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Is vitamin D a vitamin or a hormone?
Some people like to say that vitamin D is a hormone.
A simple set of differences between hormones and vitamins is described here.
Vitamin D is not (for the most part) absorbed through food but created by our body when our skin is exposed to the sun, so it does look more like a hormone than a vitamin.
Another difference listed is whether it has catalytic action or not (that I don't know what it means - answers with an explanation would be nice).
So, is vitamin D a hormone? And if so, why is it called vitamin D?

It's called "vitamin" D because it was discovered before scientists knew it could be created by the body. In a way, it's both, as it can be created by the body or provided through food.

@BillDOe the link I provided offers another differentiating statement, i.e. whether it has catalytic action. Do you know the answer to that question?

From researgate chat related to this topic they rather call vitamin D biomodulator vitamin, which means it is capable of gene regulation

@user, a catalyst is a chemical that helps enable a chemical reaction that otherwise wouldn't occur without the catalyst, or different physical conditions, and itself remains unchanged from initiation of the reaction and the end, though it may be modified during the reaction itself. So as far as how vitamin D transports calcium, magnesium, etc. I'd have to answer that it seems to fit the definition of a catalyst. However, this and that article both call vitamin D a hormone.

There's an open access article "From vitamin D to hormone D", which explains the difference(s). Vitamin D is a family of substances, but for humans the most important one from this family is vitamin D3 aka cholecalciferol. "Hormone D" (1α,25(OH)2D3, the substance that normally regulates calcium etc.) aka calcitriol is closest to vitamin D3. So if one wants to be technical about it, the vitamin(s) and the hormone are slightly different substances. Vitamin D itself is more aptly called a prohormone (i.e. a hormone precursor):

Vitamin D[3] is not technically a vitamin, ie, it is not an essential dietary factor; rather, it is a prohormone produced photochemically in the skin from 7-dehydrocholesterol. The molecular structure of vitamin D is closely allied to that of classic steroid hormones (eg, estradiol, cortisol, and aldosterone) in that they have the same root cyclopentanoperhydrophenanthrene ring structure. Technically, vitamin D is a secosteroid because one of the rings of its cyclopentanoperhydrophenanthrene structure has a broken carbon-carbon bond.

The above view is also endorsed by Horst et al., but they have a much more detailed discussion, including the fact that in vitamin D poisoning, calcifediol (25(OH)D3)--an intermediate compound in the pathway between the vitamin and the hormone--can itself act as a hormone, i.e. it has some binding affinity to the calcitriol receptor, but only at at very high doses.
As for how the vitamin label came about, "historical accident" is one way to put it...

Considering the fact that now we accept that the biologically active form of vitamin D [what the other paper calls "hormone D"], namely 1a,25(OH)2-vitamin D3, is a steroid hormone, it is somewhat ironic that vitamin D, through a historical accident, became classified as a vitamin. It was in 1919/20 that Sir Edward Mellanby, working with dogs raised exclusively indoors (in the absence of sunlight or ultraviolet light), devised a diet that allowed him to unequivocally establish that the bone disease, rickets was caused by a deficiency of a trace component present in the diet. In 1921 he wrote, "The action of fats in rickets is due to a vitamin or accessory food factor which they contain, probably identical with the fat-soluble vitamin." Furthermore, he established that cod liver oil was an excellent antirachitic agent.
Shortly thereafter E.V. McCollum and associates observed that by bubbling oxygen through a preparation of the "fat-soluble vitamin" they were able to distinguish between vitamin A (which was inactivated) and vitamin D (which retained activity). In 1923 Goldblatt and Soames clearly identified that when a precursor of vitamin D in the skin (7-dehydrocholesterol) was irradiated with sunlight or ultraviolet light, a substance equivalent to the fat-soluble vitamin was produced. Hess and Weinstock confirmed the dictum that "light equals vitamin D". They excised a small portion of skin, irradiated it with ultraviolet light, and then fed it to groups of rachitic rats. The skin that had been irradiated provided an absolute protection against rickets, whereas the unirradiated skin provided no protection whatsoever; clearly, these animals were able to produce by uv irradiation adequate quantities of "the fat-soluble vitamin", suggesting that it was not an essential dietary trace constituent. In parallel studies, Steenbock and Black at the Biochemistry Department of the University of Wisconsin found that rat food which was irradiated with ultra violet light also acquired the property of being antirachitic. However, because of the rapid rise of the science of nutrition -- and the discovery of the families of water-soluble and fat-soluble vitamins -- it rapidly became firmly established that the antirachitic factor was to be classified as a vitamin.

As an amusing parallel to this, calcifediol was identified in 1968 as an active metabolite of the vitamin, but it wasn't until 1971 that calcitriol was properly identified as the metabolite that exercises the hormonal action under normal circumstances. (cf. DeLuca)


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Do hornets return to the same nest after winter each year?
I have what I think is a hornet nest on the soffit of my house.

The nest has been removed, however, the hornets keep rebuilding. Also, they have started to swarm the sewer vent pipe (not shown in photo).
If fail to get rid of the hornets this fall, will they return to the same nest next year (or overwinter and continue to live there)?

I'm not sure if this is relevant or not:
To give you an idea of what kind of winters I am dealing with, I am near Toronto, Ontario; the temperature goes down to -25 degrees Celsius.

The picture isn't that clear and fails to show the insects involved, but based on your description and region you are probably talking about a paper wasp, not a hornet, though in common vernacular in the region 'hornet' is used. https://en.wikipedia.org/wiki/Polistes_dominula most likely.

If fail to get rid of the hornets this fall, will they return to the same nest next year (or overwinter and continue to live there)?

No. The nest, likely made of wood pulp (and maybe mud), will/should degenerate to unusable over the winter, though the bulk could remain for a couple of years. All wasps die, except for the new queens (fertile, mated females) who overwinter in sheltered crevices somewhere.
In spring, it is a single wasp that starts a hive: the new queen. She builds a new, small hive in which to lay eggs, which is added to initially by the queen and then by workers who have hatched.
While she will not return to an old hive, the conditions which appeared advantageous to one queen (shelter from rain, intense sunlight, winds, etc.) will also seem advantageous to other queens, which is why nests appear in the same places year after year.
Edited to add: It appears most likely that the queens that overwinter are "new queens", that is, mated female offspring of the queen. H/T @Brian Krause.

As a minor correction, I think the overwintering population is mostly young mated females, though I don't know for certain whether queens who produced nests the prior year can also overwinter.

@BryanKrause - I believe you are correct; edited. Thanks!

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

sort: votes


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Why is CLL B-Cell leukemia t(12;21) more responsive to chemotherapy?
Chronic Lympoid Leukemia targeting B-Cell (with the particular translocation mutation on chromosome 12 and 21) is known to be more responsive to chemotherapy. Is there a known molecular mechanism for why?

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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Orangish-coloured insect living in wood chips
Can anyone Identify this organism?
I dug it up in a pile of 5 year old wood chips in Cleveland, Tennessee, United States. It is about 4 inches long.

That is the pupa of a unicorn beetle, Dynastes tityus. https://arthurevans.wordpress.com/2010/09/15/453/


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Why exactly does the immune system weaken with age?
Why does the immune system become weaker with age in humans and in some other mammals?  Let's try to be more specific than just "everything degrades with age."

We don't know.
More precisely, we know of many, many different reasons why the immune system deteriorates with age, but we don't really know which are different measures of the same thing, which are independent factors, which factors actually cause problems and which are harmless and incidental, and so on.
There are too many age-related phenomena to try to list. There's a nice recent review Aging and the immune system: An overview which spends time on

Aging and the immune cell repertoire
Cell Intrinsic defects in lymphocytes
"Inflammaging" ("an overall decrease in the ability to cope with different stressors, accompanied by a progressive increase in the organism's pro-inflammatory status")

Each of these broad topics can be broken down into dozens of sub-topics, and the molecular and evolutionary mechanisms underlying each are rarely well understood.
It's a huge area of research, and it's not possible to give a single concise answer.

