Equilibrium and Metabolism: Can cells exist at STATIC equilibrium? What about dynamic equilibrium? I understand that in closed systems, once reactions reach equilibrium, they can no longer be used to power other reactions. If a cell was a closed system (which it is not), being at equilibrium would mean that it's dead, for it needs a continuous input of energy from the environment.

I know that the cells are open systems, and my teacher mentions that cells can never be at equilibrium. But, I am confused because can't cells be at dynamic equilibrium (where rates of reactions = rates of products)? So my next question is: can the cells not exist at static equilibrium? I am not quite understanding the differences between equilibrium, dynamic, and static. And, when something is at dynamic equilibrium, why does this mean that the concentrations of reactants and products are not necessarily equal?

There are some things that should be addressed first.

Chemical-Equilibrium
This is a condition at which the forward reaction rate is equal to the backward reaction rate for a reversible reaction.
$$\ce{A<=>[k_f][k_r]B}$$
In this case, $k_f.A=k_r.B$, at the equilibrium, if the reactions are first-order. If $k_f>k_r$, then the concentration of B would be higher than the concentration of A, at equilibrium point.

Steady-State
It is a state of the system at which the overall concentration of all the components (reactants and products) remain constant with time, or oscillate at a constant amplitude and frequency. Mathematically, the differential equations that denote the system (as mentioned by Dexter) would equate to zero.
If this condition applies only for one or more but not all the components of the system, then it is said to be in a Quasi-Steady-State.
If there are only two species which inter-convert but do not get formed or degraded, then steady state would be same as the chemical equilibrium. However, it is to be noted that chemical-equilibrium is a property of a reversible reaction whereas steady state is the property of the system.

Coming to your main question, I do not know what your teacher really had in mind, but this is my explanation.
According to the above definitions, you cannot say that the cell is in equilibrium because the cell is a system and not a reaction. The usage of the term "equilibrium" varies between different fields of study and physicists do use steady-state and equilibrium interchangeably. However, this is not the practice among chemists and biochemists.
Having said that, I would say that a cell does attain a steady state. I think what your teacher wanted to imply was that a cell constantly responds to the external stimuli (which is randomly changing) and therefore never remains at any given steady state for a long time.

Can the cells not exist at static equilibrium?

No, they don't. In fact the term "static equilibrium" in never used in chemistry because it never really happens. At a static equilibrium all the rates have to be zero, whereas in a dynamic equilibrium the rates have to balance each other out. Static equilibrium usually applies only for macroscopic objects (which do not include molecules).
A note on stochasticity: Chemical reactions follow probabilistic kinetics i.e. the reactions occur with some probabilities, instead of fixed rates (these probabilities can be unequal for different reactions). Chemical systems can be approximated by deterministic models at the thermodynamic-limit which reflects the "average" behaviour of the system.

when something is at dynamic equilibrium, why does this mean that the
concentrations of reactants and products are not necessarily equal?

See the first section. Similar logic applies for steady-state. The steady state concentrations depend on the kinetic parameters.


How did zootoxins evolve? I've always wondered how toxins in certain organisms have evolved. Particularly, organisms that produce toxins as a deterrent to predators as opposed to organisms that use it to paralyze their prey.

Where did this toxicity come from? How did it develop to what it is today?

There must've been a drawn out period where evolution 'tested' and 'fine-tuned' the toxin. Presumably until it was somewhat efficacious to the target.
What are the current popular theories on this?

General overview.
Each toxin and poison probably have their own evolutionary "arms race". Generally, an organism contains a compound that is a bit harmful to other species. As a predator or prey species becomes tolerant to low doses of this compound through natural selection, the compound efficacy could be increased (again by natural selection) on a molecular level, or at a dosage or concentration level.
Below are a few examples of where this has become the case, and some more general examples of how venom evolved in the first place.
Examples.
California Newt.
These newts contain tetrodotoxin (you may be familiar with this from the fugu fish). It is preyed on by a species of garter snake. This is a textbook arms race as the garter snake is naturally selected to have beneficial alleles that are tolerant to the toxin.
Dart Frogs.
The golden dart frog Phyllobates terribilis contains enough batrachotoxin to kill 10 people. That is apparently overkilling for any predator it would surely have to face especially given that the only animal alive that is immune to the poison is the frog itself. However, the snake Liophis epinephelus can tolerate massive doses of batrachotoxin (although I've heard it gets pretty poorly after eating a frog, rather understandably). These two species are locked in an arms race that drives the frogs to produce an unbelievably fatal cocktail and the snakes to become ever more tolerant.
Snakes.
Modified sweat glands evolved to damage the prey as much as possible for immobilisation, partial digestion, or defence. There are textbooks about snake venom and toxins. Here is a neat article I found with a cursory search or if you want to sink your teeth into the topic (heh.) check out this article.
Long story short: venom sacks are modified saliva glands from non-venomous snake ancestors. The diagram shows generally just how modified these apparatus have become!

Platypus
Let's not forget the weird and wonderful monotremes. It's hard to pinpoint exactly what drove the platypus to develop venomous barbs on its elbow (last time I looked into it, it was still disputed if they were for defence or hunting).

But what we can learn from this is that venom can independently evolve. Although the venom producing proteins are different, they produce the same venom as some snakes.


Are 'homeothermic' and 'endothermic' synonymous? I got this question from the comments below this answer. So, do homeothermic and poikilothermic have the same meaning as endothermic and ectothermic, respectively?
 A user also suggested that the terms such as poikilothermic and homeothermic have become obsolete. What is the reason for them being obsolete?

Traditionally, the terms poikilotherm and homeotherm were used to refer to organisms that don't regulate their body temperature and that regulate their body temperature, respectively.

However, those terms are not the best ones, regarding their etymology. For instance, poikilos (Greek ποικίλος, "many-coloured") means "diverse", "varied", while homoios (Greek ὅμοιoς) means "similar", "resembling". But some fish, which we define as a poikilotherm, may have a lifetime body temperature variation of 1℃ or less, while some mammals like a squirrel, which we define as an homeotherm, may have a daily body temperature variation of more than 20℃.

Then the terms ectotherms and endotherms appeared, as a new and modern terminology. And they are indeed meant to be that.

The problem is that a lot of people simply thought that ectotherm was a new name for poikilotherm and that endotherm was a new name for homeotherm, as if they were synonyms. But they are not. Follow me:

(A word of caution before we proceed: unfortunately, there is no organisation that regulates the terms used in the various branches of biology, as IUPAC does for chemistry. Thus, the acceptance of a term depends largely on the consensus among the researchers and the book authors. My answer here describes the nomenclature used by Whithers, Comparative animal physiology, in my opinion the best book on comparative physiology.)

Thermoconforms and Thermoregulators

According to Withers (1992), animals can be classified in two groups, regarding the ability to regulate their body temperature:

Thermoconforms: animals that don't regulate their body temperatures. Their body temperature is pretty much the temperature of their surroundings.
Thermoregulators: animals that actively regulate their body temperature. Their body temperature, therefore, may differ from the temperature of their surroundings.

In Withers' words:

  Most animals are unable to control their body temperature, and Tb passively conforms to their thermal environment; these animals thermoconform [...] Some animals, in contrast, regulate their body temperature often against a substantial thermal gradient between their body and the environment; they thermoregulate.

By the way, this suffix pattern of _conform and _regulator is common along the book. For instance, Withers talks about osmoconforms and osmoregulators (capable or not of regulating their body osmolarity), and so on.

So, thermoconform and thermoregulator are terms that describe if the animal is capable or not of regulating its body temperature. But those terms do not describe the source of the thermal energy.

Endotherms and Ectotherms

Here comes endotherm and ectotherm. In short:

Endotherm: the main source of heat (thermal energy) is the organism itself.
Ectotherm: the main source of heat (thermal energy) is the environment.

According to Withers:

  The terms ectotherm and endotherm are perhaps the most useful for describing the thermal capabilities of animals because they have a mechanistic basis. An ectotherm is an animal whose thermal balance is predominated by external sources of heat, and its metabolic heat production is insignificant. [...] Endotherms are animals whose thermal balance is predominated by their endogenous metabolic heat production.

Now we can try to combine those terms, and that will led us to the comprehension that none of them is synonymous neither of poikilotherm nor homeotherm:

All thermoconforms are ectotherms, that's not problematic. But things become complicated when it come to thermoregulators: thermoregulators can be ectotherms or endotherms.

For instance, most reptiles are ectotherm thermoregulators, but some dinosaurian reptiles, such as the birds (and most probably all other Dinosauria), are endotherm thermoregulators.

This table (ibid) summarizes the possible combinations very well:

Conclusion

It's clear that the terms poikilotherm and homeotherm (or even worse, cold-blooded and warm-blooded) are outdated and inadequate.

But they should not be simply replaced by the pair ectotherm/endotherm. Ectotherm and endotherm are terms that refer only to the main source of heat. The most adequate terms for describing the ability to regulate the temperature are thermoconform and thermoregulator (which, by the way, are not synonymous with poikilotherm/homeotherm either).

Source:

Withers, P. (1992). Comparative animal physiology. Forth Worth: Saunders.


Neuroscience behind the crash After experiencing things like stress, intense exercise, or using drugs such as caffeine and amphetamine, subjects often assume a depressive and lethargic state afterwards, known as a "crash." What is the neuroscience behind it? Could it have to do with the depletion of neurotransmitters such as the catecholamines, or a downregulation of certain receptors in response to the overproduction of such neurotransmitters?

(This question is a remix of a previous question I posted, which was not focused enough)

The "crash" effect is typically perceived as a deterioration in affect. With drugs, this deterioration happens as the drug is cleared from blood circulation, particularly cerebral circulation. With the ingestion of amphetamines, there is a brief reuptake of certain neurotransmitters, particularly dopamine and norepinephrine. Amphetamines also temporarily prevent the 'recycling' of said neurotransmitters, so the reuptake effect can last anywhere from 4 to 24 hours. The brain regulates internal homeostasis of mood based on perceived 'high' and 'low' elevations; thus, after an extended elevation in mood, there must be a 'comedown' period, or a deterioration in affect.

