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Are there any fluorescent proteins capable of transforming 500-600 nm light to 400-500 or 600-700 nm?
In order to improve photosynthesis, which doesn't use 500-600 nm light, I wonder if that light can be transformed into useful light?
The idea is to transfect photosynthesis organisms with the gene for that protein to improve growth.

Fluorescence always absorbs photons of higher energy and emits photons of lower energy so transforming light to 400-500 nm won't be possible.

@Cell Only in most cases: https://en.wikipedia.org/wiki/Fluorescence#:~:text=In%20most%20cases,%20emitted%20light%20has%20a%20longer%20wavelength


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Can all oxygen be provided cutaneous in humans?
What partial pressure of oxygen is needed on the skin to completely replace the lungs function as oxygen receivers? Respiration has other functions too. I am only asking about oxygen intake.
Oxygenation through the skin could eventually be used against ischaemia like gangrene and covid clotting.
The skin might eventually be kept wet to improve oxygen diffusion through the skin, as this is the case with animals.
In normal conditions cutaneous respiration is 1-2% in humans. This means that with an atmosphere of close to 100 % oxygen and pressure of 10 bar, 50-100 % of a humans oxygen intake can be through cutaneous respiration.

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What advantage does an enzyme serve over catalysis by the addition of heat energy?
I understand that an enzyme lowers the activation energy, allowing the reaction to run faster, however I am not sure, how it may be favorable during the addition of heat energy. Wouldn't that lower the activity of the enzyme since the enzyme is sensitive to heat?

Enzymes have two benefits over raising the temperature:
First, reducing the activation energy by reusable enzymes is far more energy-efficient, apart from the fact that the required temperature would vary for different reactions.
Second, enzymes are able to be controlled by allosteric mechanisms, which facilitates metabolic control by feedback loops, feedforward motivs and receptor-mediated processes. In the example of glycolysis this enables the cell to fine-control its supply with energy equivalents (see figure from Wikimedia Commons below). This mechanism may be the most important function of enzymes.

Reference

William C. Plaxton: Principles of Metabolic Control. In Kenneth B. Storey (ed.): Functional Metabolism: Regulation and Adaptation, John Wiley & Sons, Inc. 2004

The enzyme does only one thing: It lowers the activation energy which is necessary for the specific reaction to happen. It does not change the speed of the reaction, nor does it change the rection enthalpy or the quilibrium of the reaction. See the figure for clarification (from here):

Without the enzyme the Ea (activation energy) would be so high, that the reaction would be possible in the cell. Either because this high amount of energy is not available or because the amount of energy would destroy the cell or the reaction. So the lowering of Ea allows this specific reaction to take place.

By reactions there is an energy barrier called activation energy. Your substrate molecules have kinetic energy (they move, rotate, etc...), so when they collide properly, their kinetic energy can be used to overcome the activation energy and so the reaction takes place. According to the Arrhenius equation the reaction rate depends on the temperature, which is evident, because the kinetic energy of your molecules is higher by higher temperature. Enzymes lower the activation energy, because they help the substrates to collide with the proper orientation.
Enzymes are mostly composed of amino acid chains. These chains must have proper folding. Increasing (or decreasing) the temperature can disrupt this folding and make the enzyme useless. This inactivation can be reversible or irreversible depending on the enzyme type, the temperature and other environmental factors e.g. pressure, osmotic pressure, etc...
To answer your question, every enzyme have an optimum working temperature. At this temperature the inactivation is slow enough to be compensated by the increased reaction rate.

figure 1 -  optimum temperature of a single enzyme - ref

figure 2 - optimum temperatures of multiple enzymes - ref

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What happens to the umblical cord inside the mother?
After giving birth to a child, the umblical cord is cut (and stored if they want). The end connected to the child's navel will fell off eventually but what happens to the end inside the mother?
Will it be removed right after birth by doctors or what happens?

The umbilical cord is connected to the placenta, which is expelled shortly after birth.

Labor is typically divided into 3 stages:

Stage 1: From the onset of contractions (true labor pains) to full dilatation of the cervix (which is about 10 cm) - this takes about 12 to 18 hours
Stage 2: From full dilatation of cervix to expulsion of fetus - This takes about ~ 30 minutes
Stage 3. From expulsion of fetus to expulsion of placenta - this takes about ~ 15 minutes. During the third stage, the umblical cord which is attached to placenta is expelled along with the placenta. This would be the answer to your question.

Source:Hympath.com

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Arm at Heart Level when Measuring Blood Pressure
How come that one's arm has to be at heart level so that the blood pressure can be measured accurately. I've tried researching this question, but most answers to it were just "if the arm is above the heart level the blood pressure is too high and vise versa," but I want to know why this is so.

This page (and many others) explain the idea rather well. This is more of a physics than a biology question, but the fundamental concepts are the same.
In fact, contrary to what you wrote in the question, the measured blood pressure should be lower than expected if the arm is elevated above heart level.

When you reduce the pressure on the bent pipe, the water level on the side where the pressure is reduced rises.
Similarly, When the arm is elevated, it is equivalent to the right hand side of the image, where the right hand tube's water level is higher than the left hand side. Raising the arm above heart level, with the pressure of blood at the heart level remaining constant, will result in a lower pressure being measured, due to the heart effectively having to pump the blood up the distance.
For the same reason, giraffes have very high blood pressures (double that of humans) due to their long necks. If their blood pressure was at the level of humans, they would faint when raising their necks, due to the blood pressure falling to zero at their brains.


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How does most of lymph get back into the blood stream? (I don't mean the lymphatic system)
I once read that it was because of osmotic pressure that it returns to the blood stream, by entering the venules. But why? If lymph originated as plasma how come that the solute concentration is higher in the venule? Doesn't plasma contain solutes such as salts, nutrients, oxygen, etc. ?

Could you please define what you mean by lymph? Are you just talking about the non-cellular material that lymphocytes are transported in, or what?

@MattDMo With lymph I mean a fluid which originated as plasma; most of this lymph returns to the blood stream simply by defusing back inot the venule.

I think you have confused oncotic pressure with osmotic pressure

Technically 'lymph' is used to refer to the fluid found within the lymphatic system. If it's not in the lymphatic system, it is not lymph fluid. Thus, your question is really asking about interstitial fluid or the plasma that was filtered out of blood capillaries.
The answer to your question is based on the Starling equation. Normally fluid leaves a capillary due to a net pressure that favors the interstitium. This net pressure is based on the hydrostatic pressure within the capillary being greater than the interstitial pressure of the surrounding tissues, and the oncotic pressure of the capillary (that draws fluid in) being weaker than the hydrostatic pressure of the capillary (that pushes fluid out). At the venule end of this system, the capillary oncotic pressure is stronger than the capillary hydrostatic pressure, drawing fluid back into the circulatory system.

Remember that albumin is the most important component which establishes the oncotic pressure within a vessel, and that this protein is normally NOT released out of a vessel during filtration. Thus, it passes from the capillary into its corresponding venule directly.

Yes, plasma that enters the interstitium contains many of the same components as when it is in the blood, but the main difference is the protein content, losing the majority of proteins as it enters the interstitium.
Now, if you are asking how the majority of LYMPH fluid re-enters the blood stream, the answer is through the R lymphatic and L lymphatic (aka thoracic) ducts, at the location of the R subclavian or R internal jugular, and L subclavian veins, respectively. Once fluid enters lymphatic capillaries, it goes through a system of lymphatic vessels, trunks, and finally, the above mentioned ducts to rejoin blood.
References:

http://www.biog1445.org/demo/06/lymphaticsys.html
http://intranet.tdmu.edu.ua/data/kafedra/internal/in_mow/classes_stud/uk/med/medprof/ptn/англійська%20мова%20за%20професійним%20спрямуванням/2/№%2003.%20Heart...htm

Nice elaborated answer!


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Can cells straddle different anatomical systems in the body?
I'm reading Periphery by Moses V. Chao, and the author explains that the peripheral nervous system consists of the portion of the nervous system outside the brain and spinal cord. But, if I understand correctly, the cell bodies of motor neurons are in the spinal cord (or even further upstream?), whereas the nerve fibers themselves are just bundles of really long myelinated axons going all the way from the spinal cord to the nerve endings. So these seem to be cells whose cell bodies are part of the central nervous system, but whose axons are part of the peripheral nervous system. Is that how neurologists think about it? I would have thought things would be subdivided in a way that each cell is in one system or another.
I see this related question, but I don't think its answer is a clear answer for this question. That answer does seem to suggest that the cell bodies of the motor neurons are part of the PNS, not the CNS, even though they're physically in the spinal cord, but it's not really explicit about that point.
Alternatively, it's perfectly reasonable to have overlapping systems. I'd just like to know the way the lines are drawn.

The answer in your link does answer your question: "The distinction [central vs. peripheral] is slightly arbitrary... the most important part is that together they are parts of the nervous system, rather than being distinct systems..." IOW, yes, the motor neurons are just long mylinated anons.

Does this answer your question? Why are spinal nerves considered a part of PNS while the spinal cord is a part of CNS?

The answer in the link says: " 'CNS consists of brain and spinal cord, and PNS consists of everything else.' That's really it. The distinction is slightly arbitrary, I'd think of them as the central (nervous system)..." I could read that answer two ways. One is that the cell bodies of the motor neurons aren't really considered "part of" the spinal cord, since those cells are part of the PNS. The other is that the bodies are part of the spinal cord, and it's only the axons that are part of the PNS.

Have you considered the ganglia? This might be what's tripping us both up re. our communication.

Yes, but I don't think all peripheral nerves go to them. Do they? Also, it occurred to me that, if the nerve itself is only the bundle of axons and not the cell bodies, then that other answer did answer my question, but then my question becomes, "Is a nerve just the axons, or is the collection of cell bodies part of the nerve too?"