Here is one known factor. A key component of the immune system is the skin and the protection provided by insensible perspiration, and the antimicrobial peptides in perspiration. However as humans perform less exercise with age, the proper habituation of the eccrine sweat ducts fails. The ducts normally balance the passing electrolytes, in particular conserving sodium chloride. The antimicrobials are only effective with the correct balance of electrolytes. If the balance is not correct, normal skin bacteria are able to enter the ducts and block them. With the ducts blocked the eccrine glands force sweat under pressure into the surrounding skin, destroying capillaries, and depriving the skin of oxygen. The protective live barrier is compromised and the skin becomes wrinkly. Extreme examples of the effect can be seen, particularly on the lower legs, in aged persons where the skin has a parchment type appearance.

Hi and welcome to the site. Please add a source to support your answer (it is much appreciated by people who want to do more reading about it.)


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about the muscle's tension's variables
I'm reading the paper "THE PROBLEM OF THE INTERRELATION OF CO-ORDINATION AND LOCALIZATION", which is written by N. Bernstein.
The paper said
"The degree of tension of a muscle is a function, in the first place, of
its innervational (tetanic and tonic) condition E, and, in the second place,
of its length at a given instant and of the velocity with which this length
changes over time."
I don't know why the tension of a muscle is the function of those values.
If that is just assumption, why the assumption can be established?
Thanks!

In physics, tension is proportional to strain and strain is proportional to change in length per unit length.. so second part seems like a standard result i.e., Hooke's Law

So does the variable E roles like Young's modulus? I understand that the tension is the function of the change of length. But isn't young's modulus constant value? The paper said E also means the degree of excitation. Can you explain me what E can mean?

E in your question is not Young's modulus. It's innervation condition, as you put it, and I've no idea what it is. Young's modulus is indeed constant. Whenever length changes, there'll be a corresponding change in tension so that Young's modulus is constant.

In the paper, E is like the additional force to operate active motion. I didn't know about that because I didn't read that after that content. Thank you for the advise.


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Please help to identify this shrub

Please help to identify this shrub in Hong Kong:
- dark green fruit with white spot
- fruits cluster at top of stem
- upright growing of green leaves
The shrub was from Hong Kong MacLehose Country Park Trail in Tuen Mun (somewhere near a reservoir), route 10. The place was of an altitude about 200m (600 feet from sea level) hot and humid. Hong Kong weather is South of the tropic of Cancer which is equal to Hawaii in latitude.

It would help if you tell us where it grows, and whether it's wild or cultivated.  Some indication of scale would help, too.

The shrub was from Hong Kong MacLehose Country Park Trail in Tuen Mun (somewhere near a reservoir), route 10.  The place was of an altitude about 200m (600 feet from sea level) hot and humid. Hong Kong weather is South of the tropic of Cancer which is equal to Hawaii in latitude.

The plant was confirmed as Mussaenda pubescens. Common in Hong Kong but most people recognized the plant by its yellow flower and white leaf (fruit was mostly not seen concurrently).
My friend used a reversed image search smartphone app to get the suggested plant name in 30 seconds.
Mussaenda is a genus of flowering plants in the Rubiaceae family. They are native to the African and Asian tropics and subtropics.
( Mussaenda philippica in Singapore. Mussaenda pubescens in China. Mussaenda erythrophylla in China etc.)

Sources of reference are such as from:
Hong Kong - http://www.hkwildlife.net/Forum/viewthread.php?action=printable&tid=5497
Taiwan - https://bruce0342.blogspot.com/2014/08/blog-post.html

@RudyLaw You should post what was confirmed as an answer to this question, instead of a comment.


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are clones siblings to the original?
i have a question about cloning, if a person had his/her DNA sample like hair or blood used to make a clone wouldn't that clone be that same person's brother or sister since they share the same genetic makeup? also, what if a person had heterozygous genes and had two clones? but the clones had their alleles swapped making one clone have most of that person's dominant genes while the other had that person's recessive genes making the clones homozygous, would that make the person a father of mother to those clones or a blood related brother or sister?

This actually isn't a biology question, it's a moral, legal and semantic question. "Siblings", biologically, are offspring of the same parent(s). A clone, as developed through human technology, isn't the offspring of any parent in the usual sense. It was not generated from a pair of gametes that came from two different parents; it came about via a completely different biological process, one that doesn't really occur in nature (there are many natural processes that result in identical copies we call "clones", but none of these does exactly the same thing as technological process we call "cloning").
Biologically, a clone is a clone, siblings are siblings, and they come about via very different processes.
None of this means that legally, or morally, or by the dictionary definition, we cannot redefine "sibling" to include clones. And it makes perfect sense to do so. It could also make sense to define clones as "offspring" instead. This could be based on genetic similarity, or on other things.
The thing is, there isn't an obvious single answer to how they should be redefined if human cloning were a thing. This isn't an issue human society has had to deal with yet so none of these redefinitions have happened.
For an idea of what they could look like though, I'm reminded of Lois McMaster Bujold's science-fiction Vorkosigan series, that deals with cloning (in books like Brothers in Arms in particular). Different societies in her books deal with cloning in different ways, and human clones have different statuses. One of those societies (one of the more sensible ones) considers a clone to be the child of the cloned person if it's an adult cloning themselves to make a baby, but to be the sibling of the cloned person if the person's parents decided to clone their child. Basically, in that society the people who decided to make the clone would be considered its parents, and the clone's genetics would have nothing to do with it.
Note that even in our society, siblings and parents aren't only defined by genetic similarity or any biological process, but by a legal relationship, shared history and responsibilities. Adoptive parents and siblings are considered in many (most? all?) countries to be legally equivalent to biological parents and siblings.

but you just said "A clone, as developed through human technology, isn't the offspring of any parent in the usual sense." then said "It could also make sense to define clones as "offspring" instead." so would a clone be a sibling or offspring to the original? also, to be a sibling to a clone is exactly what i meant if someone was cloned off of since it's that same person's DNA being replicated.

@sarahdan I am saying that right now, there is no definition of "sibling" or "offspring" that includes clones. My second paragraph was about how we might change the definitions to include clones, but I can't tell you in advance what the governments, ethics commissions, supreme courts and people of the world will change them to if human cloning happens, because that hasn't happened yet. Do you understand what I mean by this not being a biological question? Adoptive siblings are siblings but that has nothing to do with biology, wouldn't you agree?

i agree, but i can't help but feel that if you were cloned you and your clone would be siblings since you share the same genetic code.

@sarahdan to put my answer differently, your question seems to assume that "siblings" and "parents" are defined by genetic similarity. But this is not true. Parents and siblings are defined by how an individual came to exist. If it was formed from the union of two gametes, the organisms the gametes came from are its parents. If other organisms came from the union of gametes from those same parents, they are siblings. All other systems for making new organisms involve extending the definitions or using new words.

@sarahsan in nature plenty of organisms reproduce by making copies that share the exact same genetic code, and those are usually referred to as "parent" and "offspring" but it depends on context. They are also sometimes seen as parts of a same, larger clonal organism. So you see "same genetic code" doesn't mean "siblings". You assume that because in humans, the only people with identical genes are twins, who are siblings by the standard definition (children of the same parents). But humans don't reproduce by cloning, so we have no words or definitions for the relationships between clones.