Further essential to this idea of homeostasis are the stress hormones, cortisol and adrenaline. Upon release, these hormones may raise blood sugar levels, blood pressure, and/or heart rate. As heart rate increases, the flow of blood goes to the heart, with less going to the brain. This causes the groggy and tired feeling afterwards that might be associated with a 'crash'. Stress hormones also impact the thyroid (which controls how fast the body uses energy, and controls hormonal sensitivity) as well as the central nervous system.

Exercise also leads to increased heart rate, as well as muscle fatigue. However, exercise itself doesn't typically lead to a depressed, lethargic state, as exercise promotes the release of endorphins (which are known to improve general sense of well-being). However, it is not uncommon for some people to experience "endorphin withdrawal" after suddenly stopping excessive exercise, which could mirror the crash that comes from the 'comedown' after drug use.


Is it possible to discriminate tetrachromacy using sRGB color? Hi I'm a physics grad student who has lots of interest on color perception.

I have recently learned that some people (mostly women) have another active cone cell which makes them possible to discriminate more colors than usual people like me.

Is it possible to discriminate tetrachromacy using sRGB color, I mean, is it possible to test it out on computer monitor? I guess so, because even though computer use combination of only 3 colors, it seems possible to make 2 combinations different in which is only perceptible to tetrachromacy. However, I'm not sure about that point because I'm not expert on that.

Anyway, if I'm right, it would not be so hard to make a test which resembles dyschromatopsia test, that can distinguish trichromacy and tetrachromacy. I couldn't find such a thing on internet. Test I could find seemed not valid. Even I could pass all the tests, but I'm not clearly tetrachromatic person.

Can somebody help me?

All the combinations of three sRGB primary colors are distinct for a trichromat. This immediately precludes any way to find out whether you are capable of more: if even a trichromat can distinguish all the colors, tetrachromat even more so.

But in principle, three colors are sufficient to check for tetrachromacy, but they can't be the sRGB primaries. The three colors you need must lie on one line on the chromaticity diagram, so that multiple mixtures of them could appear as the same color to a trichromat. Then a tetrachromat may be able to distinguish the two mixtures, which are metamers to a trichromat.


Why do frogs and toads only appear when it is dark outside? I noticed outdoors how frogs and toads only appear when it is dark or cloudy. Such as only after it rains or during night time. Why is this?

I see them,( or their ripples after they jump into the water ) during the day; I have 2 small ponds in the yard. I see tree frogs in my patio plants during the day but they are sleeping. The frogs/toads certainly make more noise when it rains ,has rained, or is going to rain. even during the day. They are certainly more active at night . I expect more bugs around then . I only see the geckos at night ,near the lights.


Can female Drosophila melanogaster lay eggs without males? Can female Drosophila melanogaster lay egg without males?

I maintain our lab stock but find a line that seems to have all females (or all males). The flies have been in the vial for two weeks, but I don't see any eggs hatching or become larva.

Yes, I regularly have to collect female virgins (12500 of them in the last week). They will lay eggs especially when there is extra yeast available. It is actually a good way to check virginity (in case a fly hatched early and was already mature, or a male made it through sorting etc.) - put some extra yeast grains in the vial when you collect them, leave them for a few days and then check for larvae, if they are not virgins there will be eggs and larvae, if they are virgins there will only be eggs!


Can someone tell me what these cocoons are? I am camping in Slovenia and have found some cocoon like materials.
They look like nests of some kind and are about 30cm long and 10-15 cm wide. Can anyone help me find out what these things are?
Found in Tolmin, Slovenia

I think you are actually looking at dried bottle gourds, a squash relative.  These are probably in the genus Lageneria.  These come in an extreme variety of shapes, and have been put to many ornamental uses. They were important as containers for early cultures.  Good background here and here.  Search for "dried bottle gourd" images and you'll see plenty.


Polymerase Chain Reaction Specifics While going over PCR in my biology lecture this week I have come across a few questions I have about this process.
First, since PCR focuses on trying to replicate a specific targeted DNA sequence many times in a short amount of time, are the primers used in every cycle the same sequence? I understand the forward and reverse primers would not be the same but the forward primer for one strand in one cycle, would it be the same as the forward primer for a daughter strand of let's say the 8th cycle?
Second, why are primers not reusable for different cycles? I think this would be based off of the answer to my first question. If the primers are essentially the same sequence, why do new primers have to be used for every cycle?
Thank you in advance!

The primer is incorporated into the start of the new strand. The number of dna strands produced is limited by the number of primers.


After vasectomy, where does the sperm go? After vasectomy, where does the sperm go?

Vasectomy Procedure cuts only vas deferens, But Our Testes still produces sperm, if there is no output for sperm, where does it go?

A vasectomy [...] is a contraceptive procedure in men in which the vas deferens, or sperm duct, is cut and the cut ends are sealed in order to prevent the transportation of sperm. Sperm is still produced, but does not leave the body. Vasectomy is usually done as a means of sterilization and is sometimes reversible.
(from http://urology.med.miami.edu/specialties/male-urologic-health/vasectomy)

When the vasectomy is complete, sperm cannot exit the body through the penis. Sperm are still produced by the testicles, but they are soon broken down and absorbed by the body. Much fluid content is absorbed by membranes in the epididymis, and much solid content is broken down by the responding macrophages and re-absorbed via the blood stream. Sperm is matured in the epididymis for about a month before leaving the testicles. After vasectomy, the membranes must increase in size to absorb and store more fluid; this triggering of the immune system causes more macrophages to be recruited to break down and re-absorb more solid content.
http://en.wikipedia.org/wiki/Vasectomy

A vasectomy only blocks sperm and does not affect your sexual drive, your ability to have an erection, orgasm or ejaculation or your ability to have and enjoy sex. Sperm is only a small fraction of the total liquid in your semen(almost 4-5 %). The amount of fluid, intensity – even color and texture – does not appear to change when sperm is absent.
...
The body absorbs unused sperm cells normally – whether or not you’ve had a vasectomy. After the procedure, the testicles will continue to produce sperm, but they will not leave the body in the semen. They dissolve and are simply and naturally absorbed by the body.
(from http://urology.med.miami.edu/specialties/male-urologic-health/vasectomy)

Sperm are produced in the testicles.  They are stored and reach maturation in the epididymis, a tightly coiled, muscular tube that is 15 to 18 feet long and leads into the vas deferens.   The muscle of the epididymis and the vasdeferens contract to propel the sperm through these structures and into the urethra at the base of the penis so the sperm eventually can fertilize an egg.
http://vasectomyreversalcenterofamerica.com/microsurgical-vasectomy-reversal/faqs/

Sperm are produced in the seminiferous tubules of the testes, and this does not change. A vasectomy does not affect the function of the testes. It is a physical separation of the vas deferens from each testis, so that the sperm cells cannot be ejaculated. However, the rest of the semen, which is made in the seminal vesicles behind the bladder and which is stored in the prostate, is ejaculated so the male reproductive experience will not change. He can still ejaculate, but there will be no sperm cells in the semen, so there can be no fertilization of an egg cell during intercourse.


Are memory updates local in mammals? What I mean is, during long term potentiation (LTP) or long term depression (LTD) for a particular memory, do the strengthening and/or weakening of neuronal connections only occur in a small patch of neurons or regions spread out in the cortex?

LTP and LTD are processes that operate on single synapses. We don't know how "memories" (there are several types of "memory") are encoded in the human nervous system. As a consequence, we don't yet understand the explicit link between some group of synaptically connected neurons, and a given memory.

So the short answer is "we don't know". Take a look at some of the other questions about memories in human brains: 1, 2


Are there issues with filling PCR tubes to capacity? I'm planning to scale up a PCR reaction, and I'm wondering if filling the PCR tubes to the maximum volume of 200 ul would be a problem. It would mean a lot less pipetting as I would only need 1/4 of the tubes.

The typical protocols I've seen always use 50 ul for a PCR reaction, I'm wondering if there are any issues with larger volumes, e.g. differences in heat transfer, that could cause issues if I scale up the volume in one tube.

Is scaling up the volume problematic? Any specific aspects I should consider?

Too long for a comment: I would say it depends on the PCR. I have personally used maximum volumes of 50ul, if I needed to prepare higher volumes, I made one mix which subsequently got distributed to more tubes with 50ul max.

The problem with big volumes is to get a fast and homogeneous heating and cooling. If the outside of the tube is faster, the reaction there starts already while this may not be the case in the middle. This can lead to uneven denaturation and amplification of your template. The later is especially problematic when you amplify short sequences. There the amplification time might already be over and the PCR program is moving on before the template is finished, which will result in less of your full-length product and the enrichment of shorter versions.

There is another problem that might occur in big reactions: Due to gradients in reactivity because of temperature gradients I think it is possible that reagents (dNTPs, Mg-ions) can form gradients which further inhibit a good yield.

Finally I tested one thing on one of our PCR machines: The PCR tube is set into the heating/cooling block. It is not completely set into the block but stick out partly, so if you fill it up to maximum capacity, the upper 75-100ul (approximately) would be outside the heating block and we have a thermal problem. The reaction mix there would only heat up due convection.


How does alternative splicing work? I am trying to find out what controls what exons are spliced out, and I keep coming across the term cis regulator, but I cannot seem to find a clear explanation of what happens...

Thank you in advance :)

EDIT: to clarify, I have tried to read the Wikipedia article on alternative splicing and I get the main idea (some exons being cut out of the mRNA with the introns to produce the mature mRNA, I think...) but I don't understand the 'mechanism' section, I.e. What controls which exons will be cut out? And what enzymes 'splice' the mRNA- how do they do it in the right place, and stick the mRNA together again?