"Nerves" needs a definition, I think. I think of nerves as the long fibers that transmit impulses from the center to the periphery, and vs. versa. Those consist of axons and the cells that myelinate them. That's different (to me) than a neuron. And yes, all impulses go through ganglia except at C1, I believe. My memory of neuroanatomy has long ago degenerated into simple stuff. Apologies, I should let the neuroscientist(s) answer this.

Answering my own question:
Yes, cells can straddle anatomical systems in the body.
In particular, the spinal cord is part of the central nervous system while spinal nerves are part of the peripheral nervous system, as described in this question. And nerves are bundles of axons, supported and held together by additional cells. The cell body to which the axon belongs is not part of the nerve. Instead, for spinal nerves, it's a part of the spinal cord and hence in the CNS.
It was surprising to me that the boundaries of anatomical structure don't always correspond to the boundaries between cells, but that makes sense when I consider that the field of anatomy began as a macroscopic endeavor, a scale on which it makes sense to treat the boundary between nerve and spinal cord as the point where they meet.
Thanks to anongoodnurse who basically led me to this answer in the comments.

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Cytoskeleton made of only actin?
I am aware that the cytoskeleton has three structural components: actin, microtubules and intermediate filaments. I was wondering if any cell could possess a cytoskeleton made only of actin. Or made only of microtubules, for that matter. Is it possible for actin to perform the functions that microtubules ordinarily perform in a cell? Or vice versa?

If you are talking about an eukaryotic cell, I'd say no, due to the reason that the three types all have some different, irreplaceable functions. For example, microtubules form the mitotic spindle; actin filaments are greatly used for movement protrusions and cell adhesion; intermediate filaments are what convey the cell its structure, being the strongest. As the cell system is already tuned differently around these 3 types of filaments (proper linking proteins, enzymes, ...), my idea is that taking any out would probably make the cell unviable

1) Can cells survive without any of the different cytoskeletal components?
Yes, most certainly. At least for actin and microtubules (MTs) there are plenty of eukaryotic cell types that can survive without them. MTs can be disrupted by cold-shock (see for example here https://www.ncbi.nlm.nih.gov/pubmed/16505977). How well the cell survives depends on the type of cell, but the ability to survive without MTs can range from minutes to hours as far as I'm aware. Once the temperature goes back to normal, the MTs just grow back. Of course, the cells won't behave normally in the meantime, because many processes do depend on MTs. Actin can be disrupted using various drugs or genetic constructs, or they can be cut using femtosecond lasers (see for example https://www.ncbi.nlm.nih.gov/pubmed/28324605). Again, many processes are disrupted, particularly cell motility, but most cells can survive without actin for a while.
I'm not aware whether any eukaryotic cells exist that have no intermediate filaments or can survive at least for some time without them.
2) Could a cell function normally while lacking one type of cytoskeletal component?
First, to my awareness there is no eukaryotic cell without MTs or actin. We do commonly use actin and tubulin promoters for transgenes and assume that all cells will express them. So I'm taking this question hypothetically.
As with every hypothetical question, the answer then purely depends on the restrictions that you define. Can the cell possess arbitrary new proteins that currently don't exist? Then yes, definitely you could get eukaryotic cells with just MTs or just actin or just intermediate filaments. You just have to bend all the other things the cell does to fit with that filament type, and then enjoy arguing whether that's still a eukaryotic cell or not.
But I think actin would find it easier to take over the other filaments' jobs compared to the other way round.
MTs are large and rigid. They can't operate on scales below 25nm like actin can, and the individual tubulin dimers can't do anything useful until a tube of some minimal length has been formed out of many dimers. Intermediate filament monomers are pretty thin, but very long. Actin monomers are small and globular, and a supershort actin filament made of a handful of monomers can already function as a filament, branch out, form networks, pull on things etc. Actin-mediated endocytosis crucially depends on this (https://www.ncbi.nlm.nih.gov/pubmed/25675087 for example). It would be difficult to find workarounds for these small-scale functions of actin if MTs or IFs were to replace it. On the other hand, actin filaments can very easily be made into large, thick, rigid rods like microtubules. Many cell types do this constantly when they form filopodia. Actin meshworks can also provide similar mechanical support (both stable and flexible) as IF meshes. With minor shifts in the regulation of where, when and how to organise filaments, actin could probably take over the other cytoskeletons' functions. It would probably require a quite sophisticated regulatory system though to perform all the different functions at the same time in one cell.

@EliKorvigo Noted, thanks for the correction.

I think sperm is only having microtubules (axoneme) in them as a part of the cytoskeleton. Different types of cytoskeletons evolved to perform the different function so generally they will not exchange their function but are precisely evolved to carry out their individual functions.
(From textbook Molecular Biology of the Cell. 4th edition https://www.ncbi.nlm.nih.gov/books/NBK26914/)In tail section of sperm, which is a long flagellum.The core of the flagellum is composed of a structure called an axoneme.The axoneme consists of two central singlet microtubules surrounded by nine evenly spaced microtubule doublets. These dense fibers are stiff and noncontractile, and it is not known what role they have in the active bending of the flagellum, which is caused by the sliding of adjacent microtubule doublets past one another. Flagellar movement is driven by dynein motor proteins, which use the energy of ATP hydrolysis to slide the microtubules.
But I would like to correct my answer, as sperm also contains actin for capacitation and acrosomal reaction.So I think sperm is a eukaryotic cell where you can only see 2 types of the cytoskeleton.Here is the link for the paper https://www.ncbi.nlm.nih.gov/pubmed/15749953

Welcome. Can you add sources and references to your claims to allow other users to background read on your answer?

Yes ,see this link please https://www.ncbi.nlm.nih.gov/books/NBK26914/

Could you add it into the answer proper, please?

Sperm cells, like all eukaryotes (with some pretty rare exceptions), contain actin. "So I think sperm is a eukaryotic cell where you can only see 2 types of the cytoskeleton" – by virtue of having a nucleus, sperm cells also contain lamins – intermediate filaments.


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Why did viruses evolve in the first place?
This question might seem kind of strange, but it's something I've been chewing on for ages, and I can't really think of a good answer.
Viruses just seem to be floating around passively until they encounter a host cell. Then they enter the host cell, wreak havoc and use the host cell machinery to make more copies of themselves. Then these copies float around passively, until they find host cells.
So what's the point of all this? Infecting the host and causing so much trouble for the host, I mean. The only thing I could think of was something like the "selfish gene" hypothesis, i.e. the genetic material of the virus wants to make as many copies of itself as possible, and in order to secure the machinery for replication, it must infect a host cell. But it's not a very satisfying answer, somehow. All other living organisms at least have their own replication machinery. Then what kind of organisms are viruses? (Are they even organisms?) How and why did they evolve and stay around on the earth for so much time (till the present), if they depend on hosts for their replication?

The simple answer to why anything in biology happens is always: "Because it works". As long as a thing is able to replicate itself, it will do so. Viruses have found many different ways of getting replication to work, and so they continue to replicate until one day it doesn't work anymore (like it should have been the case for poliovirus a long time ago).

They float passively until they encounter the right conditions, the same could be said of any spore or seed. The point of viruses is to make more viruses, the point of any biological product is to spread the genes that created it.

I don't really think there's a point to anything. Things just happen, and we try to understand how things happen, and the consequences of things happening. Everything you do and think is only but the result of some chemical reaction. Just like how everything a virus does is nothing but the result of some chemical reaction. I do however believe that viruses are a beautiful example of self-preservation. Viral DNA/RNA truly is the most well adapted in terms of finding a way to continue replication.

The are different theories about virus evolution, some speculate that they were evolved before the cells, some speculate they are evolved to spread genetic information, a sort of specialized conjugative pilus others say that they are cellular parasites. Still, none has the final answer yet, but thanks to the boost of DNA sequencing, many new pieces of the puzzle come out lately so keep updating your knowledge!
Whether they are alive or not is also matter of discussion and it pretty much depends on the definition of life itself.
If you define life as the property of reproducing, transmitting genetic information and evolve, then viruses are life forms. But if you want to include in the definition that a life form must have all the biomolecular machinery encoded in the DNA (I really disagree on this point), then they are not. To me, they look quite a living thing.
About your sentence:

So what's the point of all this? Infecting the host and causing so
  much trouble for the host...

I think you are looking only at the "negative" side. Viruses can transfer useful genetic information, plus they are involved with the evolution itself. We humans have lot's of viral DNA in our genome, so no viruses, no humans as we know them. Think about it ;)
There are plenty of resources around to get a better insight please have look at the following links to get started.
https://en.wikipedia.org/wiki/Viral_evolution
https://en.wikipedia.org/wiki/Evolution_of_influenza
http://www.sciencedirect.com/science/article/pii/S0042682215000859
https://link.springer.com/article/10.1007/s00239-013-9601-0
https://www.nature.com/search?order=relevance&q=evolution%20of%20viruses

I think you are looking only at the "negative" side. Viruses can transfer useful genetic information, plus they are involved with the evolution itself.  Downvoted because of this profoundly misleading sentence which suggests that there's a goal to evolution, and that organisms "should" only evolve if they have "good purposes".

@iayork Where do you read this exactly? I did not suggest any goal whatsoever. I just suggested that there are positive effects of virus infections, including broader secondary effects like humans evolution. My sentence was meant to point out that you have to consider the variety of effects, not only the "negative" one. But definitely, there is no suggestion of any goal or a "good purpose".

My sentence was meant to point out that you have to consider the variety of effects, not only the "negative" one.  Exactly my point; that's a profound misunderstanding of evolution.

@iayork how can be misleading something like "consider the variety of effects". I really don't get you...

The fact that you don't understand my point demonstrates that you don't understand evolution.

That's definitely not a mature nor scientific way of putting it.