@sarahdan and the fact that twins are the only humans that have identical genes, and happen to be siblings, is pure coincidence. If humans could reproduce asexually we might think it normal for children to have the exact same genes as their parents.

but that would be kinda weird to define something that has the same genetic makeup as you as your kid. i mean, if the two pair of chromosomes you have was used to create another being, surely the product of that would be your sibling like how you explained if a parent were to clone a kid they already have their current kid would have a sibling that was cloned off him/her.

@sarahsan why would it be weird? It's exactly what we do with aphids when they reproduce through parthogenesis. When we talk about a cell asexually splitting into two cells, we talk about the new cells being daughter cells, not sister cells. Why would it make sense for something that has the same genetic makeup as you to be your sibling? Human siblings don't typically have the same genetic makeup, anymore than human parents and children do.

yeah i know asexual is normal but cloning like ding somatic cell transfer seems to come off more as something where your genetic material such as hair, skin, or blood consisting of your entire two chromosomes to make a clone would be the end result of you and your clone come off as siblings, thats what i wonder.

@sarahsan ...why would cloning make people more like siblings than asexual reproduction does? I mean, do you actually "wonder" here or do you think the answer is "yes" and you're just fishing for confirmation? If not, how exactly have I not answered your question here? Just repeating the question won't help.

i said somatic cell transfer, in other words, EX: you take hair from a person named tom and a egg from a person named samantha who donates her egg but has her sex cells removed from it making it be a nucleus that holds tom's hair to make a clone, after undergoing the process, an embryo is formed and placed in samantha to give birth to the said clone. (this is what i'm talking about wondering if the clone is an actual sibling of tom)

and just to be clear, you did say in order for a clone to be a sibling to the original the original has to be cloned by the parents, but isn't this the same thing?

@sarahsan again, why does somatic cell transfer say "sibling" to you? Human siblings don't come from somatic cell transfer. Please answer my questions instead of just repeating yourself. And I did NOT say that "in order for a clone to be a sibling of the original the original has to be cloned from the parents". Please read what I write more carefully. It sounds like you're confusing something I said about an IMAGINARY law in a SCIENCE-FICTION book with an actual statement about reality, and that's not even what the imaginary law I mentioned said.

@sarahsan actually for a direct example of somatic cell transfer not resulting in something people called "siblings", Dolly the sheep's DNA donor was generally referred to as her mother.

i already gave my answer as to why somatic cell transfer is saying "sibling" to me you should read carefully, and i'll say it again more clearly, the reason why i see somatic cell transfer as a cloning process to where the original being cloned off of is a sibling, it's cause like identical twins they themselves are close to that of being clones, but naturally different from cloning, but most of all in this case, it's because of two beings sharing the EXACT DNA structure should/could be that of siblings since there are no shared 23 chromosomes/sex cells between two people.

@sarahsan that is true, all those are things you've said, and not only did I read them at the time, I addressed every one of them so I don't know what you are looking for here. Except for the twins thing, which you haven't brought up before but I also addressed (though I could add that one difference between twins and clones that affects how they "come off" is that twins are always the same age & from the same pregnancy, clones not). Do you still have a biological question that needs to be answered here, or do you just have an opinion on how words should be used that you want me to agree with?


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Purpose of Fc Region
Could someone explain to me the role played by the Fc region of an antibody as well as the purpose of isotype switching? According to Wikipedia, it's to allow the antibody to be usable by different Fc receptors, but I don't get what Fc receptors are for.
For context,

I'm reading about affinity maturation and learning about how ecological and evolutionary processes --- division, selection, and mutation --- drive the maturation of B cells leading to high-affinity plasmocytes that can better target a foreign antigen. Because all this happens on the Fab fragment, it makes sense to me why the Fab region is important in the antibody.
I'm not trained in cell biology.
My goal is to understand the general purpose of the Fc region and how isotype switching may be a major determinant for specific immunological or physiological outcomes, although I'd love to hear anything interesting!

Thanks in advance!

Preamble
From the point of view of understanding I think it is better to talk about the constant and variable regions of antibodies, rather than Fab and Fc, as these are historical designations for fragments of the molecules that were useful in research, but do not exist as separate entities.
Cartoon representation
It is possible to represent the immunoglobulin molecule diagrammatically as shown below. In the left-hand diagram V = variable and C = constant, and the suffixes H and L refer to the heavy and light chains. The right-hand diagram, which purports to be more three-dimensional, shows how the variable regions are responsible for binding the antigen — different manifestations of the variable region have different antigen-specificity.

The different iotypes for an immunoglobulin with a particular antigen-specificity are shown next, with a pre-colour scheme that focuses on the difference between the constant regions of each isotype.

Functions of the constant region of different isotypes
The variable region of an immunoglobulin does the exciting stuff — it binds an antigen, but that is not sufficient for its action. As well as the specific discriminatory action of the variable region, there are roles in presentation and disposal that are the same for all antibodies of a class, but may differ between classes. That is what the constant regions do.
I am not an immunologist (although had to teach the biochemistry at one time in my life — hence the diagrams) so the examples I present are simplistic and incomplete. However here are a few:

IgM is made early in the immune response and hence is not very abundant. In order to enhance its response it forms pentamers in which the constant region of the heavy chain interacts with an additional J chain.
IgA is involved in immune protection in mucous regions of the body exposed to the exterior. It is directed there by interaction with a receptor on the appropriate epithelial cells, which binds the constant regions of an IgA dimer attached to a J chain.
IgE stimulates mast cells to produce histamine. These mast cells have receptors for the constant region of the heavy chains of IgE.

There are many sources on line dealing with this topic, including a section in Berg et al. that has a similar structural approach to that presented here.

Many different cells express Fc receptors that bind to the antibody constant region and act on that signal. Wikipedia has a fair page on Fc Receptors.

The Fc region is composed of the two heavy chain constant regions, and its amino acid composition differs between the different classes of immunoglobulin (antibody). The Fc region of the five immunoglobulin (Ig) classes (IgA, D, E, G, and M)confers upon each class of Ig certain capabilities or properties. For example, IgG can cross the placenta, has a long half-life in serum, and it is opsonic (i.e., binds to Fc-gamma receptors on macrophages, facilitating phagocytosis of microbes), IgE binds to mast cells stimulating hayfever-type allergies, IgA is secreted onto mucosal surfaces, and IgM (and IgG) can activate the complement system, etc.

1.The Fc region is used as binding site for different immune system cells after the opsonisation of a pathogen.
2.Complement protein C1 binds to Fc region of antibody bound to an antigen to trigger classical complement pathway which leads to destruction of that antigen-antibody complex or opsonised pathogen


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How is the role of ethylene in ripening demonstrated in biology (or agriculture) education?
I want to know what are some typical experiments performed in the course of biology education (or possibly in applied biology education e.g. agricutlure education) to prove to the students (or have them prove to themselves) the autocatalytic role that ethylene plays in ripening. I'm interested in both how ethylene production by plants might be demonstrated/measured as well as the demonstration of the role of ethylene on ripening.
I'm aware of some historical experiments e.g. that of Gane (1934). Is it commonly repeated in biology labs in an educational context today? Or is something else used?
I found a lab manual aimed at Indian "class XII" (I guess that's the terminal year in high-school over there); the experiments aren't well detailed but they suggest keeping a sample in open and one packed in polyethylene, or treating one with ethylene. These aren't exactly quantitative though: no suggestions for measuring anything but by eyeballing/tasting. I guess that's the best on can do with limited resources. I'd like to know about college-level experiments, if there are any.
I also know how ethylene is measured in industrial/pro-lab settings:

Ethylene
  can be measured successfully with a portable gas chromatograph fitted with a
  photo ionisation detector capable of measuring ethylene to a concentration below
  0.01 uL/L. EASI-1 uses a proprietary ‘nanoporous gold sensor technology’ for
  “accurate real-time measurement of ethylene gas concentrations”. This is licensed
  from Fluid Analytics in USA, which offers a claimed sensitivity to ethylene in
  the air at levels as low as 10 ppb.