21joanna12, look into snRNPs.  These are parts of the splicosomal apparatus and some of them (the U1 and U2, U11 and U12 snRNPs) are also the guideposts that bind near the splice junctions at the end of introns.  These help guide the splicing apparatus to the splice sites. There are also proteins that bind RNA and interact with the splicing apparatus to switch alternative splicing, such as SP proteins.
https://en.wikipedia.org/wiki/SnRNP
https://en.wikipedia.org/wiki/SR_protein
https://en.wikipedia.org/wiki/Exonic_splicing_enhancer

Here's a recent review that might serve as an entry into the literature: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4232567/


Arsenic (V) Reduction to Arsenic (III) by Microorganisms I am currently doing research on arsenic toxicity in microorganisms, and I learned about arsenic (V)/(III) cycling. Arsenic (III) (usually in the form of arsenite) is generally 50 times more toxic to biological life; however, most bacteria (or at least some) reduce the less toxic arsenate into arsenite. I just do not understand why these organisms would reduce arsenate into something more toxic. This doesn't seem to be an accidental reduction in which the microorganism mistook arsenate for phosphate, as there are plasmids specifically encoded with genes that reduce arsenate. Why is this happening? How would this be an advantage in these organisms and not a disadvantage?

You can find a great and recent review on this topic, which is thankfully also free to access, here: https://www.sciencedirect.com/science/article/pii/S2319417016000159

Arsenic resistance is ubiquitous among bacteria, they virtually all maintain the ars operon. Among Arsenic-resistant bacteria, this is not an advantage, but Arsenic was and remains a ubiquituous substance and being resistant to it confers an advantage over those that aren't; which is why bacteria that save themselves the effort aren't abundant.

The core to your answer is in the very last summary paragraph:

  ArsM transforms inorganic arsenic into a highly toxic organoarsenical species that kills off by competing the bacterial species and may also be responsible for carcinogenesis in animals. Competing microbial species have responded to this environmental pressure by evolving detoxification mechanisms for MAs(III). Some produces ArsI that demethylates MAs(III) to less toxic inorganic As(III) while other produces ArsH that oxidizes MAs(III) to nontoxic pentavalent MAs(V). It is likely that all of these processes are taking place in environmental microbial communities as bacteria, archaea, fungi, and protozoans constantly fight for dominance.

Summarised in Figure 5: https://ars.els-cdn.com/content/image/1-s2.0-S2319417016000159-gr5.jpg

The reason why ArsC and other arsenate reductases (reducing Ars(V) to the more toxic Ars(III)) evolved in the first place, setting off this whole Arsenic methylation cycle, is that

  they are required for resistance to arsenate, which became the predominant arsenic species after oxygen appeared in the atmosphere.

Simply put: If I can make a poison that kills you but not me, why shouldn't I make it?


Nernst equation and equilibrium potential Solutions A and B are separated by a membrane that is permeable to Ca2+ and impermeable to Cl−.
Solution A contains 10 mM CaCl2 , and solution B
contains 1 mM CaCl2.
Assuming that 2.3 RT/F = 60 mV, Ca2+ will be at electrochemical equilibrium when

(A) solution A is +60 mV

(B) solution A is +30 mV

(C) solution A is −60 mV

(D) solution A is −30 mV

(E) solution A is +120 mV

(F) solution A is −120 mV

(G) the Ca2+ concentrations of the two solutions are equal

I eliminated A,B and E because of the +ve sign immediately, and G because it doesn't take into account the electrical potential factor.
I also understand the general idea (that Ca2+ ions will cross the membrane but Cl- won't so it will stop when solution A is negative enough for the electrical gradient to be > concentration gradient) but I don't know what to do next.
Using Nernst equation (here's the version in my book) I got that the equilibrium potential is about -60 mV (I did -61log(10/1))
But the book's answer is D which makes me think I might have a huge misunderstanding in the principle itself.

The Nernst equation should be:

RT/(zF)*ln(Out/In) = 2.3 RT/(zF)*log10(Out/In)

You substituted for 2.3 RT/F (approximately 60 or 61 mV: use 60 because your instructor asked you to), but forgot about z. Calcium is divalent (and positive) so for calcium z=2. Substitute this and you can see how you get your answer.

(Also note the "out/in" which is how you get negative numbers when z is positive and out < in )


Which predators only eat some parts of their prey? (Warning — graphic content) In an small city in middle-east somewhere near a desert, an unknown predator attacks sheeps, goats and chickens. These attacks began a few weeks ago and until now more than 150 sheeps have been attacked. It causes panic and rumors among people and despite official investigations no result has been achieved yet.

In the pictures shown above only the soft part of the animals have been eaten. This is common for most predators as these are the easiest parts to eat.

Correct me if I am wrong but the animals seem to not have severe bite marks around the neck. This means the predator was not big. You can pretty much rule out anything around the same size or bigger than the sheep.

To exactly identify what killed them just from a carcass is hard, and even harder over the internet. However, it looks like you are dealing with feral dogs, coyotes or wolves, although with wolves and dogs there would generally be more scarring around the neck of the sheep.

Dogs: I have seen this behavior in dogs. These are normal tame dogs that have discovered the kick of hunting. Where I come form in South Africa the farmers tend to shoot dog packs if they see them on their land. This is because it is a common problem for the packs to attack chickens, sheep or even calves.  They get an immense kick from hunting the sheep but in most cases don't eat it, not like the photos shown at least.

Foxes: Although it may be hard to believe foxes have also been known to kill sheep. However, in your case it is not likely to be foxes. Foxes hunt alone and tend to kill lambs.

Coyotes: Coyote packs have almost identical behavior to dog packs. The difference being that they pick one sheep and kill it quickly. They do not do it 'for the kick' like dogs and rather for the food. Judging from the photos I would say it is possible that this was done by wild Coyotes, if they are found in your area. Coyotes are also not very shy, and will often hunt close to where people live.

Wolves: While possible, I would rule out wolves because of your geographical location. Wolves also tend to be more shy and will stay away from places with lots of people, like a city.

Source:
http://www.omafra.gov.on.ca/english/livestock/sheep/facts/02-029.htm


Why did the face of human species changed so much during the course of its evolution? I recently watched this video which showed the evolution of facial features of the modern man
https://youtu.be/-69K7E0UlBI

I'm wondering what evolutionary advantage did we get by having our face from this-

(reconstruction of the face of Australopithecus)

To this-

(Homo sapien sapien)

"In other words for what advantage did nature selected our present face?"

There are many things going into the evolution of our face. It is not as simple as discussing a single trait. Your question is therefore quite broad. So I will just pick up three different traits and talk a little bit about them. Those traits are

hairs
size of the jaw
cranial capacity

As I will only say a few words, you will have to look for more advanced information by yourself if you want to deepen your knowledge.
But first, let me make a few other comments
A few comments
Panselectionist view of evolution
When you say what advantage did nature selected our present face?, you seem to assume that any evolutionary had to be brought about via a selective pressures. Yet, there is so much more to evolution than just natural selection. Not every trait has been selected for (otherwise we would not have any genetic disease). There is for example genetic drift who is also a very important evolutionary force.
On this subject, you might want to have a look at the paragraph Did you say Natural Selection? of this answer to Why don't mammals have more than 4 limbs? and to Why do some bad traits evolve, and good ones don't?
Accuracy of your Australopithecus's face
In the reconstruction of the appearance of a extinct lineage, there is always some part of artistic representation to fill the gap of what we don't know. One should investigate the exact method used to recreate this image before assuming that Australopithecus looked exactly like that.
For more information have a look at In reconstructions, how are various shapes of facial features determined from skull only?
On top of that, please note that there is variation in faces within a species. This is true for Homo sapiens today and it was true for other great ape lineage. More importantly, there were at least 6 species of Australopithecus (see wiki > Australopithecus).
Human species or hominini lineage?
Your question is

Why did the face of human species changed so much during the course of its evolution?

When we say "human species", we typically refer to H. sapiens (or even H. sapiens sapiens). Based on your images, you seem to rather ask about the evolution of faces in the hominini lineage and not only in H. sapiens as Australopithecus is not the same species as us. Australopithecus is actually a genus (other than Homo) containing several species.
Evolution of a few facial traits
Hairs
We've lost plenty of hairs! Have a look at the post Why did humans lose their fur? to understand why.
Size of the jaw
Here is a timeline of evolution of hominini

As you can see, Australopithecus did not know how to cook. They did not know how to control fire. The first to have a good control of fire were probably Homo erectus.
By cooking, we pre-digest our food, leaving much less work for our digestive system, including the physical mastication performed by our jaws and teeth. As a consequence our jaws reduced in size (Wrangham and Conklin-Brittain 2003, Lucas et al. 2006; See also this book from Lucas).
Size of the brain
H. sapiens cranium is about 3 times the size of Australipithecus cranium (Leigh 1992 and Smith et al. 1995).
Cooking allowed us to save much energy, which could then be used for higher cognitive abilities. Without cooking, it is likely that our brain would never has gotten to the size it has today. Our brain consumes about 20% of our energy today (which is very unusual if you compare to other species). Cooking therefore also lead to an increase in brain size.


Shape of feces in herbivores Why do some herbivores like sheep, cow, and others excrete feces in a pellet (or biscuit or other) shape, while other species including humans do not do so? What is the reason for such an adaptation in herbivores? Is it beneficial to them, and if so, how?

I don't think it is an adaption, but the that diet plays a dominant role. The feces of cows in intensively fertilized agricultural fields, with grasses rich in protein, has no shape at all. See picture below.