Some folks like mimat get a bit pedantic. "Viruses are not life because we've defined life in such a way that viruses are not alive". Circular reasoning much?
The ocean contain something on the order of 10-15 viral particles for every bacteria. Viruses are clearly an integral, if less-understood, part of modern ecosystems. The question of where they came from, and how they relate to the other domains of life (bacteria, archaea, eukarya) is an interesting one to explore, if unsatisfying because we don't have a lot in the way of answers.
Why do humans exist? From our genes' perspective, we exist as replicative machines whose primary function is to make more of our genes, enabling them to exist in perpetuity. It's the same with viruses. They exist because the mechanism of viral replication is effective at making more bits of viral genetic information.
Asking 'why' something arose in the first place isn't a very useful way of phrasing. Mutation in evolution doesn't occur with foresight, instead it's the random element of evolution. (Natural and Sexual Selection being totally non-random.) Asking 'how' is a better question.
Thinking about viruses not being alive because they lack the ability to make everything they need for replication. This is more than a bit pedantic: are then humans not alive because we lack the ability to make some thing we need (vitamins)? Viral capsules are machines built by genetic sequences that allow those sequences to replicate in perpetuity - same as us. I certainly think they're a form of life, and like almost all other life, they are dependent on existing in an ecosystem with other forms of life.
As to where life came from, or a particular type like viruses, very interesting question. LUCA, or the last universal common ancestor, has been inferred to have been a protocell using something like methanogenesis or acetogenesis, had a cell membrane, and either DNA or RNA for storing and replicating genetic information. Going earlier in time to the RNA world gets interesting.
Think about a given genetic sequence. While any given instance is transient and fragile, there may exist billions of copies of it at any given time on earth. An exact copy of that sequence may have existed for hundreds of thousands of years. Inexact copies for millions, and if you are generous and think of gene families, genes may have lifetimes measured in billions of years.
Microbes are far more 'promiscuous' with their sharing of genetic information than we usually think about, as multicellular organisms. You could think of microbes as systems that are very flexible, while multicellular systems have traded that adaptability for in-system optimization. That is, to us viruses make us sick, but to a bacteria a plasmid or virus might be costly, but potentially advantageous if it brings with it new, beneficial genetic information.
Viruses could be thought of as a super-spore. A spore is a dormant, but very tough capsule that allows its parent genetic sequences to survive hostile times, and then resume metabolism and replication when better times or environments come. To a virus, every environment is a hostile one except the insides of their specific target cell. In a way, you could think of a virus as 'sleeping' or dormant until it enters a host cell, and only truly active or alive when it is. Think about the actual genetic information as the 'alive' entity, and anything constructed by it as a machine.
Viruses probably predate LUCA.
Time to get super-super-speculative.
Among many ideas as to how life arose, in particular cell membranes, one hypothesis is that early cell membranes arose abiotically. According to this notion, life only gradually gained the ability to modify and eventually synthesize membranes. The original membranes may not have been composed of modern stuff at all, as long as it performed the essential functions of being a selectively permeable barrier. Early oceanic vents provide a place where protomembrane molecules could have been abiotically generated and condense on porous rocks.
Likewise, there is a question as to what came first, or if this is a good question: metabolism or genetic information replication. How do you have one without the other? Well, again, early oceanic vents seem a good candidate for abiotic metabolism to have begun building precursor molecules. Get a precursor molecule with the ability to make something like it, and voila: replicators! Personally, I think the order is this: replicators first and gradual control of metabolism and cell membranes later. You could almost think of metabolic machinery as simply being the means of recreating the conditions that existed in those early vents, or the porous rocks around them: conditions that enabled replicating machinery to replicate.
Who knows if this concept is true! But if something like this is how life got started, then at some point before luca, the original replicator more closely resembled a virus as it exists inside a cell, than it resembles modern cells. If replicators in their early days lacked much control over metabolism and/or membranes, that kind of sounds like viruses. Before early life 'took off' in its modern cellular state, early genes needed to connect with other genes for replication, but not necessarily for distribution. Maybe this took the form of physical connection via protochromosomes. Perhaps branches of genetic life that became many viruses opted for an alternate strategy.
Multiple genes that are located on the same chromosome (circular or linear, doesn't matter) have opted to link their evolutionary futures as closely as possible. They are literally, physically linked. The link may not be physical: our genes, even if located on different chromosomes, still have linked fates, marred only by recombination and sex. Remember that microbes are much more fluid and genetically flexible. From a gene's perspective, a cell is simply a location with other friendly genes, which which the 1st gene shares an evolutionary trajectory. If the 1st gene happens to be on a plasmid, however, its fate might be more independent, as copies get swapped into other cells. Microbes have many ways of swapping genetic information. To the extent that this information can be swapped around, the evolutionary future of those swapped bits is less dependent on the exact nature of the other, more cellular bits. Viral genes have opted for an even more independent evolutionary trajectory than plasmids and similar structures. I mean, really, what eats a virus? They build themselves protective capsules and are only really vulnerable when they are inside a host cell and actively replicating. If I were a genetic sequence with billions of physical instances at any given moment, and potential information lifespan in the billions of years, that honestly doesn't sound like a bad way to replicate.

Welcome to Biology.SE and thank you for your comprehensive and expansive answer. Could you maybe add some reference to your claims (peer-reviewed literature is preferred, Wikipedia etc. is very much okay for common knowledge) - this allows others to follow your arguments and increase their understanding by further reading. Please also consider taking a look at what is considered a good answer on this site and take the tour. Thank you!

Viruses are not considered alive because they cannot reproduce independently and are therefore not organisms.
As to the answer to 'why' something arose in evolution is always the same: because at that moment in time this specific set of traits was able to function and create a lot of offspring (or copies). The virus 'might create a lot of trouble for the host' but that does not matter, a lion causes a lot of trouble for antelopes but that does not get questioned.
Evolution as a process is not teleological, nothing evolution does has a purpose or end goal, a combination of traits simply works better than what came before in a specific set of circumstances.
You already mentioned the selfish gene hypothesis, in my personal opinion that is the best explanation.

Viruses actually have RNA. Due to this property of genetic material, RNA organisms are faster than DNA organisms!
Secondly, they have a protein coat that acts as another important thing which makes allows them to live in contact with organisms!
But every coin has two sides. It is much used in biotechnology to transfer important genes in plants and animals by disarming their pathogenic properties!
When they come in contact with host DNA, host DNA starts to replicate its virus genetic material and then its own! For example, in the case of HIV.

See in the image how reverse transcription the most important process converts RNA -> DNA then creates an infected DNA strand in host and host produces its RNA which is infected!

Hi Welcome to Bio.SE! Please provide some support for you answer to avoid having it downvoted or closed. Supporting answers with credible references is a best-practice that we have come to expect on this Stack Exchange site. Thanks!

Your answer doesn't seem to answer the question. Please edit your answer to avoid having it downvoted/removed. See here for a guide to writing good answers.  ... Also, I tried editing a bunch of your answer to try to improve grammar, spelling, punctuation, etc. I hope that you use this as a learning tool to create higher quality posts of your own in the future. Thanks.

There are a lot of factual errors in this answer, you have both RNA and DNA viruses and these have little to do with speed. Naked viruses do not have any proteins so that is also wrong


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What is the mass or range of weights of individual microbial spores and or cysts?
Also looking for the overall physical dimensions of spores/cysts.  I am trying to estimate how much static charge a spore/cyst would require to overcome the pull of gravity.


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how long after death can a body exhibit an immune response
I suppose this is part of a larger question - at what point do the body's coordinated systems (Endocrine, Autonomic nervous system etc) begin to fail? Within hours? Days? Minutes?
Of course this must vary widely with the means of death but let's assume for the moment a sudden brain embolism or some such that would leave the organs intact.

You might be interested in this.


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What’s the largest animal in the evolutionary history of birds?
I know that birds evolved from dinosaurs (or a related clade).  However, some dinosaurs are large and others are small.  Did birds evolve only from a line of dinosaurs that stayed small throughout evolutionary history, or did the ancestors of bids get large at some point and then shrink?
Concretely, what’s the largest known animal among the ancestors of birds?

I think you need to clarify this a bit.  First, how do you measure "large" for birds, body mass or wingspan?  And are you asking only about ancestral species, or include lineages that have died out?

@jamesqf: Good point, I meant mass, since the goal was to include non-bird ancestors.  And by "ancestors of birds", I meant ancestral species.

It is basically impossible to identify direct ancestor, the best we get in paleontology is something closely related to the ancestral lineage.

consider Herrerasaurus the most primitive therapod, which is bigger than a human https://en.wikipedia.org/wiki/Herrerasaurus

The largest bird was Vorombe titan, 3m tall and weighing 650kg. It is likely that this was larger than any of its ancestors.
Working back through the lineage of birds in Theropoda, the animals that are on the avian linage are small. One finds some early therapods that may be close to the common ancestor that were "largish" but smaller than V. titan.    Going back to basal Archosauriformes one finds a side-genus like Proterosuchus, a crocodile-like animal that could be 3m long, but not as massive as V. titan. It is possible that there is a large semi-aquatic creature in the archosaur lineage, but it is more likely that the common ancestors of crocodiles and birds were smaller. The megafauna of the Permian were all synapsids and more closely related to modern mammals than to birds.
Prior to that, there are lizard shaped creatures, salamander-like creatures, back to lobe-finned fish and so on. No megafauna.
None of these potential ancestors is as large as V. titan.  I'd conclude that the largest animal on the "bird" lineage is this type of Elephant Bird.
Perhaps this is not so surprising.  Large creatures are vulnerable to extinction. The common ancestors of the extant clades tend to small adaptable generalists.

I was going to answer that, but V. titan isn't an ancestral bird, it is one of the extinct clades within Aves, just like any number of more recent species - passenger pigeon, dodo etc.  For it to be ancestral it must have direct ancestors now.

@bob1 I assume you meant it must have direct descendants, right?