There also exist industrial scrubbers for ethylene so the air concentration can be reduced. I don't know if either of these are commonly available on college campuses though, even in biotech or agriculture departments.
(N.B.: I don't care about proving the effect in the kitchen, which is the topic of a question on Skeptics.)

One way (I don't know how easy it is to get hold of the compounds in your locality) would be to have three sealed containers containing apples, one in standard conditions, one in elevated ethylene, and one with 1-methylcyclopropene which competitively binds the ethylene receptor, and observe the differences in ripening rate.

As titled and phrased, this is a question that only a professional teacher could answer. Is this your intent or are you really asking for ideas of nice, compact demonstrations that could be done in a classroom?

@JimYoung: I want to know how it's done (if it is) in existing education, not for radom ideas how it could be done. And it's not just that a "professional teacher could answer". Lab manuals etc. anyone can read.

This is a Biology list, not an education list. So it's OK to ask how it was shown that ethylene has a role in ripening — although we'd expect you to show that you'd tried to find the answer yourself — but I think it's off-topic to ask how to do it in the constrained circumstances of a teaching course.

@David: really? Let me ask on meta here. Actually, it was asked already, and you seem to be wrong: https://biology.meta.stackexchange.com/questions/3162/questions-about-teaching-biology-off-limits "questions that ask for ways and methods to teach specific biological concepts or techniques (lab or field) should be on-topic." (that's the only answer) Also "All questions asking for this type of advice should be narrowly defined, so that the scope of possible answers isn't too wide." Not asking about hypothetical but only about actually used methods seems to satisfy that well.

A question was asked on meta and one person replied that he thought they "can" be on-topic and seven people agreed with him. That does not define the scope of SE Biology or mean that I am wrong. The scope of SE Biology is laid out in the Help and my reading of it is that it does not include questions of your type. I suggest you do some research on the subject and state what you think are the problems of repeating the experiment in the classroom. Then I and others will consider whether it is or is not off-topic.

@David: I already know of some historical experiments in general terms; see my answer on Skeptics. (The details only appear in obscure publications from the 1930s that are hard to get--not online, etc.) If I take the time to read some lab manuals myself, that would make my question here moot, unless I want to waste my time typing an answer to my own question (which seldom gets any appreciation anywhere on SE). I don't see what's wrong with my questions as-is.

I second the idea that asking a forum of biologists "which typical experiments are performed in the course of biology education" is missing the area of expertise that you can expect here. During the course of my education, there have been no such demonstrations, which probably answers your question on whether such demonstrations are routine in biology classes in schools around the world. I also guess most research biologists today have had no such demonstrations in school. @NatWH already has suggested an experiment, if you are interested in a specific way to demonstrate this in a classroom


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Is this is a parasitic wasp, which I found in Blackpool Lancashire?
A wasp I photographed on my van window in Blackpool just before it attacked me.
Is it true that it’s rare to see them in the UK?

Excellent picture!  Someone will know this species.

Quite similar to Mellinus arvensis.

Yes it is ! If you look closely at the wing patterns, they are characteristic of the Ichneumonidae family, as you can see below*. This family contains thousands of species which all are parasitoids. Species identification is very tricky for this family, but the patterns on the abdomen (2nd and 3d strips are yellow, the others are black, yellow spot at the tip) and on the tibia (yellow strips) are very characteristic of the species Ichneumon stramentor, which parasitizes caterpillars.

Based on the width of the abdomen, this is probably a female (ovipositor is not visible for this species).
It's actually quite common in the UK (they live in habitats such as hedgerows or woodlands), but not so frequently seen on windows!

*Image source : DrawWing.org
Derived from: Comstock J.H.
(1918) The wings of insects. The Comstock Publishing Company, Ithaca, N.Y.

Can you please provide the source of the image?


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During what phase is the cell polyploid?
During what phase is the cell polyploid? Why is it polyploid at this point--what has happened to create this state and why is it important to the process?

I assume that you mean phase of cell division. First off all i will write down a definition of word polyploid. Polyploid is cell which has two or more pairs of homologus chromozoms. There are two basic types of cell division are meiosis and mitosis

Technicly you can say that in reduction meiosis when chromozomes go from diploity to haploid state (which is first anaphase in this process), but ussually polyplidy occure when something goes wrong in cell division.

The major cause of polyploidy is found to the non disjunction of sister chromatids during the meiotic recombination events. Prior to meiosis chromosome numver doubles followed by chromosome separation during gamete formation (anaphase).
Artificial generation of polyploidy have been found to be useful both in research as well as economic purposes. Colchicine, the chemical which inhibits formation of spidle apparatus is widely used.

Unfortunately colchicine is only used in mitosis. Result of this process is new cultivars of plant specious.


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Fungi growing in pH 1 FeCl₃ solution
I have a FeCl3 tank that I use to dip spruce wood in. After 2–3 weeks a fungus appears in the tank and it keeps growing with time. The fungus has a white colour and is spread throughout the whole tank. It looks like mainly on the surface but its everywhere in the fluid.
The FeCl3 solution has pH 1 and that doesn't change with time.
Can anybody tell me what it might be? What's the best way to make sure it doesn't occur anymore?

I would suspect an iron oxidizing extremophile bacteria not a fungi. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5023253/


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Why do dozens of preys run away from a clearly outnumbered predator? (e.g. zebras and lion)
We are all familiar with scenes where dozens (if not hundreds) of zebras, sheep, or other preys are chased by one lion, one wolf or other predator. Examples are all over youtube, but here is one of lion versus zebras. In that video you can count at least 30 zebras. Even more, zebras (particularly adult ones) are bigger than lions. There is also evidence of prey defending itself against predators, but this seems to be not the norm.
So my question is, why do high numbers of preys always run away from a clearly outnumbered predator?
Surely evolution would have already taught these animals that numbers can make a difference, so that coordinated defense strategies would be part of their natural repertoire, or of their social learning. Why nature seem to be so oddly incapable of making use of relative numbers as defense strategies?

This definitely doesn't always happen. I've seen videos of groups of larger prey standing their ground against predators, e.g. walruses against polar bears, elephants against lions.

Why run?
To some extent, selfishness. Remember that natural selection acts within species.
Combat is dangerous. Very dangerous. Even if you are not immediately killed and successfully fend off a predator, wounds can weaken you, damage your senses, and/or kill over time with infection.
If you are a zebra, or a sheep, and you are in a group of other conspecifics, the safest action for you may be to not be the individual that is attacked. Sometimes, you might achieve this by simply advertising being a tough target. Other times, your best bet is to run away. This concept is sometimes humorously discussed in the context of humans and bears: you don't have to be faster than the bear, you have to be faster than the slowest person with you. This is called selfish herd behavior.
Fleeing predation is likely to be the default behavior
If you imagine an allele that changes an animal's behavior to combat an attacking predator (when other conspecifics predominantly run from predators), it is difficult for this allele to grow in the population. Individuals with the allele will get in fights, and although they may reduce predation of the herd as a whole, they will individually be selected against.
Similarly, imagine an allele that changes an animal's behavior to run from an attacking predator (when other conspecifics predominantly attack predators). Individuals with this allele will avoid fights, stay healthier, and breed better than their conspecifics that are getting beaten up, and eventually the herd will be mostly escapers.
Exceptions to the default
However, as pointed out in a comment by gardenhead, not all prey try to escape.
To avoid the 'default' escape behavior, there must be some other motivation: fighting back has to be special some how. In the context of group selection, fighting back may be selected for if it means improved survival of related conspecifics. This behavior is often seen in defense of offspring, but can expand to larger related groups. However, even defense of offspring can be risky, and it is not uncommon in nature for mothers to abandon offspring they cannot defend. It may be safer and more productive in the long run to survive and produce new offspring next year.
Another alternative would be some sort of social/sexual selection, where strong individuals who defend the group (likely males) have increased likelihood to mate.