The feces of cows in natural areas has much more structure. (image has copyright, so can only link)


Plant's phylogeny tree to identify which of them are closer (genetically) with another plant I'am trying to create a phylogeny tree from some plants, as the post's title says, to help me conclude which of those plants are closer genetically with another one plant.

So let's say that this is the plant list:

Nicotiana tabacum , Zea mays, Oryza sativa, Solanum lycopersicum,    Solanum tuberosum, Erythranthe guttata, Hordeum vulgare, Vitis vinifera, Prunus persica, Glycine max, Populus trichocarpa, Medicago truncatula, Phaseolus vulgaris, Morus notabilis, Citrus clementina, Setaria italica, Theobroma cacao, Acacia mangium, Cicer arietinum, Triticum urartu, Brachypodium distachyon, Aegilops tauschii, Panax ginseng

and i want to see which of those species is closer with Sorghum bicolor.

Is there any easy way to conclude something like that or it needs to get results out of bioinformatics using a specific gene , align it , and then see the tree ?

In general for plants, before you start trying to make your own phylogeny, you should try to find an existing phylogeny. Phylogenetics is complex, and a lot of people have already done the hard work. You can start by looking at the Angiosperm Phylogeny to figure out which species are most closely related. To make use of the tree you will usually have to look up each species to figure out what order or family it is in.

In this particular case, Sorghum bicolor is a grass, so of course it's going to be closed to Zea, Oryza, Setaria and Brachypodium (all grasses) than any of the others. You can see where it places relative to the other grasses by looking at a grass-specific phylogeny. Because all three are model species, their phylogenetic placement relative to one another is well established. A simple Google image search for [grass model species phylogeny] gives you your answer (from the Setaria genome paper):

This shows you that Sorghum is closest to Zea out of the species you listed.


Tap vs. mineral water for drinking I was told a human should drink a small glass (0,3 liter) of mineral water per day to get the minerals. What is the rationale behind this? What is the difference between tap water and mineral water in terms of nutrition facts and effects on human health?

Values for tap water in my area:

How good are the values regarding nutrition facts?

The mineral content in tap water differs from area to area as well as the source. The mineral content in bottled water is regulated by the companies that manufacture them, in particular the Mg and Ca content(reference).

  Death rates tend to be lower in areas with tap water containing higher
  levels of Ca and Mg. It has been shown that deficiencies in magnesium
  are capable of producing heart disturbances, including 215,000 fatal
  heart attacks in the U.S. each year, and as many as 20,000,000 fatal
  heart attacks worldwide (reference).

Different brands of bottled water will differ in their mineral content as well (reference). The place where you stay might be lacking in a particular mineral that your body requires which is why your doctor has specified the use of a particular brand of mineral water.


How large might a paper wasp nest become? About two weeks ago I noticed a new wasp nest in my back yard. I generally leave them as long as they aren't interfering with anything, but this nest has suddenly grown quite large and they are swarming when I mow the lawn. From the nest appearance, I was afraid these were bald-faced hornets, but up close they look more like yellowjackets, I'm uncertain of the species. This is as close as I dared to get with the camera.

I am willing to live and let live until October (when the nest is vacated), but I have two concerns that may change my mind:

How large might this nest become?
If I leave them this summer, are they likely to return to the same place next year?

According to multiple reports (here, here and here), a 7m (22ft) paper wasp nest was found in an abandoned home in San Sebastian de La Gomera on the island of Tenerife (~100km off the shore from Morocco)!! The nest was estimated to be home to over 22,000 wasps! The picture is included below:

This nest broke the previous world record, a nest discovered in Waimaukau in New Zealand in April 1963 that was an impressive 3.7metres, or 12ft 2ins long, more than 5ft in diameter and 18ft in circumference!

Other big nests? ...

According to this site a 10 ft x 7ft x 2ft nest buzzing with about 400,000 yellow jackets was found in a camper in SC, U.S.
Here is a video of an apparent giant (6.5ft x 8ft) yellow jacket nest found in Florida, U.S. in 2013. A Picture of the nest is below:


The new DNA study showing that we have two DNA codes and not only one unique code I am looking for a study that i read maybe 2-3 years ago that i cant find at the moment.

Scientist has always believed that humans only have one unique DNA code that makes us who we are, but a couple of years ago scientist found that we actually have two DNA codes, something that the scientists called mysterious and that this changed what we always have belived regarding humans uniqe DNA code that makes us who we are, now this was not true anymore with this new finding, since we have two codes which means that who we are could be more complex and not only be information stored in one DNA code. I cant find this study when i look for it on google, do you know which study i am speaking of? i would like to find it again, so that i can see if there is any updates by the scientists, and i also think it is extremely interesting and don't want it to get lost, i forgot to save it in favorites before.

Perhaps you are referring to so-called "duons" (dual-use codons) discovered by Stergachis et al.. This paper was published a bit more than six years ago. A recent paper within the last 2-3 years references duons implicated in photosynthesis.

Duons essentially extend the idea that conserved coding DNA encodes proteins, but can in fact also preferentially encode sites which bind transcription factors, at the same time. DNA can code proteins as well as code that controls regulatory regions, which in turn are switches that control how proteins get made.

Disclaimer: I am a contributing author in the linked Science paper.


Examples of humans intentionally introducing non-native species where everything went well? It's easy to find examples of humans introducing non-native species to solve some problem (e.g. for food, to control the population of a pest), but later regretting it as the introduced species upsets the ecosystem.

Rabbits in Australia
Mongooses in Hawaii

Are there any examples of this going as expected?

I guess, since I'm really interested in how well humans can predict this sort of thing, what I'm looking for is examples of a situation where there were no unintended consequences. (Rather than beneficial, but unintended, consequences).

The best examples are for when non-native pest species arrive, and then a search for their natural enemies in their native countries is undertaken to bring them back and control the invaders. This is called "biocontrol", and there are many examples of it going well, under carefully controlled conditions. https://biocontrol.entomology.cornell.edu/success.php
However, you are right to note that it is very difficult to predict.


Can you use images taken at different exposure times in western blot image analysis? I am doing Western blot data analysis where I have images from a number of experiments (where the samples in the experiments are biological/technical replicates). For each experiment, I labelled the membrane with antibodies against the same proteins of interest.
I want to combine the data from these experiments so that they are all displayed on the same graph.
I took my images at a variety of exposure times (e.g. 5 sec, 30 sec, 1 min, etc). For one protein X, I have found that the images taken at 30 seconds exposure are the best for analysis, as the bands are saturated at higher exposure times.
However, for one experiment, for the protein X labelling, I cannot use the 30 second exposure image for my analysis as there are ghost bands. I have an image taken at 5 seconds exposure which I can use instead.
I was wondering when combining data from western blot images from different experiments, for a specific protein of interest (e.g. protein X), do all the images have to be taken at the same exposure time? All the protein X images I will be using were taken at 30 seconds exposure except for one which is taken at 5 seconds exposure.
Any insights are appreciated.

Generally no, you can't directly compare them and you can't easily compare across gels. I have done many hundreds of western blots, a large proportion of which were for quantitation, and in general quantitation on western blots is difficult (because of inconsistency run to run) and not highly quantitative - a 2-fold change is detectable and probably real, but a 10% change - unlikely to be real.
If you want a real example of how to compare and observe this (works with the Bio-Rad system or others where the transfer is in the same space) - run exactly the same amount of protein on two identical gels, place them both into the same transfer tank. Compare protein stain on the membranes after transfer. The one closest to the black terminal will have stronger staining = better transfer.
However, what you can do is convert the numbers you get into a relative expression on each of the blots and then use those numbers for comparison.
For example you compare expression of protein X to a normalizer (often B-Actin) and get fold-change data out of that, or you can compare Sample X untreated to treatments A, B, C and get data out that way.


Can Eskimos be regarded a distinct species from Kalahari Bushmen based on morphological differences & geographic isolation? I was motivated to ask based on the answer to another SE Biology Question that uses the following argument to conclude that two varients of snake are indeed a different species:

  To test whether [Dendrelaphis ashoki and D. girii  were a separate
  species of snake] they (Vogel and van Rooijen, 2011) compared 9
  individuals of D. ashoki with 34 individuals of D. pictus, and found
  statistically significant (p<0.05) differences in five morphological
  characters....

Further:

  The authors didn't rely just on morphological evidence: they note that
  D. ashoki, which is found in the Western Ghats, is also geographically
  isolated from other populations of D. pictus, which are found in
  Northeast India, Myanmar and South East Asia.

Minor differences in morphology of a snake: Why designate it a different species?

My question is, why can't we on the bases of an analogous argument conclude that (say) Eskimos & Kalahari Bushmen are, forget the race debate, but two entirely  distinct species?

I mean if "number of infralabials touched by the first sublabial" can count as a legitimate species-distinguishing morpohological factor, then so can heights, eye colors, hair texture, skin color etc. right? And we won't even have to fish too hard to gain statistical significance given how different Eskimos are from Kalahari Bushmen morphologically.

Further, the geographical isolation must have been pretty strong too.

I think that species delimitation is not a science, or at least not a coherent one. Different fields use different criteria, for practical or historical reasons. For instance, in plants, loads of fertile hybrids exist between species. It seems that botanists do not split based on the traditional biological definition of what a species is: they apparently tend to split more (see the splitters and lumpers notion).

My intuition is that humans are generally interfertile. There even seems to have been interfertility between H. sapiens and H. neandertalensis which have been (or maybe still are?) considered as distinct species. But how are the actual genetic exchanges across the human populations?

In my opinion, if it were proven that genetic exchanges between human populations living very far apart and having evolved very different ecological adaptations (like populations from the arctic and from the Kalahari) were almost reduced to zero, then it would not be absurd to call them different species. Humans would form a continuum that can be considered a unique species (if interfertility is to be taken as a criterion), but with isolated extremes being in the process of forming separate species, somewhat like the extremes of a ring species. Maybe there even is some degree of reproductive incompatibility between very divergent human populations. The thing is that it is not ethically acceptable to experiment with this. We need to rely on "natural" experiments happening. Globalization could potentially tell us in the future, by facilitating encounters between individuals from very distant populations, whether such reproductive incompatibilities exist or not. That said, I doubt that the origins of parents are recorded in a scientifically usable manner when a couple has problems having children.