@bob1, that is a very reasonable interpretation of the question, in which case it is likely that the African ostrich is the answer to the question: extant birds are descendants of generally smaller ancestors, though there may be some theropod ancestors that were larger. As your answer implies, we probably don't have actual fossils of theropods on the line to modern birds, we only have various side branches, but if we do, it is very hard to establish which, if any are ancestors and which are cousins. My interpretation is "clade Aves and ancestors", and V. titan is certainly in Aves.

I should say that “the largest ancestor is a large current or recent bird” is a good answer to the underlying motivation of whether the ancestral line went large and then shrunk or not, which is why I accepted the answer.  I should probably have phrased my question this way explicitly rather than trying to concretize it.

@GeoffreyIrving in that case the question should have been "what was the largest bird ever?", not a specific ancestral bird. BTW, Dinornis robustus was taller but probably not heavier than V. titan, having said that, there were Dinornis species that were about the size of a turkey too...

This is actually a very difficult question to answer - because how far back do you go. The clade Avialae which includes the true birds is fairly recent and contains a lot of new dinosaurs(! -debate over feathers), but the clade Avialae is included in the theropod (Theropoda) group of dinosaurs, which includes such things as Tyrannosaurus rex, Spinosaurus, and Giganotosaurus, all of which are fairly large. However, these are almost certainly sister clades to that of the birds rather than actual ancestors.
However, Avialae is a made up clade with no actual fossil representing it; it is purely hypothetical as an ancestral marker for birds.
It seems that there is quite a bit of debate among paleo ornithologists as to which groups of dinosaurs are most closely related to birds. It is thought that things like Archaeopteryx are part of the bird ancestral clade, but even this much is uncertain, as there are a number of other feathered dinosaurs within the larger clade, that definitely did not evolve into birds. You might consider Neotheropoda a suitable cut-off, as this contains the true birds, but is still quite diverse. You could also cut off at Averostra, which includes Aves, and Ceratosauria, a group of quite large feathered dinosaurs.
Having said all that, we are very unlikely to even know which species are directly ancestors of birds, it seems that there are a lot of species that are very similar and all closely related, but making the choice of which is down to experts and a paucity of specimens. See this bit on Birds for some of the difficulty in defining them. If I had to make a choice, I would probably go with Ichthyornis as a definite ancestor, but I am no expert (I'm a virologist...).

Interesting, thank you!  I suppose in the absence of known common ancestor species, answering this kind of question might require some entirely difference source of information to separate sister clades off, such as the presence or absence of genes related to large size.

@Geoffrey Irving: I doubt that genes for large size would work, considering that the elephants are closely related to the hyrax: https://en.wikipedia.org/wiki/Hyrax  Or that the dodo is descended from pigeons, or the considerable size variation among domestic dog breeds.

@jamesqf Not sure what your mean by that, since we know that, in humans, size is mostly genetic. So there are definitely genes for size.

@Konrad Rudolph: But those genes are obviously not... is stable the word I want, or maybe conserved?  Anyway, my point is that size can change drastically in relatively few generations, either through natural evolution (see e.g. "island dwarfism" and "island gigantism"), or by selective breeding.

@jamesqf I think it’s mostly that height is a complex, polygenic trait: hundreds of pleiotropic genes all have a tiny influence, and these genes are mostly not in linkage disequilibrium, so they are inherited independently and are subject to different selective pressures.

@Konrad Rudolph: Yes, and it doesn't seem as though there's a purely genetic constraint on size.  As with dogs (or indeed, with humans), the size can be increased until it causes other health problems.  Given a few million years to weed out those problems, and the proper evolutionary pressures, it seems like the only constraints are mechanical.  Consider whales and their much smaller ancestors.


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A fish with 3 paired fins
Many species of fish have 2 or 4 fins combined into pairs. But is there a fish with 3 (or even more) paired fins? Or has it ever existed in the past?

Holocephalans exhibit auxiliary appendages called pre-pelvic claspers (PPCs) that are located anterior to the pelvic fins... [which] could represent the only example of an independent third set of paired appendages in an extant taxon, if they articulate independently from any pelvic fin basal cartilages, challenging the current paradigm that extant jawed vertebrates are constrained to two sets of paired appendages. Two extinct groups, including Placoderms and Acanthodians, exhibit variation in the number of paired appendages, suggesting this may be a plesiomorphic trait.
... microcomputed tomography scans revealed that PPCs are not modified propterygia, nor do they articulate with the propterygium. They articulate with the anterior pre-pelvic process on the anterior puboischiadic bar (or pelvic girdle), suggesting that while they are associated with the pelvic girdle, they may indeed represent a third, independent set of paired appendages in extant holocephalans.

Are vertebrates constrained to two sets of paired appendages? The morphology, development, and evolution of pre-pelvic claspers in the Holocephali


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How can I retain cells in suspension for comparative microscopy?
I am working on a digital holographic microscope. I would like to compare its imaging properties with an actual phase contrast light microscope. My aim is to do this cell by cell, creating a z-stack that shows the same cells in suspension, in a volume with approx. 1-2mm side length. In order to do this, I need to fix each cell firmly in one XYZ position to be able to move them between microscopes.
I am not a trained biologist and I am wondering if there is known procedures/agents to do this. Here's a couple of (non-)requirements I could think of so far:

the cells don't need to live through the process
they should however retain their form for at least couple of minutes (acquisition time)
the agent should be close to translucent and not form bubbles

you can embed the cells in a matrix. You can use agarose, geltrex or fibronectin. I am not sure about their optical properties though.

@alec_djinn Thank you. Someone has pointed me to low-melting-point agarose before.. 600 EUR for 50g though, what in the name of God..

You can use normal agarose as well, it is much cheaper. A 0.5% will do the job.


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Gibbs free energy and entropy in enzyme catalysis
In enzyme catalysis, the formation of the enzyme-substrate complex causes a reduction in the entropy of the system. If entropy reduces, the gibbs free energy will become less negative. How then is enzyme catalysis favorable? Are there any other factors that off-set this?

Enthalpy.......

And is it impossible to decrease the entropy of a molecule? And does an enzyme reaction stop with the formation of the ES complex? And what exactly is the second law of thermodynamics?

As @canadianer hinted, the answer is enthalpy.
ΔG = ΔH - TΔS
For binding to be a spontaneous process ΔG must be negative. If the binding of a ligand to a protein decreases system entropy then ΔS is negative and the entropy term -TΔS is positive. However ligand binding involves the formation of various protein-ligand interactions (hydrogen bonds, ionic interactions, van der Waals interactions) all of which make a negative contribution to the change in enthalpy, so ΔH is negative. If |ΔH| > |TΔS| then ΔG will be negative.
This simplified account ignores the parallel changes taking place due to the ligand 'dissociating' from the solvent.


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Aerobic respiration
I read a sentence in my biology book while i was reading respiration chapter.  i wasnot able to understand it. It was in the process of oxidative phosphorylation"
"as the proton pass through channel their electrical potential energy is used to synthesise ATP in a process called CHemiosmosis" Can anyone plz explain that from where this energy came in proton and how is it transfered during facilitated diffusion.!


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Insect Identification needed
I found this sitting on my window, could not understand what it is. Any help would be appreciated.

Where did you find it?

Size and location would help a lot!

size - 3 inches max and location is Rajarhat. It can fly. Is their any moth that comes similer? Its my guess though.

It is a moth, maybe Miresa clarissa but not sure, so not an answer.

@anongoodnurce Thanks. I checked several other pics of this insect and the pic I clicked. Its almost looked the same and most probably the ans you have provided is correct.


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Coalescent Theory - Probability for $k$ alleles that of one coalescence event occured $t+1$ generations ago
From this textbook
Under the wright-Fisher model of genetic drift and under the assumption that all alleles are neutral, the probability that $k$ alleles had $k$ distinct parent alleles the previous generation is
$$Pr(k) = \prod_{i=1}^{k-1}1-\frac{i}{2N} ≈ 1-\frac{{k \choose 2}}{2N} $$
The chance of two alleles not coalescing for $t$ generations is $\left(1-\frac{1}{2N}\right)^t$ , and the chance that they coalesce in the next generation is $\frac{1}{2N}$. Therefore, the probability that 2 alleles had a common ancestor t+1 generations ago is
$$\frac{1}{2N}\left(  1-\frac{1}{2N} \right)^t ≈ \frac{1}{2N}e^{\frac{-t}{2N}}$$
I understand up to this point!
The probability that the $k$ alleles do not coalesce for $t$ generations, and then one pair coalesce to give $k-1$ alleles at $t+1$ generations ago is as follows:
$$Pr(k)^t \left[ 1-Pr(k) \right] ≈ \frac{{k \choose 2}}{2N}exp\left[ -\frac{{k \choose 2}}{2N}t \right] $$
Can you help me to understand this last part? (both the left and right part of the equation)

Is this the exact text from the book? The left side seems to represent the probability for

"No coalescence in $k$ lines in $t$ generations (i.e. the $Pr(k)^t$ term), and at least one coalescence among those lines in generation $t+1$ (the $1-Pr(k)$ term)"

which is the same event as

"First coalescence event in $k$ lines is exactly in generation $t+1$".

The right hand side is derived analogous to the second equation, with $1-\frac{1}{2N}$ ("no coalescence in two lines") replaced by $1-\frac{k\choose2}{2N}$ (approximation for "no coalescence in $k$ lines):
$$
\begin{align}
Pr(k)^t \left[ 1-Pr(k) \right] &≈ \left( 1-\frac{k\choose2}{2N} \right)^t \left [1 - 1 +  \frac{k\choose2}{2N} \right] \\
&\approx \exp\left( - \frac{k\choose2}{2N} t \right) \frac{k\choose2}{2N}
\end{align}
$$
were is first approximation is due to your first calculation. The second one seems to use a first order Tailor approximation of $\exp(x)$:
$$
\exp(-xt) = exp(-x)^t \approx (1-x)^t
$$

+1 Ok, I got the idea. No, that is not exactly the same text than in the book. I summarized it. Thanks a lot for you answer. The answer would be perfect if you could just show that $$\frac{1}{2N}\left(  \prod_{i=1}^{k-1}1-\frac{i}{2N} \right)^t ≈ \frac{{k \choose 2}}{2N}exp\left[ -\frac{{k \choose 2}}{2N}t \right]$$

I extended my answer to show the equation. I have never seen this approximation of $\exp$ before...


