm where it is called (early) endosome. The cellular membrane components of this endosome are recycled and gave back to the plasma membrane. The endosome pH decreases and it is now called late endosome.

Meanwhile, peptides (which will form the future hydrolases) are produced in the ribosomes of the endoplasmic reticulum and mannose 6-phosphate is added to these peptides. They are further transported to the Golgi apparatus which "packs" them into lysosomal vesicles.

The lysosomal vesicles fuse with a late endosome and due to the acidic medium of the endosome, the peptides dissociate from mannose 6-phosphate. This process turns the late endosome into a mature lysosome that is capable to digest material taken up via endocytosis.

  My book wrote: lysosomes are formed from ER or golgibodies.

ER and Golgi help supply the enzymes to endosomes, thus turning them into lysosomes.

References:

Wikipedia contributors, "Lysosome," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Lysosome&oldid=635272974 (accessed November 30, 2014).
Cooper GM. The Cell: A Molecular Approach. 2nd edition. Sunderland (MA): Sinauer Associates; 2000. Lysosomes. Available from: http://www.ncbi.nlm.nih.gov/books/NBK9953/


Publicly available genotype data? I am a statistician and I'd like to test my new method on biological data. For this I am looking for genotype data for a number of individuals. That is, I am looking for something like this:

                    | Individual 1 | Individual 2 | Individual 3 | Individual 4 | ....
Chromosome 1 SNP 1  | AA           | BA           | AB           | BB           |
Chromosome 1 SNP 2  | AB           | AA           | AB           | BA           |
Chromosome 2 SNP 1  | BB           | AB           | BB           | AB           |
etc.

I don't really care about the species. Ideally I'd like to have data for complex and less complex genotypes (different number of chromosomes and number of SNP's).

Are there any publicly available data sets like this? I have been searching the internet, but I can't find any.

that's the stated purpose of the thousand genomes project.

the thousand genomes project has.. 1000 genomes.

its all downloadable.

http://www.1000genomes.org/


Can DNA be flattened? DNA is always shaped like a double helix. But could you flatten the double helix (which is essentially just a twisted ladder) and would DNA still be able to duplicate and control cells?

Flattening the double helix, i.e. making it look like a ladder (like in the usual diagrams of DNA, shown in the first figure below), would not be possible because of bond angles.

Figure 1

Figure 2

The only way for everything to be flattened out completely (as in Figure 1), is for all the bonds to be planar. However, we know that this is not true, as the C1 (carbon 1) is sp3 hybridised, not sp2, which means that the bond from the sugar to the nitrogenous base is not planar. The bond with the phosphates is also not planar. Hence it would be impossible to flatten DNA out like paper.

Moreover, there are relatively strong London dispersion forces between the layers of bases in the 3D structure (helical form). You can see on Figure 2 that the bases lie parallel to each other in each "step" of the helix. This adds to the stability of the molecule.

To answer your second question about whether DNA would be functional if flattened out, the answer would be no. The helical shape of DNA means that there is a minor groove and major groove, which is a property of its 3D shape. This is where proteins bind, which will help the process of replication (duplication) and transcription ("controlling" cells).

Figure 3


Which countries do not feature mosquitoes? Please, I am so itchy, I need to know: which countries are free of mosquitoes?

According to India.com, Chris is right and Iceland has been declared mosquito free.

The science behind this is quite interesting and there are various hypotheses regarding as to why Iceland doors are shut to mosquitoes. The most preferred hypothesis by scientists, according to New York Times is >>

  When mosquitoes lay eggs in cold weather, the larvae emerge with a
  thaw, allowing them to breed and multiply. Iceland, however, typically
  has three major freezes and thaws a year, creating conditions that may
  be too unstable for the insect’s survival.


Why asexual reproduction? When I took a course on genetics and evolution, I learned that recombination and sexual reproduction is advantageous compared to asexual reproduction. Sexual reproduction allows more combinations of DNA because of recombination, allowing more variations of species, causing natural selection to "choose" different variations of species to reproduce and share their genes to help the species from dying out. On the other hand, asexual reproduction doesn't allow recombination. So species can only rely on mutational changes to keep a species safe from extinction. Therefore, why don't we see more sexually reproducing species than asexually reproducing species? Sexually reproducing species have an advantage, don't they?

When you say, why don't we see more sexually reproducing species than asexual, I presume you are referring to bacteria, protists, archaea, some fungi, etc.

Most multicellular organisims do reproduce sexually, which makes sense since an organism would need to be multicellular to have cells specialized for gametes. As you stated, the advantage is that sexual reproduction offers an advantage by allowing more rapid generation of genetic diversity, allowing adaptation to changing environments.

However, look at the single-celled organisms that reproduce asexually. Asexual reproduction is beneficial in many circumstances in that it can create individuals rapidly and in large quantities. For example, yeast can duplicate every hour under the proper conditions. For yeast, that means survival by sheer numbers. For us, it means we can make bread in a few hours.

If you believe asexually reproducing organisms are at a disadvantage due to lack of genetic diversity, consider bacteria and antibiotic resistance. The rapid generation times allow mutations to be selected for in particular circumstances. Penicillin was introduced in 1941. Two years after this landmark event, strains of Penicillin-resistant S. aureus had already emerged. Now, perhaps 2% of Staph. aureus (SA) is susceptible to penicillin, and some SA are "superbugs" with multidrug resistance: good for Staph, bad for us.