How is the Concept of Simple Diffusion Possible How can a substance pass through a lipid membrane in a cell through simple diffusion? In order for something to be able to go through the membrane, in simple diffusion, it must be hydrophobic, or non polar. The reason for this is that in order for it to easily interact and pass the fatty acid part of the lipid membrane, which is hydrophobic or non polar, it must also be hydrophobic and non polar. But in order for this substance to pass the phosphate part of the membrane, which is hydrophilic, or polar, doesn't it also need to be polar and hydrophilic?

Simple diffusion is the movement of solutes from an area of high solute concentation to an area of low solute concentration.

Here are a few ways molecules will make it through membrane into cell:

(A) Fuse with the membrane and enter due to like polarities i.e non-polar subtance fuses with non-polar membrane and passes through membrane

(B) Small polar molecules CAN move into cell but at a much slower rate

(C) Through transmembrane integral protein channels such as aquaporins, K+ leak channels, and other channels that DO NOT require energy, and are ALWAYS open

If you want to understand how it was determined which molecules were able to pass through the membrane look for some resources about Overton's Plasmolytic Method.

Alongside that the definition of the partition coefficient will give you some insight on how fast molecules will pass through membrane, if at all.

Good luck on the searching!

@ Ro Siv - Simple diffusion is not facilitated diffusion


Help with analogy: Competition among similar species I'm not from this field, but I'm trying to make a biology/ecology analogy for companies with similar products competing for the same market segment.

I was thinking of using the competitive exclusion principle to illustrate that the products will have to each find their own niche, or disappear from the market.

In a market, when opportunity arises (lots of capital available, and interest from the consumer side for an new product) many competing products spring up, and then we slowly arrive at an equilibrium similar to the exclusion principle mentioned before.

My question is this: Is there a similar "opportunity stage" of this process in nature? Like an increase in resources available that drives many different species to "appear" and compete for the newfound wealth?

Pointers to Wiki articles etc. for further research will be appreciated.

Here are some definitions of interest to you

Ecological succession is the process of change in the species structure of an ecological community over time. The time scale can be decades (for example, after a wildfire), or even millions of years after a mass extinction.
A seral community (or sere) is an intermediate stage found in ecological succession in an ecosystem advancing towards its climax community. In many cases more than one seral stage evolves until climax conditions are attained.1 A prisere is a collection of seres making up the development of an area from non-vegetated surfaces to a climax community.
In biology, a disturbance is a temporary change in environmental conditions that causes a pronounced change in an ecosystem. [..]  Because of these and the impacts on populations, disturbance determines the future shifts in dominance, various species successively becoming dominant as their life history characteristics, and associated life-forms, are exhibited over time.
Ecological facilitation or probiosis describes species interactions that benefit at least one of the participants and cause harm to neither.1 Facilitations can be categorized as mutualisms, in which both species benefit, or commensalisms, in which one species benefits and the other is unaffected. Much of classic ecological theory (e.g., natural selection, niche separation, metapopulation dynamics) has focused on negative interactions such as predation and competition, but positive interactions (facilitation) are receiving increasing focus in ecological research.


At what age do babies begin to synthesize their own antibodies? When babies are first born, they receive their antibodies from their mother (I assume because they do not yet have the capacity to synthesize their own).  So my question is, at what age do babies begin synthesizing their own antibodies?

In the graph above the darker blue line refers to the antibodies the baby receives from the mother in utero, as you mentioned in your question.

As you can see, the red line indicates that babies begin to produce low levels of their own antibodies between 3 and 6 months before birth.  However, these are IgM antibodies, immature 'rough draft' versions.  These have much lower affinity for antigens then their mature IgG counterparts which are the classically thought of antibody.

Levels of an infant's own IgG start to rise after birth, however don't reach a reasonable level until after the child is roughly 1 year old.  Maternal antibodies start to tail off at around 3 months leaving a period highlighted in blue on the graph where infants are particularly prone to getting infections.


Enzymatic error rate I am aware that each enzyme generate a certain amount of misproducts.
This is well documented, for example, for the DNA polymerase.

I am interested in enzyme involved in biochemical processes, so for example methytransferase, oxidoreductase, carboxylase and so on.
I have been looking for any reference that could report the error rate or the amount of misproduct for any of these enzymes, but I was not successful.

Does anyone know a reference reporting the error rate, or any other information about the misproduct generate by these enzymes?

EDIT

I will try to clarify a bit better my question.
Let's assume that we are considering an enzyme that add a methyl group to a molecule, we can choose propionic acid for example.
In theory the correct product would derive from the addition of a methyl to the C3.
For the biochemistry study we know that the activation energy is decreased by an enzyme for example by orienting the molecules in the right way to react with the second molecule.
Therefore, if the enzyme in question will not be able to orient the molecule in the right way there is a certain probability that there will be a mis-product.
For example the methyl group could be added to the C2 and not the C3. Now. the probability for this process is quite low, but it cannot be excluded from happening.
My question is, if there is anything known about this type of error rates in the different type of enzymes.

I hope this make things a bit more clear

EDIT 2

Lets consider the imagine below that was taken from here

In B you can see the interaction of the active site of the enzyme with a substrate (for the example it does not matter if it is the real substrate or an inhibitor). I would say that among al possible interaction that this active site can make with substrates there are some much more likely than others. An hypothetical chart could be created considering the free energy of the complex enzyme-substrate, higher the free energy lower the stability.
Therefore among all possible enzyme-substrate combination we will have just few possibilities that have a low free energy. In the first place we will find the "correct" substrate, then we will find eventual competitors and other molecules that have similar chemical features as the substrate. Even though with low probability these interaction, enzyme-competitors, will happen.
This might led to the formation of "unwanted product" that I refereed to in my question as "misproduct".

I am interested in reading some paper that are considering thie phenomenon and also quantify its rate. I am also curious if this phenomenon can happen with different rates in different enzymes.

First it is important to define what actually an error is. What you call misproduct is actually a right product for a different substrate. The enzyme has a low specificity; but you won't say hexokinase is error prone because it has wide substrate specificity. The question is — is specificity critical?

Coming to the example of DNA polymerase, you should note that DNA polymerase only adds a nucleotide to the DNA strand. Here the template DNA strand acts like a co-enzyme and it is the template DNA that provides specificity to the reaction. In this case the specificity is really critical and there are mechanisms that help in ensuring that.

Other enzymes also make errors and the probability of making errors depends on different parameters. Take the example of restriction enzymes that are supposed to cut at a specific site. When this specificity is lost we say that the enzyme is showing a "star activity" i.e. non-specific cleavage. This depends on different parameters such as buffer composition, enzyme concentration etc.

In general specificity is provided because of high affinity of binding towards one molecule compared to the other. These binding reactions are second order — a high affinity substrate will bind to the enzyme even at a low concentration, however if you increase the concentration of the low affinity substrate or the enzyme, then at some point the rate of binding may be significant enough to create a "wrong" product.

Sometimes there are cases where the enzyme can bind to a wrong substrate but cannot create a product. This is the typical case of a competitive inhibitor. It is also possible that a certain molecule is good at binding but the conversion rate is slower.

To conclude, these kinds of "errors" happen with many enzymes but it is very critical in case of DNA polymerization. You can get information on star activity of restriction enzymes (just google it).


Hydrophobia Outside of Rabies? RELATED:

  Why does rabies cause hydrophobia?

  Agony, Hydrophobia and viruses in the light of evolutionary principles

Has hydrophobia been found outside of rabies?

I have only seen it being mentioned as a symptom of rabies.

You are correct that hydrophobia is often considered pathognomonic of rabies. However, I offer for your consideration:

Hydrophobia as a rare presentation of Cotard's syndrome: a case report.1

Cotard's syndrome itself is a bizarre psychiatric condition that the authors of the above paper define well:

  Cotard’s syndrome is a rare condition where the central symptom is a nihilistic delusion, which, in its complete form, leads the patient to deny his own existence and that of the external world.

The patient described in this case report harbored delusions that his internal organs were shrinking. He asserted that his abdomen would rupture if he internalized anything. The hydrophobia was secondary to this concern. When given a glass of water he showed a panic reaction and attempted to keep away. Orientation and memory remained intact.

The authors go to length to point out that this was not, in fact, a case of rabies (as thought that were in question at this point!). Also, the patient himself was not aware of symptoms of rabies, ruling out "rabies hysteria" (a hypochondriacal delusion that one has rabies).

Hydrophobia, then, is a rare manifestation of a rare psychiatric disease in addition to the more frequent and well-known association with rabies.

1. Nejad AG. Acta Psychiatr Scand. 2002 Aug;106(2):156-8; discussion 158.


Is there a name for this principle in biological contexts? This is mostly a question about usage.

There is a probability-related idea that has been used in at least two biological contexts. The idea is that if something happened, it was probably likely to do so.

This has been used in discussions about evolution, in which it is said that while we have trouble imagining circumstances in which self-replicating forms arise, the odds were probably in favor of their emergence when it actually occurred. And in discussions of the existence of intelligent life--it may be prevalent if we make the somewhat natural assumption (among others) that our own emergence was not highly improbable, given the existence of a suitable planet and so on.

Is there a name for this principle? I am familiar with the idea in the context of probability but have thought of it as an 'argument from likelihood' in biology. Also if there is a good description of the idea in a biological context a reference would be appreciated.

The tag is a little arbitrary. Thanks for any suggestions.