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How do I calculate the change in allele frequency in a haploid population under selection?
From this book

For simplicity, let us consider a haploid organism and assume that the frequencies of alleles $A_1$ and $A_2$ are given by $x$ and $y=1-x$, respectively. We also assume that the fitnesses of $A_1$ and $A_2$ are $w_1 = 1$ and $w_2 = 1-s$, respectively. In this case the mean fitness $\bar w$ is given by $x + (1-x)(1-s)= 1-sy$, and the allele frequency change per generation becomes
$$\Delta x =  \frac{dx}{dt} = \frac{sxy}{1-sy}$$

If I would have to find what $\frac{dx}{dt}$ equals I would use the Wright-Fisher equation and find that:
$$\frac{dx}{dt} = \frac{w_1 \cdot x}{\bar w} = \frac{x}{1-sy}$$
, which is obviously not the same result as what the author found...
What am I missing? How did the author find out this result $\frac{dx}{dt} = \frac{sxy}{1-sy}$?

Recheck all the equal signs in the second equation (looks strange).

Well that's just reformulate the same equation differently. I got rid of everything in the parenthesis hoping things seem more clear. I edited some other stuff hoping things are clearer. Thanks for your help @fileunderwater

Hey remi, given your info I've managed to derive the answer. Check my answer below and ask me if you need any extra explanation, this is important since I gave you an answer but I am still unsure how you went wrong.

Here's a simple consistency check to show that $\Delta x = \frac{x}{1-sy}$ can't possibly be the right answer: in a pure monomorphic $A_1$ population, there obviously cannot be any change in allele frequencies through selection, so $x = 1$ should imply $\Delta x = 0$. Your formula, however, yields $\Delta x = \frac11 = 1$ in that case.

Ps. As a mathematician, I'd like to register my objection to using the notation $\frac{dx}{dt}$ for "allele frequency change per generation"; it properly denotes the rate of allele frequency change over time (presumably in a continuously breeding population, for such a rate to be well defined). Even if we measure time in (average) generations, it's not hard to come up with examples where the two are not equal.

Here is my full derivation to the book example you gave, hopefully it'll help you clear up what went wrong:

You need to remember that after there is selection acting on the population, you no longer have a total of 1 after selection. Think of selection as "killing" individuals, which means the total is now 1 minus what has been "selected out". sy is what is selected out, therefore the new total is 1-sy. Which means you now divide each of your frequencies by 1-s*y (see picture).
Please comment if you need more explaining.

Ok, I totally understood my error. That was very simple. Thanks a lot for this good explanation.

The great thing is that you've grasped the "hardest part" in population genetics modelling. The procedure, of breaking down the steps via table and normalising, is the same procedure for diploids but instead of A1 you have A1B1, instead of x you have 2pq, where p is f(A1) and q is f(B1)), after selection A1B1 is simply 2pq - s(2pq), etc. Even if model multiple separate loci, and where each locus may have >2 alleles, just: (1) tablate all possible genotypes as columns, (2) tablate the frequencies at each stage of the life cycle, (3) and make sure to normalise if there is selection. :)


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Evolution: How could all useful traits evolve simultaneously?
I have a basic question about evolution, for which I never found an answer. I understand how evolution works if we focus on one specific organ or trait. With each generation, some organism is more likely to reproduce, so the trait that leads to success gets more frequent. My problem is understanding how all the traits can evolve simultaneously.
Looking back to our ancestors, we evolved many different kinds of adaptations (in unrelated areas like eyesight, kidney efficiency or a healthy fear of predators, digestion of certain nutrients, balanced walking etc.).
Natural selection can only work with what's there, so mutations are important. But if  mutations are rare, it seems unlikely that many (thousands of) properties of organisms get improved in a single generation. You'd need to get very lucky to randomly improve all the genes responsible for it.
So, if we look back to our ancestors again, did they just improve on a single or a handful of traits in each generation? In that case we would need hundreds of generations before we have improved somewhat on each "front". By then, the other properties could "drift" back to a not-so-advantageous version. (This was supposing that each generation improves on a random trait, as opposed to long sequences of generations each improving on the same).
Or were there always some super lucky organisms that randomly got an improvement on almost all different traits? But just having some of those super lucky ones is not enough. The good traits don't guarantee success, just improve the odds. So we'd need many very lucky ones in each generation.
Has anyone calculated or simulated how the adaptation for many different traits can happen simultaneously?

Has anyone calculated or simulated how the adaptation for many different traits can happen simultaneously?

There are a lots of studies on the subject but I don't fully understand what is your issue. So I'll try to give some words hoping that helps a bit but it is possible that I'll totally miss the point you want to make.
The mutation rate in humans is around $1.25 \cdot 10^{-8}$ per base pair per individual per generation. The human genome contains about 3400 Mpb, meaning that you probably carry $1.25 \cdot 10^{-8} * 3.4*10^9 = 42.5$ mutations that none of your parents had in their genome. Now if you consider the population size, you'll see that a fairly big amount of mutations occurs each generation in the human population. So mutations are not that rare! It might unfair to take human as an example though as human's population size is very big. Anyway, the great majority of mutations are deleterious. In consequence, you are right, probably not many beneficial mutations will occur in a given population at one given generation and especially not in the same individual (except if you think of viruses!).
Now, depending on how beneficial is the mutation you are considering (selection coefficient), depending on its dominance, depending on the (effective) population size, your new mutations might take quite a bit of generations before reaching fixation in the population. In this time other mutations might occur. And then, the question is very interesting. Imagine a population of asexual individuals where two beneficial mutations exist (at two different loci [=position on a chromosome]). Because there is no recombination (by definition of what is an asexual population) never these two mutations will be found in the same individuals and in consequence if one mutation reaches fixation, it necessarily mean that the other mutation would have disappear. In sexual population it is different. Recombination allow that the two mutations, once they reaches a sufficient frequency will probably be found in the same organism and therefore, the two mutations can reach fixation.
Hope that helped a bit

Thanks. I think sexual recombination is the key to the answer to my question. It would allow the population to mutate in many different directions in parallel and then "merge" the successful mutations together later on. Very interesting! I never realized that recombination is so crucial in this regard.

@quorilla You might want to go for few lectures concerning the concept of "Muller's ratchet". The absence/presence of recombination is a very interesting subject. For example, it is the absence of recombination between the chromosomes X and Y that causes the Y chromosome to shrink.

Well, it depends which study you look at (consider finding some numbers on bionumbers). I would personally tend to think that the standard error for this kind of study is large enough so that whether or not we consider genomic rearrangements is negligible in the estimate as those mutations are relatively rare. That is just my opinion though.You might find some estimates of the relative frequencies of the different types of mutations in the work of Sharp

I think the main issue you have is in this paragraph:

But if mutations are rare, it seems unlikely that many (thousands of) properties of organisms get improved in a single generation. You'd need to get very lucky to randomly improve all the genes responsible for it.

There are two basic misconceptions there:

Mutations are not rare. They're actually very common. One of the cells in your body probably just developed one while you were reading this answer.
It is indeed unlikely that thousands of properties get "improved" in a single generation. That is not how evolution works. You need to remember that species evolve, not individuals. So, say I have been selected for because I run faster and my mate has been selected for because she's smarter, our child might incorporate both characteristics. Now extrapolate that to all individuals of a species and add a few million years and you get both intelligence and speed selected for.

Finally, luck has very little to do with it. We're talking about a very slow process that works over millions of years. Evolution does not occur over single generations, the mutations driving it might but not the evolutionary process by which these mutations become incorporated into the genome of the population at large.

Thanks. The key sentence is "So, say I have been selected for because I run faster and my mate has been selected for because she's smarter, our child might incorporate both characteristics."
This way we receive the good properties from an exponential number of successful ancestors in the past, each of which might have mutated in different advantageous ways.

The basic idea is that mutations improving different traits can occur in different individuals, and then be brought together by recombination. So the frequency of recombination roughly sets the maximum rate at which the population can acquire good mutations. Nick Barton and I calculated it, and found that a population can gain about one good mutation per chromosome per generation:
http://www.plosgenetics.org/article/info%3Adoi%2F10.1371%2Fjournal.pgen.1002740#pgen-1002740-g008


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DNA replication, why complex
When the DNA replicates, it first attaches RNA since the DNA polymerase can't attach DNA in the 3' end. Why the replication is happened this way?
If the DNA polymerase can attach DNA from the 3', the replication process will be much simpler.
Is there a special reason for this?


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Why don't Australian magpies in Tasmania swoop at people?
I'm currently living in Tasmania (Australia) and I have noticed that Magpies don't swoop at you here, yet they do in other parts of the country.
Just wondering: does anyone know why?

@havefun I reckon he means Tasmania

If it is Tasmania are we talking about Magpie (Pica pica)? (an introduced species). Or Magpie-Lark? Or the Australian Magpie?

It appears that there are attacks in Tasmania.There is a different agpie alert page for Tasmania. Still very few though.
https://www.magpiealert.com/SwoopingMagpieMapTAS.php

Tasmania has been inhabited for 40,000 years. Chances are, they used to trap them with nets, hit them with sticks, or throw boomerangs at them. Some genetic factor can also have made them larger and bolder on the mainland, like hybrid vigor from a large population. Different prey and local predators could have also made them swoop less often.