References
Fischhoff, I. R., Dushoff, J., Sundaresan, S. R., Cordingley, J. E., & Rubenstein, D. I. (2009). Reproductive status influences group size and persistence of bonds in male plains zebra (Equus burchelli). Behavioral Ecology and Sociobiology, 63(7), 1035-1043.
Hamilton, W. D. (1971). Geometry for the selfish herd. Journal of theoretical Biology, 31(2), 295-311.
King, A. J., Wilson, A. M., Wilshin, S. D., Lowe, J., Haddadi, H., Hailes, S., & Morton, A. J. (2012). Selfish-herd behaviour of sheep under threat. Current Biology, 22(14), R561-R562.
Sjare, B., & Stirling, I. (1996). The breeding behavior of Atlantic walruses, Odobenus rosmarus rosmarus, in the Canadian High Arctic. Canadian Journal of Zoology, 74(5), 897-911.
Smith, W. P. (1987). Maternal defense in Columbian white-tailed deer: when is it worth it?. The American Naturalist, 130(2), 310-316.
Wood, A. J., & Ackland, G. J. (2007). Evolving the selfish herd: emergence of distinct aggregating strategies in an individual-based model. Proceedings of the Royal Society of London B: Biological Sciences, 274(1618), 1637-1642.

Thanks! A lot to digest. Just to start, I don't see how the phrase "Remember that natural selection acts within species." fits into the picture. Do you mean that individuals only care about the survival of their own genes and have no regard for those of their fellows? So, in this sense, there is no probability of species survival function to maximise, which could help understand why such strategies might gain little traction in selection processes?

@luchonacho "Do you mean that individuals only care about the survival of their own genes" - to a primary extent, yes. When you talk about natural selection of alleles, you are talking about variation of allele frequency within a population, which means individuals that can interbreed. Interspecific competition is separate. On some macro scale you might think some of the ideas of natural selection apply across species that compete for the same ecological niche, but really only by analogy.

@luchonacho You should also be aware of the idea of the "selfish gene" which takes the individual-centered approach to selection even further and says that individual genes are 'selfishly' self-promoting. There are criticisms of that approach, but if you apply it to this particular case like the 'default behavior' paragraph in my answer you will find it works.

why do some animals like elephants team up and fight the predators?


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Non-coding DNA correlation with rate of evolution
Non-coding DNA can be helpful in generating useful mutations that can go on to become new features/functionality of an organism.
Non-coding DNA also indirectly reduces chances of mutation of useful/functional genes.
So if an organism has a larger proportion of non coding DNA it'll be safer from mutation. Humans have 80%-90% non-coding DNA. But this number is far lesser in many other species especially plants. Some plants have as few as only 3% non-coding DNA.
My question is, do these species with less non-coding DNA undergo evolution faster? Because their functional genes are more susceptible to mutations (which would be disadvantageous on average I guess). Would it be fair to say that evolution tries to keep expanding this proportion of buffer DNA? Lastly, is my question related to C-value paradox?

My assumption that non-coding DNA indirectly offers adaptive advantage (evolutionarily speaking) seems to be questioned. Let's consider the following case:
Let A and B be two genomes of equal size. Let A have 80 % non-coding DNA and 20% coding DNA. And let B have the opposite i.e., 20% non-coding DNA and 80% coding DNA. Let both A and B be exposed to the same amount of UV radiation for the same amount of time. All conditions being the same, let's assume that this causes the same amount of mutation in both A and B, say 10%. Now what is the probability that this mutation happened in non-coding DNA (which means it doesn't harm the organism) in each of A and B? Evidently, the probability is higher in A meaning it's safer from mutation caused due to UV radiation. So A has an advantage of surviving over B.

Humans have 80%-90% non-coding DNA Wasn't it 98% as per as my limited knowledge is concerned?

@FailedScientist 98% was the popular understanding which is now changing due to broadening of the definition of what is 'functional' part of DNA sequence.

“Non-coding DNA also indirectly reduces chances of mutation of useful/functional genes”  — It does?! How? The rate of mutation doesn’t change because of the size of the genome.

@yathish “functional” ≠ “coding”. Regardless of the definition of “functional”, the percentage of coding (= protein-coding) DNA has barely changed.

@KonradRudolph Let's assume mutation is bad and it can happen anywhere on the genome with equal probability. If non-coding DNA is 95% of the genome then the probability of mutation happening over coding DNA is only 5%. I understand functional!=coding.. it's a broader definition.

@yathish Again, the rate of mutation is independent of its size. Yes, if you add 95% non-coding DNA (= 20-fold increase in genome size) then only 5% of mutations happen on the coding fraction, but the absolute number of mutations also increased 20-fold, so the number of mutations on coding genes remains identical! In sum, non-coding DNA does not “indirectly [reduce] chances of mutation of useful/functional genes”. And to your other comment, it’s still wrong to speak of “80%–90% non-coding DNA”, the actual number is roughly 98%.

Thanks for adding the explanatory paragraph to your question. Unfortunately, as my previous comment and David’s answer explain, your calculation is wrong. You need to think more carefully about what “10% mutation amount” means. In fact the term “mutation amount” is vague and problematic. That’s why we instead speak of “mutation rate”, and this rate refers to a per-base probability.

@KonradRudolph I'm assuming that the genome size is same. We merely vary the proportion of coding and non-coding DNA within the given genome. Is it wrong to assume that the genome size could be same? Regarding 98% please refer to latest sources (ENCODE project) or Wiki. This 98% figure was revised over time as it was discovered that certain non-coding DNA is also 'functional'.

@yathish “Is it wrong to assume that the genome size could be same?” — No, but it is still wrong to assume that the mutation rate depends on that size (or, conversely, on the fraction of noncoding DNA — both assumptions are equivalent; reread my previous comment and think about what 10% mutation rate actually means). And, again, you do not distinguish correctly between “coding” and “functional”. The “98% coding” figure has not been substantially revised in the last 15 years, and ENCODE had nothing to say on this figure.

Let us continue this discussion in chat.

Whether or not species with less non-coding DNA evolve faster, the assumption that this could be explained by their genomes being more susceptible to mutation would seem to me to be based on a false premise.
Let us examine the logic of the assumption by making an analogy to drawing of tickets from an urn in a lottery. If you buy one ticket (coding region), and only one ticket is drawn (there is a single mutation) from the urn (the whole genome), the probability of winning (your gene suffering a mutation) decreases as the number of tickets (the size of the genome) increases.
So the question is “does mutation follow this model?”, i.e. are the number of mutations in a genome independent of its size? To answer this, let us look at two examples of known mechanism of mutation.

Misreading during DNA replication: Here (and in other types of misreading) the error frequency is, quite logically, related to the number of bases replicated i.e. it has a specific (if very low) value of n per 1,000,000 bases — not n per genome.
UV radiation: Here the source of the radiation is external and its flux will be proportional to the area it strikes — hence the larger the target area the more interactions with thymine causing dimerization. Although our linear-centric view of DNA tends to ignore its area, the larger the genome, the larger the target. The only way I can see the non-coding DNA buffering the coding DNA from radiation is if it somehow formed a protective shell around the latter. I know of no evidence that this is so.

It seems my question is unclear. May I request you to read a portion I added in the question as an edit? Assuming mutation is harmful on an average, my argument is that having more non-coding DNA in a way shields the coding DNA from mutation. There doesn't need to be physical protection - I'm only talking in terms of probabilities (averages). Note that I've also assumed the size of genomes under comparison to be same.