It may also be called as Idea of maximum parsimony. It is used in phylogenetics to construct phylogenetic trees which require the least number of evolutionary events.


Impact of Terminator Efficiency in Genetic Constructs I was looking at the iGEM Bioregistry of Terminator parts which offer varying degrees of termination efficiency. I am wondering why studies into combinatorial synthesis of genetic circuits for metabolic engineering include terminators as a variable component within their designs, such as this paper by Woodruff et al., 2017? This must come at great complexity cost to overall library size, where I would of assumed one would take the most efficient terminator and fix it within the design. How could terminator strength or sequence effect optimisation of a metabolic pathway in an impactful manner such that this extra complexity becomes worthwhile?

To add to gaspanic's answer, not all terminators work equally well under all conditions. So if terminators weren't characterized in the organism or tissue you are working in the efficiency might be different. Additionally, though rarely people might be looking to design with a leaky terminator mimicking bacterial use of leaky terminators to use one DNA sequence to create two mRNAs of different length.
[Edit] Sources for further reading
Example of terminator efficacy differences between different species
Example of terminator differences between tissues
Terminator Attenuation - stopping of termination only sometimes
Leaky stop codons as a molecular tool


How does rate of evolution/innovation scale with population size? I understand that there will be many other factors that affect rate of evolution/innovation. However, other things being equal, how will the rate of evolution vary between two populations of different sizes? Does doubling the population size double the rate of introduction of new traits?

Is this answerable for evolving life in general, or do different forms of life have different scaling laws? For example, is it different for sexual and asexual life?

Interesting question (+1) but not that easy to answer. I'll give a try!

First, the rate of evolution and rate of adaptation are two different things.

There are two main thing processes that quantitatively differ in populations of different sizes. 1) population-wide mutation rate and 2) genetic drift.

1. Population-wide mutation rate

Large populations create more mutations at each generation and therefore if the rate of evolution or the rate of adaptation is limited by the genetic variance, then one can expect large population to have higher rate of evolution and higher rate of adaptation.

--> Large populations may have higher rate of evolution and higher rate of adaptation

2. Genetic drift

However, small population have higher drift, resulting in a higher probability of fixation for new neutral (or slightly deleterious) mutations. It results that a small population will fix (fixed: frequency = 1) a higher proportions of the new mutations through time than large populations.nActually the probability of fixation of a neutral mutation is \frac{1}{2N}. Therefore, the rate at which neutral alleles fix is $\mu\cdot 2N \frac{1}{2N} = \mu$, where $\mu$ is the mutation rate. So, the rate of fixation of neutral alleles is independent of the population size.

--> Small populations have more drift but this doesn't necessarily yield to higher rate of evolution

Other and comments

Shifting balance theory

If adaptation is limited by the genetic architecture, that is, only mutation of very big effect on phenotype can be advantageous, then small population have the advantage to be able to accumulate slightly deleterious mutations, so that they can get off a local peak on the adaptive landscape and eventually manage to evolve toward a new higher fitness peak.

--> Small population may have higher rate of adaptation

Population-wide mutation rate vs genetic drift

Weighting the relative importance of rate of production of neutral (or quasi-neutral) mutations (See population-wide mutation rate above and the probability of fixation of neutral (or quasi-neutral) mutations (See Genetic drift above) depends also on the probability distribution of mutational effects (=probability distribution of the effect on fitness of a given new mutation).

Ceteris Paribus

The comparison between large and small populations are dependent on the state of other parameters. So even when saying all else being equal (ceteris paribus), we need to know what these other parameters are equal to, in order to answer the question because there are interactions between populations size and other parameters in explaining the rate of adaptation and rate of evolution.

Other impact of population size on genetic features

Population size has many impacts on various genetic features, such as pattern of genetic diversity, distribution of per locus Fst between subpopulation, and other things. This paper is likely of interest


Help me identify this Bug species I found this insect in Pune/India. Its body size was less than 1 cm. It was near light source. I suspected it to be Juvenile Thread-legged Bug, but i am not sure. Is my suspicion right or is it some other insect?

It is Pneustocerus gravelyi, a species of stilt bug that lives in India.

In both of these images, you can clearly see the the bright red coloration of the joint on each leg. The pronotum is also the exact same shape and color, and the bright red abdomen extends beyond the closed wings.

original unmodified image source


What is the evolutionary purpose of white spots in nails and how can they be characterised due to Leukonychia? Suppose you haven't hit your nails so the white spots are due to Leukonychia.

Are the discoloration i.e. the white spots due to lower porosity (less minerals absorbing) or some other factor? I cannot understand their physiobiological chareterisation and why are they created due to evolutionary terms? To show a person that he is lacking minerals? Or why do some people have them?

This is a common misunderstanding from newcomers in evolutionary biology. Not every trait is the result of an adaptation. Evolution is way more than just natural selection and is not as deterministic as you may think. There is stochasticity inherent to mutational processes and there is stochasticity in reproductive success (called genetic drift). This seemingly totally unrelated post may help you getting a quick grasp of what are the stochastic processes in evolution.

The white spots you observe very likely do not result from an adaptive process but it just happen to be the way it is. For the physiology part (but this would be the subject of another question) I have no idea what drives these white spots.


What is the advantage of indirect ELISA over direct one? I guess the answer is about indirect one giving less error due to selectivity but how exactly does that happen?

You are correct, the selectivity advantage of an indirect or sandwich ELISA comes from the fact that two antibodies are employed - one to capture the analyte, the other to detect it.

Here is the classic illustration of how this type of ELISA works. First ([1]), the capture antibody is coated onto the plate and bound via one of a number of different types of chemistry. The plate is then washed (this occurs between all steps). [2], the analyte is added, sometimes in a homogenous solution (i.e., pure recombinant protein), other times in a matrix like serum, cell lysate, etc. The plate-bound antibody has a certain specificity for the analyte — let's say it binds the wrong epitope one time in 1000. [3] The detection antibody is added, and let's say it has the same specificity of 1/1000. Finally, [4] the secondary antibody (with the enzyme linked to it) is added, and [5] the enzyme's substrate is added, producing the color or light output.

From Wikimedia

If we were to use a direct ELISA, the error rate would be 1/1000. However, by combining two antibodies, our error rate is now 1000 times lower — 1 in 1 million. Since both antibodies are required to bind properly in order to get a signal, this makes the results much more reliable.


Why are bacteria immune to snake poisons? In a test I was asked why bacteria are insensitive to snake toxins.

Is it their membrane that provides a barrier to the toxins? Or do snake poisons have specific targets and thus cannot bind to bacteria?

Short answer
Many snake poisons target specific proteins not present in unicellular organisms.

Background
The question is admittedly broad but the idea behind this question is pretty much what you indicate in your post - many venoms target specific proteins and do not simply destroy their target by, e.g., disrupting gross cellular structure (like alcohol does for example). Instead, they target specific molecules that are essential for the survival of their prey.

Snake toxins can be categorized according to the organ systems they target, namely :

the central nervous system
the cardiovascular system
the muscular system
the vascular system

Central nervous system toxins are carried by elapid snakes like cobras, kraits and the taipan. Typical targets are the nicotinic acetylcholine receptor and the muscarinic acetylcholine receptor. Blockade of these receptors at the neuromuscular junctions resulting in death by asphyxiation. Acetylcholine receptors are not present in bacteria.

Cardiovascular toxins are pretty diverse and include things like angiotensin-converting enzyme inhibitors (leading to a drop in blood pressure) and glycosaminoglycans (the sulphated carbohydrate moieties that occur abundantly in cells of cardiovascular tissues) binding proteins that lead to cardiotoxicity. Again, the targets are specific molecules involved in heart function and hormones, stuff not present in bacteria.

Muscular toxins include those that bind specifically to the sarcoplasmic reticulum of muscles or interfere with specific second messenger systems messing up muscular function. Again, quite specific targets not present in bacteria.

Lastly, typical vascular system toxins include anti-coagulants such as protein C activators and inhibitors of prothrombin complex formation. Again, specific targets.

Reference
Koh et al., Cell. Mol. Life Sci (2006); 63: 3030–3041


Why can't ciliary muscles in the human eye relax like other muscles? I had laser eye surgery a decade ago, but in recent years my eyesight has become significantly myopic. I consulted an ophthalmologist to see if this was eye strain because I work at computers a lot, or part of a natural degradation of the eye over time, or both. My ophthalmologist seems to believe that in my case I'm youngish enough that the natural degradation with age is minimal, and that it's mostly eye strain that is my problem. She believes I can get my eyesight back to roughly 90% of my post-surgery sight ability, if I can reduce eye strain. She gave me some eye drops to help with dryness, and recommended various ways to for me to help my eyes recuperate.

I decided to look into eye strain to learn more about what conditions cause it and what can alleviate it. What I learned is that the lens of the eye needs to be flatter to accommodate focusing on far objects, and rounded to focus on near objects. The way the lens becomes flat is by using spring-like connective tissue called choroids that pull it taught. Attached to these choroids are muscles called ciliary muscles that stretch the choroids out when they contract. This action causes the choroids to stop pulling on the lens, and the lens will retract into a more rounded shape. So, when the ciliary muscles are relaxed, you can see far. When the ciliary muscles are contracted, you can see close up. This diagram from the York University website was the clearest explanation I have come across:

Thus, the reason for my current inability to focus on far objects is that so much focusing on close objects, mainly computer monitors, is straining my eyes. In order to regain the ability to focus on far objects, I need to reduce strain and allow the muscles to relax. If they relax, the choroids can pull the eye to the flatter shape needed to see far.

However, I can't reconcile that model with how I understand the mechanics of the other muscles in my body. If I go to the gym and run or lift weights, or in any way expose my muscles to work, they respond by getting stronger without sacrificing the ability to stop contracting. The muscles in my body don't lose the ability to relax, no matter how much I train them. I have never heard of anyone who worked out too hard or too long such that their bicep would remain in a permanent state of contraction.