As someone who moved from WA to Tasmania 18 years ago, I discovered the Tasmanian magpies to be much more wary of humans that others I have met.
They very much kept their distance for many years. Traditionally many Tasmanians have an old fashioned approach to nature. In previous years I suspect a swooping magpie would simply have been shot and the birds have learned to keep away from us.
On the mainland you have large cities, with many parks and open areas. Ideal for magpies and full of humans. You also have lot's of cycleways and people moving about. Tasmania has a lower population, many rural areas and less of the territorial intrusion sort of behaviour that magpies resent.
I was working on a Tasmanian university campus and from my office window I often saw the local magpies swooping cyclists. Open areas, strangers moving about, the birds took exception. I was never swooped because I was recognised.

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A little late with this response but here goes. My home in Tasmania is a semi rural bush block that is also home to a primary magpie family (3 to 5), and also home to an ever changing peripheral group (upwards of 20) of older juvenile magpies. Although the magpie family make it clear the patch belongs to them, they show their superiority more with irritation, the odd sneaky peck or two, than outright aggression. As long as the other magpies defer to them when they're all in the same vicinity peace reigns.
My theory is the family, who I have a close relationship with, know I wouldn't be happy if they attacked other magpies, so they keep their disdain fairly low key.
They proved this recently when next door's free range chooks were causing a problem. I only had to chase them away for a single day before the 'family' took over and chased them away for me. But, even then, non contact swooping was applied.
Tasmania is filled with low key people who have time to take the time...just a guess, but perhaps this friendship factor is the key to the lack of magpie swooping in the state. Or, more likely, Tasmanian magpies have simply evolved to be a less aggressive breed.

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I have been a cyclist in Tasmania for decades and until recently had never been swooped by a magpie.
In November 2020 I rode the "Tassie Gift" bike-packing event and was swooped and chased at Caveside on my way to Mole Creek. There were multiple aggressive birds over about a 10km stretch and I was hit on the helmet twice as I tried to outrun them.
Then again a few days later on the trip on my way towards Cressy I was attacked again. They seemed very angry and followed and swooped for a long distance.
So unfortunately I can confirm that they do indeed swoop in Tassie but only in certain places.
They have not swooped me yet on my home trails around Launceston. But sometimes I can see them looking at me intensely and I wonder if they are thinking about it.
I hope they are not all starting to learn this dangerous and disturbing behavior.
A few hours after the second attack I saw one flat on the road that had been squashed by a car. Oh what joy and mirth that bought me, cop that you f^%ker may many of your mates meet a similar fate.

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Mitochondria - ETC
I read somewhere that the Malate aspartate shuttle transfers the electrons to complex 1 in the ETC while Glycerol phosphate
shuttle uses complex 2. Does anyone know if this is true? Also a lot of textbooks state that complex 2 can bypass complex 2. Does anyone know if this is true? I have seen this statement in the book Biochemistry by Voet and Voet.

Hello! thank you for the answer. But do you know if it is possible for these two complexes to bypass each other?

Thank you. Please let me know if you have any references for this above mentioned bypassing.


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What attaches plant cells to the cell wall?
In animal cells integrins span the plasma membrane and attach the cell membrane to the extracellular matrix. I was wondering how are plant cells attached to the cell wall? Is it just the middle lamella holding them in place or is there something else (i.e proteins)?


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Can we estimate effective population size from DNA sequence data (CR or cytB sequence)?
I have DNA sequence data (control region) of two population of a species. Can anybody suggest me any software to calculate effective population size? Is it possible and meaningful?

It sure is possible.
Very simple model
It is often hard to decompose the effective population size $Ne$ from the mutation rate $\mu$ though. But it is quite common to estimate $N\mu$. For example, it is a classical result from coalescent theory assuming a single panmictic population of constant size and no selection (and a few other assumptions) that
$$N\mu = \frac{S}{\sum_{i=0}^{k-1} \frac{1}{i}}$$
, where $S$ is the number of segregating sites and $k$ is the number of sampled individuals.
More advanced models
You will probably want a slightly more advance model though.
There exist a number of estimators including Colony2, CoNe, Estim, MLNe, ONeSAMP, TMVP and LDNe. I recommend having a look at Gilbert and Whitlock (2015) who compares these estimators under different demographic scenario.

Thanks, Remi. Request you to suggest some papers estimating Ne using mitochondrial DNA sequence.


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What kind of spider is this please?

What type of spider is this PLEASE. My friend found it in her home. She has 3 boys under 10yrs old and people are telling her its a wolf spider i really dont think it is. Please help

It looks similar to a fishing spider. Please let us know your locale so we can make a more accurate determination.

We need to know the region, and also the size of this spider.

If you are in the US there are very few spiders that bite unprovoked. It looks more like a wolf than a brown recluse. (one of the few possibly dangerous US spiders, still needs to be provoked)

https://entomology.ca.uky.edu/ef631 can you get a better photo of the eyes please?

but they look like non recluse eyes to me.

It looks like a Wolf spider to me, probably one of the Tigrosa (formerly Hogna and Allocosa) species.  The narrow central line on the 'head', and what appears to be a blocky dark central mark at the front of the abdomen, are what I would expect.  I can't tell if the appearance of bands on the legs is real or an artifact of the light and photograph.  Oh, yes - these spiders are quite harmless (to humans, anyway), like almost all spiders.  They can give you a bite if you force them to, but I've handled them a lot and have never been bitten.  I would expect it to hurt a bit like a wasp sting, though.


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Yeast contamination with fungus patch
I am working on yeast mutant and I am observing their sporulation efficiency on agar plates. One of my plates got some dark green small fungus patches. I can't grow yeast again and dump this one with fungus because I am counting at a specific time interval to compare and it will take a lot of time to go through the entire process.
What should I do? Should I remove fungus from scalpel? And does this fungus going to affect the yeast growth?

Either you can cut out the fungus and get away with it, or the fungus will rapidly overgrow your plate regardless.  You might as well try to cut out the fungus.  If it overgrows your plate the experiment with that plate is done.
This is why you should have parallel plates for this sort of experiment.  There is a saying: don't put all of your eggs in one basket.  The reason is that if you sit on that basket all eggs are broken.  If you are counting on just one plate for your experiment and you sit on it, or it gets overgrown with fungus you must start over.
The other reason to have several parallel plates going is that you can average the spore count.  One plate might have more or less for some random reason, like fungus.  But if you have several and average them out you will reduce noise.


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Help with understanding XKCD's “How Vaccine Failure due to Viral Vector Immunity Works” Why is this response a failure exactly?
Full disclosure; no biology since 9th grade, so please go easy on me!
XKCD's 2406 shows a literal wooden Trojan Horse outside a castle, but instead of bringing it inside the castle walls, the soldiers recognize the shape as horse-like:

Look! It's a statue of that horrible animal that trampled Steve!

and the soldiers decide to destroy and dispose of it rather than to let it in.
The title of this XKCD is

Viral Vector Immunity

with the subtitle

How Vaccine Failure Due to Viral Vector Immunity Works

Wikipedia's Viral_vector; Vaccines explains the basic idea, which is (I think) that the viral vector's genome is modified so that it includes a new protein on its surface that serves as an antigen, and the host builds and learns an immune response to this antigen that will then immunize the host against an infection by another organism that also presents this antigen.
Question: The XKCD shows recognition and an analogy of an immune response, so why does the subtitle call this a "Vaccine Failure"?

XKCD image License

Yes, the cartoon is a description of immune action.
Traditionally shown is first exposure being a vaccine, and the second exposure being the bad virus being destroyed.
However, this cartoon is describing viral vector immunity.
The first exposure is a viral vaccine. This alerts and educates the immune system about not just the intended antigen, but also the (harmless) carrier virus which is represented by a horse.
The second exposure is a different viral vaccine.
The immune system immediately mounts a successful response against the vaccine because is recognises the carrier virus.
So the immune system doesn't get the chance to learn about the antigen associated with the second virus.
A example of viral vaccine failure would be useful - I will see if I can find one if no-one else does.

Viral vector only serves to deliver to cells the proteins/mRNAs necessary for triggering the immune response. In this sense it is like a Trojan horse - it is not supposed to cause suspicion, since otherwise it fails.
In this case the immune system recognizes the vector as a dangerous virus, destroing it before it delivers its load.
I find this xkcd rather convoluted...

This cartoon imagines that, rather than sacking Troy, the Greek soldiers inside were planning to help the Trojans recognize dangerous aliens who were preparing to attack. The horse represents the viral vector that carries the genetic material for producing the antigens that the immune system needs to learn to detect. The vaccine fails because the Trojans recognize the horse as an invader and destroy it, killing the soldiers who they didn't realize wanted to help them.


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How to understand the biophysics and math behind a 0.2 second delay between the pulse in my arm and my ankle?
I recently had a test with six blood pressure cuffs; 2 each on arms, ankles and big toes. During the test I could feel the pulses in my arms and legs, and noticed a distinct ~0.2 second delay between the pulse in my arms and ankles.
I used my pulse rate at the time and the fraction of the pulse period between arm and leg to get the 0.2 seconds, and I unscientifically give myself a +/- 20% error bar on that number.
I was at first quite surprised, because the speed of sound in water is roughly 1500 meters per second, and since water and presumably blood is mostly incompressible I couldn't figure out what could cause such a long delay.
Then I realized that arteries must be somewhat elastic, and that the propagation of the pulse must involve the mass/inertia of the blood and the restoring force of the artery, and so this was a biophysics problem of some kind.
It turns out that the results of the test include a report of the propagation velocity which was of the order of 1100 centimeters/second. I'm not sure how that connects with my estimate of 0.2 seconds as it implies a distance of 2.2 meters and there's no way that my elbow is 2.2 meters farther from my heart than my ankle (I'm ~1.7 meters tall).
Questions: How to understand the biophysics and math behind a 0.2 second delay between the pulse in my arm and my ankle?