@yathish — Again, I question your assumptions. I do not think it valid to compare two genomes of equal size, or if you do you are asking a different question. You clearly talk about increasing the amount of non-coding DNA, not the coding DNA. For this you have to compare two sets of coding genes of equal size, but associated with different amount of non-coding DNA — something like Drosophila, with a genome with a similar number of genes (ca. 18,000) but more non-coding DNA. And for that my argument holds.

I was definitely assuming the size of genome to be immaterial. I wanted to highlight the PROPORTION of non-functional DNA and not the amount of it. Would my argument hold for species of comparable genome sizes but with widely varying proportions of coding to non-coding DNA?


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Can someone identify this brown spider in California
Spider found on transit case from California. Approx 1 1/2 inches leg span. Is it poisionus?

It looks a lot like a Kukulcania hibernalis, or southern house spider. This one appears to be a female and if it were to bite you then it would be painful, but not dangerous. These spiders typically keep to themselves so unless you find one hanging in a really bad place it's better just to leave them alone.
For further information you can look here:
https://spiderid.com/spider/filistatidae/kukulcania/hibernalis/

Joseph, once again please provide support for your answer. We as kthat all answers (especially those regarding species ID) be supported by reputable sources that are cited or linked. Otherwise, we're no better than Yahoo Answers :p. I'm sure you know your spiders, but without outside evidence, your post appears no more than a comment. Please see our help page for additional notes regarding writing good answers on our site. Adding citations/sources will surely garner you additional upvotes as well. Thanks!


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Is there a limit on how big a free living unicellular mono-nuclear organism can be?
When I looked for the largest protozoan I've found the name Syringammina fragilissima. According to wikipedia " .. Syringammina fragilissima, is among the largest known coenocytes, reaching up to 20 centimetres (7.9 in) in diameter." The catch is it is multi-nucleated organism, not exactly what I had in mind. The reason I am interested in the upper limit of the size of the free living unicellular organism is because I want to have a sense of the limitation of single center has in emitting and receiving information across a large span of space. My interest is not about non-compartmentalization (as in the case of multi-nucleated unicellularity)  rather about single center.

There are individual neurons in multicellular organisms that are meters long with a single nucleus. Certainly they are nothing near spherical, but just something to think about.

I have edited the title to only include free living organism. Apparently a too specialised and dependent cell can become very large. :)

Some bacteria form > 100 micrometers long unicellular filaments (e.g., Caldilinea tarbellica). https://cz.pinterest.com/pin/518125132116454830/


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chaperone protein names
I am studying chaperon proteins DnaK, DnaJ etc. This question sounds trivial but I would like to know what the acronym stands for. I have looked on google/google scholar. My best guess is that the name comes from the fact that these are genes whose products are necessary for bacteriophage DNA replication. Can this be confirmed? The full name of GroES and GroEL may also be helpful. Thanks!

DnaK: the recommended name is Chaperone protein DnaK; the alternative names are HSP70, Heat shock 70 kDa protein, and Heat shock protein 70 (source: UniProtKB); the name of the protein, DnaK, is derived from the name of the gene, dnaK (Yochem et al., 1978, Mol Gen Genet. 164: 9-14):

We show that a collection of 93 E. coli mutations which map between
  thr and leu and which block phage lambda DNA replication define two
  closely linked cistrons. Work published in the accompanying paper
  shows that these mutations also affect host DNA replication, so we
  designate them dnaJ and dnaK; the gene order is thr--dnaK--dnaJ--leu.

To find the recommended and alternative names of GroS and GroL, search UniProtKB . . .


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DNA replication precision
This will sound as a super stupid question, but I just read in the Molecular biology of the gene book (7th edition, Watson, Baker, Bell and al.) that one mistake occurs in 10 million nucleotides added during the replication of DNA.
However, I read in the Campbell's biology book (11th edition) that it is one mistake in 10 billion nucleotides added.
I tried to google it and kept finding these two numbers... probably because people use the same books as I do as sources. So, my question is the following: which book is right about DNA replication precision?
Thanks for your help and sorry if my question isn't very interesting.

Can you provide some longer passages from those books? I suspect one is reporting the number of errors before correction, and the other is reporting the number of errors after. That said, you should consider either number as a very rough approximation to within a couple orders of magnitude to interpret it generally.

Also, what organism are the books considering? Different organisms have different mutation rates. Trying to get something meaningful from these random numbers is useless.

The precision of DNA replication is determined by the fidelity of DNA polymerase, which depends, in part, on its proof-reading capacity. The ratio of correct:incorrect nucleotide insertions ranges from 10^3 (extremely low fidelity) to 10^10 (extremely high fidelity).


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Does a reproductively successful male have the same genetics as a reproductively successful female?
Evolutionarily, using humans as an example, it would make sense that a successful female would produce successful male offspring. If a successful female produced male offspring that weren't successful, the female also wouldn't be successful by definition and would, through evolution, stop being desired by males. Therefore, females are selected for by their ability to produce successful males and thus successful male genes must be the same as successful female genes?
However, I've heard that in humans today, males don't like rich females while females like rich males. Also, from what I've read, lascivious females used to be looked down upon in the past while lascivious males weren't. Females and males also played very different roles in society. Also, successful males often don't spend much time taking care of children and spend more time making them, while successful females spend more time taking care of them. This suggests that successful males are genetically different than successful females? I'm an amateur in biology, so correct me if I'm wrong.

One important thing that the logic of your question seems to be completely missing is that, at least for humans and many other species, no male has the same genetics as a female. In humans and related species, males have one X and one Y chromosome whereas females have two X chromosomes.

What difference does it make though? Isn't the only difference that being female decreases or increases the degree of some of the traits that a male would have and vice versa? Or are the interactions more complicated than this?

Because the traits expressed by males and females are not the same.

So your're saying that an aggressive male wouldn't necessarily make a relatively aggressive female? I somehow don't believe that.

Evolutionarily, using humans as an example, it would make sense that a successful female would produce successful male offspring. If a successful female produced male offspring that weren't successful, the female also wouldn't be successful by definition and would, through evolution, stop being desired by males. Therefore, females are selected for by their ability to produce successful males and thus successful male genes must be the same as successful female genes?

That assumption is wrong. Of course the best thing for an individual's reproductive success is to have as many successful offspring as possible regardless of gender, but in the real world there are sometimes tradeoffs. If an individual had a trait that made, say, their female offspring a lot more successful but mildly impaired their male's offspring's success, the advantage to the female offspring might outweigh the disadvantage to the male and the trait might get passed on, even though it produced male offspring that weren't very successful.
Here is a paper apparently exploring the concept in seed beetles:
http://rspb.royalsocietypublishing.org/content/early/2009/12/21/rspb.2009.2026

However, I've heard that in humans today, males don't like rich females while females like rich males.

You've heard that of humans, have you? Are you sure what you heard actually applied to all humans, and not the humans in one specific society? You say "humans today", do you mean "anatomically modern humans" or "people in the 21th century"?
You really ought to investigate this kind of thing you hear before drawing all-encompassing conclusions about biology or evolution from them. Maybe you were assuming that "in humans, males don't like rich females while females like rich males" was consensus biology; if so, well, it isn't. And given that it isn't, we can't answer your questions based on such a vague claim; you should give a source that explains more precisely what exactly is being said there.

Also, from what I've read, lascivious females used to be looked down upon in the past while lascivious males weren't.

Same thing; I'll also highlight the "in the past" when your previous sentence talked about "today". Evolution works on the scales of hundreds and thousands of generations. Why would you assume evolutionary explanations for social trends that, by your own words apparently, have changed recently?

This suggests that successful males are genetically different than successful females?