In fact, in my experience, after a hard workout, it's impossible to prevent my muscles from relaxing and resisting doing more work. When I do a bicep curl at the gym, and I do it to the point that I can't lift the weight anymore, my muscle gives up and I drop the weight. Similarly, if I've spent a long time looking at close up objects, shouldn't my ciliary muscles give up, allowing the choroids to take over, making clear far vision the unavoidable outcome?

The idea that my ciliary muscles need to relax in order to see far also seems to contradict my personal anecdotal experience. Sometimes I am able to see far away, but I can't hold it for more than a few seconds. If I try to maintain focus on far objects for too long, I get an uncomfortable feeling in my eyes that is hard to describe, but it's a form of pain that forces me to give up. My vision goes blurry, and I can only see close objects again. If my bicep worked the same way, it would be as if it hurt to let my arm hang straight down with a weight, and the only way to alleviate it would be to raise the weight, which makes no sense. I feel like the effort is in seeing far, and that when I'm tired, I can only see close up.

It's not that the case that I think that all medical research on the eye has it backwards, it must be that there is some aspect of this that I am not seeing (pun intended).

How can it be that the ciliary muscles, unlike other muscles, lose their ability to relax?

Why is it that my ciliary muscles don't become exhausted and allow the choroids to take over by default?

First of all, I should correct some points that were misunderstood.
Don't change the question because this will lead to confusion.

"The way the lens becomes flat is by using spring-like connective tissue called choroids that pull it taught."

In classic ophthalmology you don't need to think about choroid in direct relation to accommodation: choroid is a sponge-like layer between the sclera and retina and in general it is consisted of blood vessels. The anterior part of the choroid continues anteriorly to became a ciliary body which in turn contains ciliary muscle - one circular muscle per eye. From the ciliary body/muscle spread zonules (zonule fibers) and they are fixed on the lens equator.

Physiology: contraction of ciliary muscle causes zonules to became loosen and "free" the lens to became more convex and move the focus anteriorly (not choroid contracts itself). If the ciliary muscle relaxes then zonules are tighten up and the lens consequently becomes more flat (less convex) moving the focus posteriorly. In other words you can say it in the terms of depth of focus - convex lens gives less depth, less convex gives more depth of focus.

Thus, the classical choroid layer does not perform any action (look at your choroid related link - there are almost nothing about accommodation).

"Permanent state of contraction" can be physiological (=normal) as well as abnormal one, and it is very common in some conditions (muscles spasms). One example is priapism, where corporal smooth muscle contraction causes permanent and dangerous penile erection which can be medical emergency (priapism is by far more complex, so take the explanation like a metaphor).

If we refer to "accommodation spasm" there is analogy to "muscle spasm" (and partially to priapism), but I should state we believe that spasm of ciliary muscle exists - since we don't see it directly. Probably (and take this sentence as speculation, since I cannot give you reference right now) the causes of this is not a muscle spasm itself, but the state of zonular fibers which cannot come back to their base state. I like the example with iron rod - if you will contract it fast and many times, at some point it can be "loosen" as well as fractured (and probably it does happens to zonules too). Probably (I say "probably" to underline the point we do not exactly know this), the "accommodation spasm" is partially misname and in future the investigations will clarify that.

Probably, you will learn some interesting facts from definition of "pseudoexfoliation" syndrome, but I do not explain it here because it is not related directly to the question. From wiki "has been known to cause a weakening of structures within the eye which help hold the eye's lens in place, called lens zonules"

Another example for analogy for continued "spasm" is the situation when one should care something heavy for a long distance without releasing the grasp - finally one can get not only spastic contraction but also severe ischemic damage to the fingers.

Considering your case, you should know about pathological (degenerative) myopia where the eye expands posteriorly and consequently the focus is before the retina which should be corrected by minus lenses. It is well known fact that myopic eyes have longer axial length then normal eyes. Probably, it is your case.

So, as you can see, the answer to your question is not a clear cut, but assumption. The ciliary muscle does can relax, but probably the problem is more complex then only ciliary muscle related issue.

PS The image you reposted is a little bitconfusing one and is not exact. This one is classical and gives better understanding of the anatomy -


Can you identify the bird in this photo? I spotted this bird in Bangalore, atop a building on a September morning.

Looks like Butastur indicus, the grey-faced buzzard. The spotted breast and the greyish chin fit well.

A nice picture can for example be seen here


Proline Iminopeptidase v Proline Aminopeptidase We're an undergraduate independent research team and we are having trouble purchasing commercial proline iminopeptidase as it is unavailable on Sigma Aldrich and very expensive on other websites. We need to test that this peptidase will cut a series of tripeptides we are synthesizing in e coli.

Could we purchase proline aminopeptidase instead of proline iminopeptidase; will the peptidase function the same way?

This paper says that they are the same, but this paper says that they are different. Does anyone have any experience with this commercial peptidase?

There are two related enzymes that cleave an N-terminal residue. Enzyme 3.4.11.9 cleaves any residue from a peptide when the next residue is proline. Enzyme 3.4.11.5 cleaves an N-terminal proline from a peptide. Unfortunately, it appears that both are sometimes referred to as proline aminopeptidase. However, only 3.4.11.5 is referred to as proline iminopeptidase.

The vendor should certainly specify which enzyme they are offering.


Long term effects of "brain freeze" on the cerebral vasculature According to one theory, ice cream headaches are caused by an increase in blood volume of the anterior cerebral artery:

Another theory into the cause of ice-cream headaches is explained by increased blood flow to the brain through the anterior cerebral artery, which supplies oxygenated blood to most medial portions of the frontal lobes and superior medial parietal lobes. This increase in blood volume and resulting increase in size in this artery is thought to bring on the pain associated with an ice-cream headache.
(from Wikipedia)

Does repeatedly experiencing this phenomenon put someone at higher risk for some sort of cerebral vascular accident, or is it not any more harmful than a small increase in blood pressure that one might experience under exertion, despite the painful nature of the headache?

I do not have a source for the following as it was taught to me in neuroanatomy classes, the explanation given for brain freeze is that it is  referred pain through the trigeminal nerve. The  meninges (the tissue lining the central nervous system) is innervated by the trigeminal nerve in the head. Therefore the pain feels as though it is like a headache from meningeal irritation but is in fact benign.

Given that the mechanism is through referred pain rather than any vascular event it should not put you at any increased risk.

This being said if you experience repeated headaches and are unsure of the cause it would be wise to consult your doctor.


Are there any thermogenic plants which are suitable as houseplants? I have been wanting to supplement my heating system with some plants that produce heat! I have become aware that there are around 14 species which generate significant amounts of heat for example the eastern skunk cabbage.
However I have also read that many species which are thermogenic release odours such as the smell of rotting flesh. I would rather avoid plants which will make my house smell like this!
Are there any plants which produce heat which would be suitable for storing in my house?

The heat the plant produces ultimately comes from the light it uses. Unless the plant produces heat just in the wanted time (winter?) from light absorbed another time; then you would be just as warm by letting the light directly warm your environment regardless of plants.


Why do plants need oxygen through their roots? I was asking myself why plants die from over-watering and the simple answer was that they can't get enough oxygen through their roots. But this made me ask myself why they need oxygen in their roots since oxygen is a product of photosynthesis and plants even release oxygen through their leaves.

With this seeming surplus of oxygen, how can plants "suffocate" when their roots dont get enough oxygen from the soil?

Plants need oxygen but don't have a heart

Complex animals all have a circulatory system of some sort to get oxygen throughout the body for respiration. Plants also do respiration even though they are net producers of oxygen through photosynthesis.

Plants also have a bit of a circulatory system, but for the most part it isn't nearly efficient enough to deliver oxygen everywhere in the plant: plants don't have anything like circulating hemoglobin-filled cells we are familiar with in vertebrates, and although fluids flow in plant circulatory systems, they aren't circulating quickly like you are familiar with in your own body. This means that plants need to get oxygen near to where it is needed.

Roots, in particular, consume oxygen

The problem of a plant not getting enough oxygen through its roots isn't because the whole plant gets oxygen through the roots, it's because the roots themselves need oxygen to function. Roots do a lot of 'heavy lifting' in a plant, literally: they are pumping ions across membranes to pull in water, to concentrate other nutrients that the plant needs for survival and growth, and to pressurize the plant enough for those nutrients to make it up into the leaves. Those processes take energy, and in turn they need oxygen.

Additionally, photosynthesis isn't taking place in the vicinity of the roots: plants are both taking in CO2 and releasing oxygen from their stomata in the leaves and stems.

If roots cannot get enough oxygen, for example due to overwatering, the roots themselves are damaged, and this harms the plant as a whole.

Adaptations

Because there are always exceptions in biology, it should be noted that some plants are indeed adapted to wet environments and have better systems for promoting the diffusion of oxygen including increasing the amount of air space in the roots, where oxygen diffuses more quickly than through aqueous media. Other plants use fermentation in their roots to survive temporary hypoxia.

References

Colmer, T. D. (2003). Long‐distance transport of gases in plants: a perspective on internal aeration and radial oxygen loss from roots. Plant, Cell & Environment, 26(1), 17-36.

Drew, M. C. (1992). Soil aeration and plant root metabolism. Soil Science, 154(4), 259-268.

Justin, S. H. F. W., & Armstrong, W. (1987). The anatomical characteristics of roots and plant response to soil flooding. New Phytologist, 106(3), 465-495.

Laan, P., Tosserams, M., Blom, C. W. P. M., & Veen, B. W. (1990). Internal oxygen transport inRumex species and its significance for respiration under hypoxic conditions. Plant and Soil, 122(1), 39-46.