Is there an equation that relates the delay between arm and ankle pulse to the elasticity of the arteries?
How is the velocity calculated from the measure delay in this case?

Since @bob1 outpaced me with his answer, I will give just a short comment. He has correctly warned you that the $\text{PWV}$ is not equal to the sound propagation velocity. In the Moens-Korteweg equation, you can see that the $\text{PWV}$ depends strongly on the dimensions of the artery, its elastic properties, and also on the blood pressure (indirectly, by changing the elasticity $E$). From the physiological perspective, this means that the  $\text{PWV}$ is not constant throughout the circulatory system. Furthermore, measuring $\text{PWV}$ has generally a large measurement error.

Finally, the measurements of $\text{PWV}$ are generally on the order of $\text{m/s}$ (with outliers up to approx. $25 ;\text{m/s}$). Your result ($11; \text{m/s}$) seems to lie on the upper part of the distribution. Some graphs for the age and pressure dependence can be found here and here.

It's like the difference between voltage propagation down a wire and movement of the electrons themselves, if that helps

@Domen - I'm a virologist not a cardiology person at all, so I would love if you could provide a better/more complete answer. I just did some quick googling, so am sure to have missed some salient points.

So it turns out that your estimate is not bad, by simple velocity calculation, I get it to be a little over 50% out (see below), but as you say, there is some error in your measurement. However, it turns out the pulse wave velocity is much more complicated than that, and subject to some debate in the literature.
The speed at which the impulse propagates is not the speed of sound, but rather the speed of the impulse from your heart, and varies according to aterial stiffness (thinner arteries are faster, larger slower as they are more floppy). The equations for calculation are similar to those used to calculate the velocity of sound in a medium. There are two of these, where $P$ is pressure and $V$ is volume and $\rho$ is density of the blood:
The Frank/Bramwell-Hill equation
$$
PWV = \sqrt{\frac{V.dP}{\rho.dV}}
$$
And the Moens-Korteweg equation ($E_{inc}$ = vessel wall elasticity, $h$ = wall thickness, and $r$ = radius
$$
PWV = \sqrt{\frac{E_{inc}.h}{2.r.\rho}}
$$
Now these are super complicated for the average person to measure and it seems a bit difficult to work with, so it can be simplified to a the classic $velocity = distance/time$.
If you look at the structure of the arteries in the body, all the major blood ones to distal portions of the body feed off (unsurprisingly) the same source, the aorta.
Now to estimate the difference in time you need to work out the time it would take to propagate to each point.
I'm not too far off you in size (~10 cm taller), and did some very rough estimates of how far my elbow is from my heart and about how far my heart is from my ankle, and I got ~40 cm for elbow and ~135 cm for ankle.
You gave a propagation speed of 1100 cm/s, so substituting that into the simple equation:
$$
\text{time} = \text{distance}/\text{velocity}
$$
So 40 cm distance:
$$
\text{time} = 40/1100
$$
$$
\text{time} = 0.0364  \text{ seconds}
$$
and 135 cm distance
$$
\text{time} = 135/1100
$$
$$
\text{time} = 0.1227 \text{ seconds}
$$
$$
\text{Difference in time} = 0.1227-0.0364
$$
$$
\text{Difference} = 0.0863 \text{ seconds}
$$


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Subset of Protein Crystal Structures (from PDB)
Is there a well-accepted subset of the Protein Data Bank set of protein structures that:

Has only "high quality" structures (may be differing metrics of this; e.g. resolution, size, or structural completeness)
Has minimal redundancy (e.g. nothing with exact sequence identity from the same species)
Is still as large as possible, spanning as many molecules and species as possible
[Optionally but better] Is not too biased (e.g. certain classes of proteins are highly over-represented in the PDB)

It is possible to download the entire PDB and make up rules for myself, but this seems like something people might have already considered reasonably extensively. I'm hoping for a dataset I can just download and cite, in the best case. :)

Richardsons' Lab has a top8000 list.
See their paper from 2016.
They also have top500 list, but it hasn't been updated for many years.


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What are the relative roles of coding DNA versus regulatory DNA thought to be in evolution?
Intuitively, once you have the idea that some DNA is responsible for turning on and off the DNA that codes for proteins, it's possible to imagine that the regulatory DNA is actually the most important part. In the ingredients list of a recipe, you might think the coding DNA gives you the list of ingredients, but the regulatory DNA gives you the amounts of each one, plus the order in which you add them to the bowl. If that's true, then different variants of regulatory DNA should be selected for and against, and evolutionary molecular biologists ought to be tracking those variants like they track alleles of genes. But evolution always is discussed as if it's just about different gene frequencies.
Is "regulatory evolution" a thing? If so, is there an understanding of how big a thing it is? Or, if not, why not?

Evolution is rarely about gene frequencies — much research does, however, focus on allele frequencies. In any case, in a modern context a gene includes its regulatory sequences. While allelic differences resulting from changes in regulatory sequences are harder to identify they most certainly are being considered, so I'm afraid your question is based on a false assumptions about both genes and evolution!

I think the focus on gene/allele frequencies is more due to the historical reasons - notion of gene is rather old, preceding even the knowledge about the DNA, whereas the existence of regulatory DNA is recent knowledge. However, most of the discussions about genes/alleles are easily transposed to the regulatory DNA. I agree with @tyersome that gene and allele are not the same thing... but these words are used interchangeably in many contexts.

Yes, a simple google search reveals millions of academic citations talking about "regulatory evolution".
But it's a little over-simplistic to divide coding vs. regulatory DNA. Indeed, some coding DNA is in fact also regulatory at the level of determining gene expression in cis (a well-known example of this would be codon usage).
It is moreover incorrect to think that coding DNA products don't do gene regulation. This was recognized very early on in the ideas of "structural gene" vs. "regulatory gene". These days we would call the latter transcription factors, we don't really use the structural/regulatory terminology anymore. Transcription factors do most of the actual active work of gene regulation in trans, in collaboration of course with regulatory DNA.
So in conclusion, yes it's important and there are tons of studies that you can google if you want to investigate these problems. I would suggest reading more about cis-regulatory and trans-regulatory elements. Of course, there isn't an exact mapping of coding<-->trans and noncoding<-->cis, it's just a helpful simplification.


text:
Why Insect bites are itchy rather than pain?
i don't understand if some thing bites or hurt we feel pain, but its differ for insect bites, why so?

maybe because those bites cause allergic reaction

Has a wasp ever stung you? It is quite painful

You're more likely to have an allergic reaction if you're stung by an insect. The reaction can be classed as:
Minor localised reaction – this is normal and doesn't require allergy testing, although the affected area will often be painful for
  a few days
large localised reaction (LLR) – this can cause other symptoms, such as swelling, itching and a rash
systemic reaction (SR) – this often requires immediate medical attention because it can cause a potentially life-threatening allergic
  reaction (anaphylaxis)

Taken from : http://www.nhs.uk/Conditions/Bites-insect/Pages/Symptoms.aspx
You can read up on this here:
http://en.wikipedia.org/wiki/Inflammation
http://primer.crohn.ie/the-inflammatory-response
For a more detailed look, I would suggest papers like this:
Loza, Matthew J., et al. "Assembly of inflammation-related genes for pathway-focused genetic analysis." PLoS One 2.10 (2007): e1035.
or a good immunology textbook.


text:
Why do we feel cold in the lower part when we lie down?
This question is based on my personal experience. But I believe that this common for many of us.
Let us say that I am sitting on a chair in normal indoor dress. Then, if I lie down on bed, I will feel the need to cover the lower portion of my body.
As I have seen at home, I am working sitting on a chair. Then I lie down in the same dress, and i feel the need to cover my lower part. When traveling in some sleeper train, people ask for blankets when they lie down, not while they are sitting. It is not that they change their dresses when they lie down, they are in the same dress.
Why does this happen? Why do we feel colder, specially in the lower portion, when we lie down?

Could you clarify whether it's just sensation of cold or does the feet actually get cold? Please touch the feet whether when you are feeling cold, if they are warm to touch them it may be peripheral neuropathy.  Atlast welcome to biology.se

@JM97 It's just sensation of cold. My feet are perfectly warm.

Then it may be due to peripheral neuropathy? It's my opinion , please consult a doctor.

@AlwaysConfused please don't use the term "everyone". A), you don't know that, and B), it's not true.


text:
How long do tiny spiders live?
I'm pretty sure there's a spider in my ear. I feel it move and hear the scratching (i blame my cat for playing with bugs in the bed). I've gone to the doctor, but all they do is flush my ear with water and it never works. I've decide to just wait for the damned thing to die.
How long will it live in my ear without coming out? How quickly will it die if i flush my ears with peroxide once a day?
any other advice for how to get the stupid thing out?

Unfortunately this is for all it's worth a personal medical question, which is not on scope for this site. Please don't do anything yourself without asking a doctor. If the last one did not help you, try to go to a specialist. Still, be open for the suggestion that it might be there is nothing alive in your ear.

Maybe lure it out of hiding with a fly? Scare it away with a big bird? Smoke it out? Play nasty music?

It's not a spider. It might be a paresthesia (more specifically, formication) that you're experiencing, though. Spiders don't survive flushing, or peroxide. I often used to see kids with insects in their ears in the ED. Never did any of them remain after flushing. Interestingly, my son once got a spider in his ear. I did get it out with flushing. There's another possibility: a bit of fluid in the middle ear.

I was asking how long it would take to die. The doc i did see DID say there was something moving in my ear. There are no other doctors who will take my insurance in my area, so he's the only one i can see. When nothing came out after the water attempts (and 5 hours of it mind you) he just said 'oh well, go home' essentially. Hence why i'm asking //how long it would take for a spider to die stuck in an ear./// I know the ear is self-cleaning and the wax will just push it out eventually. I need to know how long it'll take.