In order for those things suggest that, you would need: 1) to establish reliably that the differences you talked about exist, 2) to establish that they have a probable biological basis; one way of establishing this could be to show that they are universal across human cultures, geography and history. If they aren't then it's more likely the explanation is cultural than biological, and 3) to establish that the biological difference is related to individuals being successful, as opposed to being random variation (which happens a lot in evolution).

competition between male and female genes is known to exist in some species, in the most extreme case sien in some mice genes on Y chromosomes that actually prevent X carrying sperm from forming properly.

Before I read this I thought biology was simple stuff. But does this answer my question?

@dan-dan I tried to answer your question, so I think so... Do you feel this doesn't answer your question, and if so can you say what's missing?


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What kind of bird is this and what does it eat?

My father found this little guy in one of the tractors of where he works (in the fields) i’m not sure what species of bird it is and what it eats. It just keeps chirping not stop and I have no clue what so ever to what it eats. If anyone knows please tell me, I don’t want to see him starve to death.

Hi Maria, if you can give a general location it’ll help us give you more accurate information. Are you in the US?

when in doubt finely ground meat can work temporarily there are very few (non-mammalian) vertebrates that cannot digest meat. not a long term solution but can buy time.

Could you provide a photo showing the little guy from the side so that one can see the pattern of the wings? Would be very helpful. Frm this view I'd say that this is some sort of sparrrow

Based on the photo, it looks like you have a fledgling American Goldfinch (Spinus tristis). Here's a photo of an adult female feeding a young goldfinch. This link has dietary information.

I would suggest contacting your local Wildlife Rehabilitation Centre or leaving the young guy where he was found. He could of jumped the nest a bit early, but typically the parents are always nearby.


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Why do proteins targeted for chloroplasts require two signal peptides?
Question #11 of the GRE Biology Practice Test says that proteins targeted for chloroplasts require two signal peptides:

Targeting of a newly synthesized protein is most likely to require two different signal peptides for which of the following destinations?
(A) Plasma membrane
(B) Lysosome
(C) Cytosol
(D) Chloroplast (Correct Answer)
(E) Endoplasmic reticulum

I can't find a reference for this.
I understand that a ribosome starts the synthesis of a protein in the cytosol and a signal peptide takes that to the endoplasmic reticulum (ER) which finishes protein synthesis in the ER lumen and then the protein is secreted in a vesicle to its destination (if it doesn't become an ER membrane protein). What's the purpose of the second signal peptide to enter a chloroplast?

Welcome to SE Biology. Please update the tags on your question to include the homework tag. Goodluck getting an answer.

@Michael_A Thanks for the welcome! I'm glad to tag properly, but I'm not currently in school, so this isn't homework. Is homework a broader tag for any test-based question?

Yes, exactly. Renaming it has been debated but it seems like we're stuck with it. Your question is a model of how to ask this kind of question and I think the tag is a minor issue but including the tag should reduce the odds of people downvoting the question.

@Michael_A Makes sense, thanks. I've added the homework tag.

Protein import to chloroplasts (and also mitochondria) can still have multiple destinations, because these structures themselves have sub-compartments:

both have an inter-membrane space as well as an 'inner space' (the stroma in chloroplasts, matrix in mitochondria).
proteins can also be targeted towards either of the two membranes
additionally chloroplasts have the Thylakoid stacks in the stroma which are separated by another membrane layer.

Due to this complex structure you need multiple signal peptides to properly target proteins to their destination.
I don't remember (or can find) all the details now but basically you (can) have:

a 'main' signal peptide that targets proteins directly towards the stroma (which will be removed there by the stromal processing peptidase (SPP)).
an additional signal peptide for import to the the thylakoid stacks (which will be 'made avaibalble' by cleavage of the first peptide)
there should be other signal peptides or at least variants that allow import to the intermembrande space and the inner membrane (via the TIC23 complex). [I couldn't find any sources for this right now]

Sources I could find:

TIC/TOC complex in wikipedia
in-depth scientific review


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Why don't phosphatases both add and remove phosphate groups if enzymes catalyze reactions in both directions?
We know that Phosphatase is a type of enzymes that removes a phosphate group.
Why can't phosphatases add a phosphate group if we know that all enzymes reactions are reversible ?

@TheLastWord I think the question was quite clear - maybe you can explain better what about it you find unclear?

@BryanKrause I am just wondering if he meant to ask if Phosphatase enzyme can in itself add the phosphate group of if we can add it externally thorough some means or he is commenting on the reversibility of the reaction in general.

@TheLastWord Does my edit help? Maybe the 'it' in the second sentence was unclear, but I feel like this question addresses a fairly common misconception to biochemistry novices so I'm fairly confident I've extracted the correct intended meaning.

@BryanKrause That should be sufficient.

Enzymes make reactions happen faster in both directions. If the chemistry favours removing a phosphate an enzyme cannot change that. Only get there faster (or maybe slower too I guess.)

I think the description of enzymatic reactions as 'reversible' is potentially a bit misleading. It might be better to think of enzymes as agnostic to reaction direction.
The big missing piece is the difference in free energy of the reaction itself. Reactions that remove a phosphate group are energetically favorable in biological conditions. A phosphatase will effectively never add a phosphate group back because one would have to supply additional energy to make the reaction proceed in that direction.
Phosphatases catalyze a reaction that results in a free phosphate ion. However, kinases that add phosphate groups are catalyzing quite a different reaction, where a phosphate group is lost from a molecule of ATP which becomes ADP. This reaction is also energetically favorable, and the reverse reaction does not occur.

The feasibility of an enzymatic reaction depends on the activation rather than reaction free energy. It is the climbing up the hill that requires effort. The effort depends on the difference in elevation between the valley and the top of the hill, not on the difference in the elevation between the two valleys on the opposite sides of the hill.

@MartinKlvana True, but the reversibility of the reaction depends on the free energy. The question is more about reactions proceeding in both directions rather than the reaction being feasible in at least one of the directions. If there is little difference in elevation between the two valleys, the reaction will go in both directions (or neither at all if the activation energy is too high); if there is a huge difference, one direction may be feasible and the other is not.

The reversibility depends on the feasibility of the reverse reaction. And the feasibility of the reverse reaction depends on the activation free energy barrier of the reverse reaction, and it is the barrier for the reverse reaction that determines the rate of the reverse reaction, not the reaction free energy of the reverse reaction. And it is the rate of the reverse reaction that determines the possibility of the reverse reaction occurring in biologically meaningful time.

@MartinKlvana Right, but the difference in the reaction directions is critically dependent on the difference in energy between the products on each side of the reaction: that is what determines the asymmetry in reaction rates. The energy of the intermediate state is the same in either direction.

Bryan, of course, the activation free energy barrier is the difference between the top of the hill and the valley, and the deeper the valley, the higher the activation free energy. But it is the height of the hill that determines the rate of each reaction, not the difference in the elevation of the valleys. We both arrive to the same conclusion as to the preferred direction of the reaction, but your reasoning does not allow you to assess the feasibility of the forward and reverse reactions, because you cannot get the rates of the reaction in the two directions from the reaction free energies.

@MartinKlvana I know we are really talking about the same thing here and going in circles around each other. I think it's maybe important that I clarify where I am coming from here...for someone having trouble understanding these concepts, I want to avoid talking about differences in the activation energy because people are taught to think about the purpose of enzymes as reducing the activation energy, which they do, but that gets confusing then when you are talking about the two directions. I want to emphasize that the reaction won't go in a direction where the products are too high energy.

Not all enzyme catysed reaction are reversible reactions .reversible reactions are those which have free energy change between product and reactant sholud  approximately or exactly equal to zero. Phosphatase canot do the reverse of the reaction because if both the reactions where done by the same enzyme in both the direction then a cell will not be having the ability to decide weather forward or backward reaction that should actually take place at any given time.