What processes regulate the sex of offspring? It is known that some species are more likely to born male than female (and some maybe vice versa). I understand that it is due to evolutionary perspective (average number of adult males is close to that of females), I want to know about how it is regulated.

What I thought is that spermatozoa are made by half as Y and half as X chromosome. Then mitosis and meiosis and the probability that one of them will die is equal for both types. So, somewhere I feel lost.

Also, can it be regulated by female body or not? According to this paper claiming that hormone levels in women affect the likelyhood to born son. Possibly it is just because they choose males that are more likely to have more Y spermatozoa than X, but if it is some chemical mechanism to regulate that I'd like to know.

I'm not asking only about humans, mechanisms can be similar in almost all mammals. I'm not asking about other species: I know some are regulated by temperature, etc. This question is only about mammals.

In theory spermatozoa are indeed produced in a 50:50 X:Y ratio. However, there are factors which can change the ratio, such as hormone-disrupting agents or even food.

Best known factor in the female body is timing. There are different theories of which The Shettles method is the most well known I think. In this theory they think that boy sperm are faster than girl sperm, but don't live longer. So to have sex around the date of ovulation highers the chance of getting a boy (their sperm is faster), but for a girl sex should be planned a few days before ovulation (they live longer). It is all theory, of course, so there are no guaranties.


How does the blood of the veins in the legs get to the heart? Does it have something to do with the valves? Thanks in advance!

The veins in your legs have one way valves. These prevent blood from flowing down, but do not actively push it up. However, normal muscle movement from walking etc will squeeze the veins to push blood through these valves, and so it will work its way up to where negative pressure in your heart atrium can begin having an effect. This does however mean that blood accumulates from long periods of standing without movement, and so exercises are needed to prevent fainting, for example, for soldiers on parade (see Pathophysiology, Homeostasis and Nursing
By Roger Watson, Tonks N. Fawcett, Josephine N. Fawcett)


Why don't cats have to pant? I understand why dogs pant and humans transpire, namely for temperature homeostasis. So why don't cats need to do either, even after expending a lot of energy on a hot day?

Transpiring and panting are ways to regulate body temperature. When sweat evaporates, it cools the skin, and panting releases heat through the mouth. Horses, humans and even plants transpire for this reason, while dogs and birds pant. But how do cats release heat?
In fact, cats sweat through their paws. It appears that a cat after it has been frightened may leave wet pawprints on the floor. Although it's all over the internet, I couldn't find a convincing picture and as a cat lover, I've never noticed this phenomenon. That aside, cat's paws have little surface area, and cannot provide much cooling power. Instead, felines have other, more effective strategies to adjust their core temperature. Like dogs, they often sprawl out on cool surfaces (Fig. 1), or they seek out the shade on hot days. They also tend to sleep a lot, which reduces core temperature and is preferable of being very active in hot times in terms of body temperature (Fig. 2).

Fig. 1. Sprawling cat. source: Columbian blogs

Fig. 2. Cats in the shade. source: Cat memes
Source
- Indiana Public Media


What is the most detailed living-tissue scan available There are a lot of ways to scan living tissue. What is the most detailed one to date? What kinds of resolutions can it produce? Is there a different answer for 2D vs 3D?

I assume you are asking what is the most high-resolution in vivo imaging that science has performed to date?

I think the best way to answer such questions is to explain the nature of the question.

This depends a lot on what kind of sample you are interested in for the question to address. It also depends on whether we are talking about time (temporal) or space (spatial) resolution, because there is usually a trade-off for imaging methods. Some things we can image with femtosecond resolution, and other things we can with femtometer precision.

What property do you want to look at? Is it a certain staining, such as a fluorescent marker? The topography of a molecule sitting on a membrane? The force generated by a motor protein?

Do you consider a reconstructed image (in 3D) from 2D slices to be a fair comparison with techniques that aim to directly image in 3D? Microscopy and imaging are quite advanced fields and we're only beginning to scratch the surface.

Some more considerations for the questioner: is your sample moving? Are we talking about imaging insects hovering near flowers, or anesthetized flatworms? What scale of the sample is being imaged? What are the requirements for keeping it alive during imaging? For instance, perfusing nutrients or imaging a microbe growing on a substrate normally requires the modification of your microscope in such a way that may limit your optical resolution. Imaging some things necessarily requires long working distance objectives, while other specimen may be visualized at short working distances. These have tremendous impact on resolution!

As a case study: let's say we are interested in looking at the human brain with high resolution. You can do this with high temporal resolution (using EEG) or with high spatial resolution using magnetic resonance! Or are you interested in the resolution of real time activity of the brain, as measured via oxygen delivery to regions? This is not possible with either of the above; you have to rely on functional imaging, e.g. fMRI!


How does Mupirocin affect in staphylococcal infection? I found this sentence confusing

Transitor carriers of staphylococcal infections 70% because of mupirocin i/n.

Mupirocin is drug which affects some way.
I am not sure if the statement means inner neuronal.

I am little confused by the abbreviation i/n.
What is the point of the sentence?

This comes from the usage of the Mupirocin: Its an antibiotic, which is used topically (on the skin, its not taken in form of pills). It binds specifically to the isoleucyl t-RNA synthetase in gram positive bacteria and Streptoccus and Staphylococcus and is used to fight intranasally (that what i/n stands for) infections with these bacteria. It inhibts the introduction of isoleucine into proteins. More informations can be found here.


What cells don't have a primary cilium? It is often stated that most cells in the human body have a primary cilium.

Which ones don't? For which cells is it unknown?

It seems that, by and large, most animal and plant cells have primary cilia. To quote from this open access paper:

  ".[..] organisms that form cilia have a basal body or centriole-like structure as their microtubule-organizing center, whereas those that do not [e.g., yeast, higher plants] use morphologically distinct structures for organization of their microtubule cytoskeleton."

Other cases where cells lack primary cilia are when they possess motile cilia (e.g., sperm are mono-ciliated, respiratory epithelia are multi-cilliated).

Fry AM, Leaper MJ, Bayliss R. The primary cilium: Guardian of organ development and homeostasis. Organogenesis. 2014 Jan 1;10(1):62-68. Epub 2014 Apr 17.


Which shades/hues of color are easiest to distinguish for humans? I'm trying to represent data graphically and am using a variation of hue/lightness to distinguish one data point from the next. I would like to use a color that would allow me to convey most information visually.

What I'm interested in is which color I should use. I've read somewhere that humans are most capable of distinguishing shades of green, that is a human can differentiate more shades of green than any other color. Is it true?

Has there been any studies to distinguish the number of shades that a typical westerner can distinguish? I'm looking for information like : ### shades of green, ### shades of red, ### shades of cyan, etc.

Thank you for your input!

I've read somewhere that humans are most capable of distinguishing shades of green, that is a human can differentiate more shades of green than any other color. Is it true?

I'd say it's plausible, depending on your definition of "Green." While your eyes do, indeed, have RGB receptors (cones) and Rods for grayscale - they don't perceive the Visible Spectrum equally. Here are a few graphs I found from Photo.net regarding the human eye and the sensitivity of the Cones (first and second) and Rods (third):

What you should be noticing above is not necessarily the Y axis, but the X axis - which represents the Wavelength, and amount of Wavelength our eyes are sensitive to each color. While our eyes perceives the most Red wavelengths and the least Blue wavelengths, Green comes in just under Red's range for Wavelength coverage. However...

When combined with our Rod sensitivity, though, Green wavelengths produce nearly double the sensitivity the Red Wavelengths - and nearly quadruple the Blue wavelengths. What that means is that in low-light situations when the Cones are unable to produce a precise color image, your Rods will be able to pick out Green things (with a slightly loose definition of 'Green') more than other colors - which is perhaps the reason why night-vision goggles often use Green since they increase the Intensity of the light, which presumably stimulates the Rods more (although not knowing precisely how the image is produced - if the green coloring is enhancing that particular bit of the spectrum of falsely colored - take this with a grain of salt).

Does that explicitly prove you can see more Green shades than others? No. Your brain does a lot of processing - the entire color Yellow is a construction of your brain, and Tetrachromats (people with 4 types of Cones) are real.

However, like I said above, I'd say it's plausible.


What would be the estimated cost sequencing? I'm a newbie to the world of NGS, but I thought it might be a suitable and cheaper alternative to doing traditional Sanger sequencing for this particular application. However, I'm not so sure on how to approach calculating this cost, so I was hoping to reach out and see if someone could help here. This is for my grad school research project.

Problem Statement

I am about to make a rational library of ~1000 protein complexes belonging to the same family of proteins. There are 4 protein's plasmids to make per complex, and they are to be made by a combination of synthetic genomic cloning methods using cDNA, and multi-site directed mutagenesis on existing plasmids. Before testing their function as a complex, I need to verify that the cloning steps succeeded by sequence verifying each plasmid.

I could do traditional Sanger sequencing on each of the protein sequences, but given that each protein is ~2kb long, I would need 4 single direction sequencing reactions per plasmid to cover the CDS. In total, per protein complex, that's 16 sequencing reactions. At USD5 per sequencing reaction, each protein complex would cost USD80 to sequence. At 1000 sequences, that would be USD80,000 in Sanger sequencing.

I was thinking of doing something else - after creating the library, say in chunks of 384, send them for NGS on an Illumina MiSeq.

Request for Help

Given that:

I am not wedded to any particular NGS protocol,
Our only goal here is to, by one way or another, sequence verify the cloned plasmids.
1000 proteins is the right ballpark for the number of proteins that need to be sequence verified. 4 plasmids per protein complex.

What would be the appropriate sequencing strategy that could help us get way below 80K for sequencing costs?

Most NGS approaches should enable you to sequence all those plasmids at very low cost-per-base values (Please see here for more on prices). The challenge in sequencing them all, if there are sequences common to all your plasmids, will be to get adapters for each sample/plasmid so that reads can be mapped back to the correct plasmids.