Also, it is possible for single-celled organisms to "share" DNA through mechanisms sometimes likened to sexual reproduction; lateral gene transfer occurs through conjugation, transformation and transduction.

Thus, both asexually and sexually reproducing organisms are well-suited to their ecological niches.


Composition of EZ-Vision® DNA Dye? I'm looking for the composition of the EZ-Vision DNA Dye for electrophoresis visualization. I could not find anything helpful on the web.

I would appreciate a lot your help :)

Contacted technical support and received the following response:
"Unfortunately, the information you requested is proprietary and we will not be able to share the images of excitation-emission spectra of EZ-Vision® Bluelight DNA Dye and the chemical structure of the dye. "


How to edit manually pdb structures? I would like to manually movement some b-sheets from a 3D structure of my PDF protein to represent a change in its structure.There some tool i can do that?

If I remember correctly pymol can edit pdb structures (as well as visualize them).

I've used a student version though (which is a free full version) and I'm not quite sure if its possible to use pymol without buying a license nowadays (though the source code is still open source, so can in principle always install it from that)


When are a female's eggs created? Since a human woman is born with a set number of eggs, and meiosis is the process by which sex cells are produced, would meiosis in a woman happen before she is born or soon after she was born?

If meiosis creates sex cells and women are born with a set number of sex cells, when in the development of a woman are her sex cells created?

Oocytes, or immature female eggs, develop in the fetus's ovaries during pregnancy. This graph (U. New South Wales) shows the oocyte population over time in a human female:

Although the x-scale is kind of confusing (months when negative, years when positive), you can see that the fetus has all the oocytes it will ever have at the peak 18-22 weeks after conception. Since age 0 is birth, meiosis in a woman happens long before she is born.


Are chromosomal microdeletions passed on? I've been looking around but can't find a clear answer: are chromosomal micro-deletions passed on (hereditary) or not?

Of course. Just like any other type of mutation.

If a mutation (incl. a chromosomal microdeletion) happens in the germ line, then the mutation can be passed on.


What species is this large bug? (South India) I found this bug in South India. What species is it? The tiles in the picture are 5x5 centimeters each. The bug was moving relatively slowly and didn't seem to fear me much.

I tried asking it directly, but it kept claiming to be a feature.

I suppose it's a whip scorpion.

  Whip scorpion (order Uropygi, sometimes Thelyphonida), any of approximately 105 species of the arthropod class Arachnida that are similar in appearance to true scorpions except that the larger species have a whiplike telson, or tail, that serves as an organ of touch and has no stinger. The second pair of appendages, the pedipalps, are spiny pincers, and the third pair are long feelers.

It is most common in India and Japan to New Guinea.


Why would an Eadie-Hofstee Plot be non-linear? Besides cooperativity between multiple active sites on an enzyme, what are the other reasons for the Eadie-Hofstee plot to be non-linear?

The reason is that the inhibition models are inherently wrong.

Inhibitors bind to enzymes with the same mass action principles as substrates do so the term that should describe their binding should mirror the form of the MM equation i.e. ([S]/([S]+km)).  However all the traditional equations use (1+([I]/Ki)) rather than ([I]/([I]+ki)).

To compound this problem the (1+([I]/Ki)) term multiplies into the Km in competitive inhibition but divides into the Vmax in the noncompetitive equation.  It is therefore not affecting these terms in the same way in these separate equations and leads to the conclusion it is upside down in the competitive equation.

The plots above are deceiving as they allow the user to look at a linear plot and assume mechanism based on axis intercept pattern without analyzing the actual change in kinetic parameters produced by the inhibitor.  Kinetic models should be only fit using global data fitting to the proposed inhibition model.  This can be done quite easily using excel, for an example of how this can be done check out Kemmer and Keller 2010, or check youtube.

Kemmer G, Keller S. 2010. Nonlinear least-squares data fitting in Excel spreadsheets. Nature Protocols 5:267-281.

By realizing that the change in enzyme kinetic properties relates directly to inhibitor binding the logical hyperbolic shift in values exactly like the hyperbolic curve of the MM equation must be acknowledged and finite changes in the kinetic parameters must be accounted for.

i.e. Km = Km-((delta Km)*([I]/([I]+Ki)))

  Vmax = Vmax-((delta Vmax)*([I]/([I]+Ki)))

While I have been told this may be over fitting as the competitive, noncompetitive, mixed noncompetitive equations define inhibition with one or two inhibition constant (Ki alphaKi), these terms eliminate the need for all of these equations and the family of equations that they spawned as they proved ineffective over the years (such as uncompetitive, partial competitive, partial noncompetitive, partial mixed noncompetitive, I could go on but I think you get the point).

Additionally the competitive, noncompetitive and mixed noncompetitive equations define the effect of the inhibitor with the equilibrium binding constants and do not allow for the possibility that complete inhibition may not occur (no delta terms), leading to the family of equation to try to make up for this, i.e. partial competitive and partial noncompetitive.

Use empirical models and stop trying to force mechanistic models, the data will suggest the mechanism with good experimental design.