@anongoodnurse wow.... I removed that comment I really thought this was impossible...

If there's something stuck in your ear after five hours of flushing, you need to see a better doctor. Hardened ear wax is dark and can be hard to remove, and can mess with your hearing.

Did it die yet?


text:
How, when, and where did the very first life in the universe exist/formed
Do we know about the very first life, how it is formed? or from where it originated in the universe?
How life is fromed in our planet earth??
Life require conditions for survival or it can create favorable conditions

To answer all your question: no.

We've never found life except on earth,  so as far as we know, it originated here. However, there are numerous theories about how.


text:
Why cornstarch for athlete's feet?
It seems like a lot of foot (anti-odor or antifungal) powders are often based off of cornstarch (i.e., as the primary filler).
But wouldn't cornstarch (which, in some places, is also a common food additive) just feed the undesired microorganisms anyway? Or, perhaps, is its dessicating effect so powerful so as to nullify whatever nutritional value it might provide anyway?

athletes foot is not a carb specialized fungus, skin is higher in protein... its more likely to develop species unfavorable to athletes foot. put a cheese  in cornstarch, it may get marred... experiment time

Talcum powder was originally finely powdered talc, a rock, but talc is technically in the same mineral family as asbestos, it is completely harmless and not the same as the dangerous mineral used in insulation at all, (it is actually used as an additive in table salt). But some early talcum powder did contain actual asbestos, as does industrial talcum* today, this only made it more confusing. Manufacturers that used talc took a lot of flack during the asbestos scare (you tricked me into putting asbestos on my child), there were many lawsuits.  Corn starch is now used as a replacement for talcum powder in many many things labeled talcum powder, baby powder, or body powder.
The cornstarch is acting as a carrier/filler, so no its probably not the best thing because the fungus can metabolize it and it does not need to be there but the companies prefer using it to dealing with misinformed disgruntled buyers.
*talc and asbestos often occur in the same deposits.


text:
Irradiation instead of pasteurization?
Can we just replace pasteurization with simple irradiation for most (if not all) foods? (For example, such as milk, to sterilize and preserve flavors)

I don't know about "replace", but it is used.

@arboviral It still doesn't answer the question. I know what pasteurization and food irradiation is, thank you ; )

Both pasteurisation and irradiation work by killing micro- (and macro-) organisms in food. The two processes are broadly similar and in both cases the objective is to reduce the number of bacteria or other microorganisms in the food rather than completely sterilise it. Due to this and other similarities food irradiation is sometimes called cold pasteurisation (for example in this paper).
Food sterilisation has some advantages over pasteurisation: for instance, it can be used on (most) solid foodstuffs, including fruits, vegetables, grain foods, spices and meats (such as chicken), while pasteurisation can only be used on liquids. However, irradiation cannot be used on dairy products or eggs as it results in changes in flavour and texture (source).
There are other reasons why irradiation is not used as widely as it might be. One is that some markets were already saturated with pasteurisation, which is an older technology. Another is that public acceptance of irradiation is lower, with (for example) concerns about safety of the products, although these are not rational concerns and Crawford and Ruff note that similar concerns affected acceptance of pasteurisation when it was introduced. This may also partially explain why irradiation is sometimes called cold pasteurisation, although by international agreement irradiated unprocessed food sold in stores (not in restaurants, or processed foods) is labelled with the Radura symbol anyway.

I also have a suspicion that the startup costs associated with food irradiation plants are relatively high, but couldn't find a reference for this yet.
Some further reading
Lester M.Crawford, Eric H.Ruff (1996) "A review of the safety of cold pasteurization through irradiation" Food Control Volume 7, Issue 2, April 1996, Pages 87-97
"Advantages and disadvantages of the use of irradiation for food preservation" Journal of Agricultural and Environmental Ethics March 1991, Volume 4, Issue 1, pp 14–30
"Food irradiation", Better Health programme, Victoria State Government website (accessed 2017-10-24)


text:
How much does sleeping correlate with daily activity?
I'm a very lazy person. I spend most of my time in a chair, at a computer; I eat more than three meals a day. I don't do any sport, at all.
What I want to know is: why do I need to sleep 8-12 hours daily since I don't waste myself physically during the day?!
Wouldn't 3-5 hours be more reasonable? With an increase to 7-10 if I were a bodybuilder or a construction worker.. something that would actually deplete my body of energy?

Physical inactivity doesn't necessarily mean mental inactivity. Heavy mental exercise may also cause a need to sleep.

@ChrisStronks yes but why? Why does heavy mental and heavy physical labor produce equivalent global fatigue when they are fundamentally so very different, down to the actual organs under load?

@tel you seem to assume that 1) physical movement uses up lots of energy, and 2) sleep is there for muscle regeneration. Both assumptions are not very true. Your body heat production, viscera function and brain function use up by far more energy, and it is not known what sleep is for, but it's more likely to be about brain self-organisation without the meddiling of a wanton, energetically expensive consciousness, than for muscle relaxation.

@rumtscho Really, just like the OP I'm wondering why both a day of hard labor and a day of hard thinking leave me similarly tired. It's a curious symmetry.


text:
What Websites Have Image Libraries for Bacteria and other Microorganisms
What Websites Have Image Libraries for Bacteria and other Microorganisms?
With age of cell phone microscopes and hand held spectrometers it would be interesting and valuable to be able to compare in-home/at-work microbiology with data-banks. To be able to test for health or enjoy the visuals of tree of life seem relevant. What websites are out there?

Sites for microscope blood analysis would be a nice compliment to this.

While I doubt that this might be possible in all cases (and I would be careful about classifications), there are indeed some great ressources, which contain a lot of images. Since there is a vast number of bacteria present on this planet, there is of course a limitation to bacteria available in photos, representing only the most common or important.
These are:

Bacteria in Photos
American Society of Microbiologies Microbelibrary
Microbiology in Photos

Then there is an information page available from the CDC, which informs about parasitic diseases. These are non-bacterial, but probably also interesting. It can be found here:

Laboratory Identification of Parasitic Diseases of Public Health
Concern


text:
Microbiome Context for Amino Acid Essentials and Non-Essentials
Given what we are now learning about the diverse mix and variance of microbiomes (aka bacterias via human gut project), is it possible that synthesis of aminos can be done by specific bacteria and therefore provide the "essentials" if atomic ingredients are available in digestive tract?

Essential amino acids are defined as those required in the diet. Non-essential amino acids as those that are not. In general this is rationalized by known metabolic pathways and rates. I don't see what connection are knowledge of gut bacteria (not baterias) have to do with this. Could you clarify your question, please.

Many bacteria are prototrophic and can synthesize the essential amino acids from other available nutrients. OP is asking whether this could be enough to supply the human host with all the needed essential amino acids. It's a perfectly good question. The answer is obviously yes in theory, but I don't have any data to suggest it happens in practice. Someone else might.

If your body was filled with highly specialized bacteria living in nutrient-rich conditions, what you suggest could happen*.
But in practice, you're not filled with such bacteria, and most of the bacteria in your body are living in rather harsh conditions for rapid metabolism.
That said, gut bacteria do produce a range of other useful nutrients. Look for a review on gut microbiome metabolism, and you will find a number of examples.
*Some basic calculations:
Say we take an optimistic estimate for productivity of 1g AA/g biomass/day. (It's what they got in this paper (one of many) that characterized a strain of Corynebacterium glutamicum engineered to produce lysine for industrial purposes and growing in a bioreactor. There are better strains now, but still, let's call that an unbelievably optimistic estimate of what a bacterium in the body might produce in the right conditions). How much bacterial biomass is in the body? Not a trivial question to answer (How much weight/volume do microbes occupy within the human body?) but let's go with the middle of the road estimate of 1kg. So 1 kg of awesome lysine-producing bacteria might potentially produce 1 kg of lysine a day. Googling around for dietary requirements seems to get you somewhere in the 1-5 g/day range. So assuming vaguely similar productivities for other amino acids, we've got plenty of room to spare if we assume that our bacteria are highly specialized for this function and are exposed to friendly, oxygen-rich and nutrient-rich conditions.


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Why are male gametes and female gametes not equally sized
Why is it that male gametes are smaller and produced in larger quantities than female gametes that are large and lesser in number. Why aren't the gametes equally sized, or their sizes the other way around. Is there an evolutionary advantage to this, or is it just how things evolved and would it not have mattered if the sizes and quantities were reversed?

Gerardo is correct that female designates the bigger gamete, so there's nothing important about the terms "male" and "female" here.  But I'd like to also respond to your initial question of how the difference in size would've evolved because I don't think it's trivial.
I can provide a rough summary of one explanation that was summarized in Dawkin's The Selfish Gene which was summarized from G. A. Parker's 1972 paper "The origin and evolution of gametic dimorphism and the male-female phenomenon."
It goes something like this:
The asymmetry could have evolved from originally equal sized gametes through the evolution of two divergent sexual strategies - a large investment strategy which opened the way for a small-investment exploitative strategy. The idea is that when gametes were all roughly the same size, some would have happened to be bigger than others. There may have been some advantage to this because the larger gamete could provide a larger initial food supply. However, this also could have created a condition for exploitation by individuals producing smaller than average gametes, especially if they could ensure their smaller gametes fused with the larger than average ones. This could be achieved by making the small ones more mobile and able to actively seek out the larger ones. Making smaller gametes would have allowed that individual to make more of them and potentially have more descendants, as they're not investing as much energy into any one gamete. The interplay of these two strategies would've continued in a runaway fashion, with the larger gametes evolving larger and larger to compensate for the ever-smaller contributions by the exploiters.  Eventually the larger gamete could become immobile since it's being sought out by the smaller gametes anyway. You can see where this is going, with the larger gamete becoming what we know of as eggs and the smaller as sperms.