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Can two proteins sharing a few domains be considered homologous?
I wonder when to say two proteins are homolog. In the current example I checked the sequence of these two proteins in pfam and as you see they have some shared domains but all domains are not shared. Can I say that these proteins are homolog? How can I be confident about my decision?

Did you do a sequence alignment of the two proteins? Homology is often judged on DNA/protein sequence similarity. Other relevant information might be the source species of the two proteins (and their evolutionary distance).

It would be better if you can summarize the PFAM results in the form of text.

I thought that PFAM visuall result better explains my purpose.

@MySky It is difficult to search the content shown in the images. You can keep the image but a text summary would be good

Worth mentioning that this was cross-posted to BioStars.

Yes this question is cross posted in BioStars: https://www.biostars.org/p/335210/

Homology means shared evolutionary ancestry. Sequence similarity is often used as a proxy for homology but inferences should be made with care.
The similarity between two genes/proteins should not just be good but has to be statistically significant (metrics like E-value) for the two genes/proteins to be considered homologous.

INFERRING HOMOLOGY FROM SIMILARITY
The concept of homology – common evolutionary ancestry – is central to
  computational analyses of protein and DNA sequences, but the link
  between similarity and homology is often misunderstood. We infer
  homology when two sequences or structures share more similarity than
  would be expected by chance; when excess similarity is observed, the
  simplest explanation for that excess is that the two sequences did not
  arise independently, they arose from a common ancestor. Common
  ancestry explains excess similarity (other explanations require
  similar structures to arise independently); thus excess similarity
  implies common ancestry.
However, homologous sequences do not always share significant sequence
  similarity; there are thousands of homologous protein alignments that
  are not significant, but are clearly homologous based on statistically
  significant structural similarity or strong sequence similarity to an
  intermediate sequence. Thus, when a similarity search finds a
  statistically significant match, we can confidently infer that the two
  sequences are homologous; but if no statistically significant match is
  found in a database, we cannot be certain that no homologs are
  present.
Pearson, 2013

Members of a protein family are descendants of a common ancestor and are hence homologous. However, in the course of evolution they would have acquired new domains or reshuffled their domains such that their sequences are no longer similar. Proteins that have full length sequence similarity are called homeomorphic (Wu et al., 2004). Therefore, members of a protein family may be homologous but not homeomorphic. However, homeomorphic proteins can evolve independently and therefore may not be considered homologous.
Identifying homologous proteins is, therefore, not a simple task. Machine learning algorithms are used for better identification of homologous proteins. Some of these algorithms are mentioned in the linked papers.
In general, global similarity, rather than local similarity should be considered for identifying homeomorphs. See What is the difference between local and global sequence alignments?

This is the definition of homology that disturbed me. you say we must consider global similarity rather than local similarity. accordingly, we can't say these two proteins are homologs, because just about 60% of their lengths have significant (above 80%) similarity and the rest of their sequence is not similar. But actually, we see that they share 4 exactly similar domains, and have 3 nonsimilar domains. according to shared domains we can say those are homolog (at least in part of their sequence). I am really confused.

Wikipedia (Protein family): Proteins in a family descend from a common ancestor (see homology) and typically have similar three-dimensional structures, functions, and significant sequence similarity. The most important of these is sequence similarity (usually amino acid sequence) since it is the strictest indicator of homology and therefore the clearest indicator of common ancestry. Proteins that do not share a common ancestor are very unlikely to show statistically significant sequence similarity.

Could you please lead me to some good papers that give me a deeper understanding of the definition and concept of homology? As I previously said, I am really confused about this.

I have updated the answer @MySky

Domain is a module. Proteins are composed of one or more domains. Proteins are modular. Homology describes the relationship between domains, because domains are the primary evolutionary units. It is possible for two proteins to be homologous in one and non-homologous in another domain.
For example, alpha/beta-hydrolases (Ollis et al., 1992, Protein Eng. 5: 197-211) belonging to different families are homologous in the alpha/beta-hydrolase domain, but non-homologous in the "cap" domain.


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Does homology of a trait necessarily imply that the most recent common ancestor had the trait?
If two different species have a trait that is homologous, does this mean that the most recent common ancestor necessarily had the same trait?

Yes, assuming you treat the term strictly.
The term homologous implies that the most recent common ancestor had the trait, although it would be possible for the term to be used in error, when something thought to be a homology is actually not.
If the trait is shared but the trait evolved separately twice, instead you would refer to it as an analogous trait rather than homologous; analogous traits are often the result of convergent evolution.
I can imagine some edge cases, however, where one could argue about homology, although I don't have a specific example in mind (maybe someone can help me out if they can think of one). Imagine you have a trait that is present in an ancestral population, becomes minimized in a common ancestor, and then multiple species descending from that ancestor start to exhibit the trait again. This is called atavism. In some ways, atavism could be seen as convergent evolution and an analogous trait: each has separately evolved that trait from the last common ancestor. However, one would expect a lot more genetic similarity than other examples of convergent evolution and therefore outside of cladistics it might be more appropriate to think of it as a homologous trait in that you can find some ancestor that shared the trait, it just doesn't happen to be the most recent one.


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How exactly does sensory substitution work?
Sensory substitution, when one of sensory modality changes into another sensory modality to help someone restore the ability to perceive defective sensory using a working sensory modality. For example, blind people who have improvements in their other senses like auditory system or olfactory system compared to normal people. Or deaf person who have enhanced vision ability than normal people.
Questions :

Does this work the same way as Alternative Sensation ?
Is there any pattern of which senses will probably improve according to which kind of senses someone's lacking ?
Is there actually any method to train which senses someone would like to improve ?

Tot start of with your definition:

Sensory substitution, when one of sensory modality changes into another sensory modality to help someone restore the ability to perceive defective sensory using a working sensory modality.

I personally like to use a more subtle definition of sensory substitution (Stronks et al., 2015):

[T]he process of obtaining information about the world through an alternative intact sensory channel [] that would normally be obtained by the deficient [sensory] system.

In other words, the information is not changed into another modality; it is simply processed by a sense normally not used for that purpose. Your definition seems to imply that the information stream is swapped. Although this is not strictly true, and hence the reason I like the second more subtle definition better, it is nonetheless true that cross-modal plasticity results in the deafferented cortical regions being taken over by other senses; for example in the blind, it has been shown that tactile and auditory information is processed in the visual regions, even down to the V1. The primary visual cortex is normally strictly associated with low-level visual processing, being the first central brain area where visual information enters the brain. Although this view is contested(V1 is also activated by tactile grids for example), in blind folks there are gross rearrangements where the somatosensory and auditory cortices take over the visual system (e.g., Pascual-Leone et al. (2005)).
To your questions

Does this work the same way as Alternative Sensation ?

'Alternative sensation' is unfamiliar to me, it doesn't pop up in a Google search, and its nonexistence is backed up by this answer.

Is there any pattern of which senses will probably improve according
  to which kind of senses someone's lacking

Yes. It depends on which senses are used most extensively to substitute for another sense. Training is an important factor in improving alternative sensory capabilities. In fact, it is the determining factor; the loss of a sensory system in itself does not propagate compensatory mechanisms (Stronks et al., 2015). Compensation being

partial compensation for [the] loss of [a sense] by developing enhanced abilities with [] remaining senses

For example, training with the BrainPort Artificial Vision Device (Fig. 1), which projects electrotactile 'images' onto the tongue using 400 electrodes, gradually improves performance in the blind, all the while the somatosensory information is funneled progressively into the visual system (Stronks et al., 2016).

Is there actually any method to train which senses someone would like
  to improve?

Pick your sensory substitution device of choice and train away; popular ones include, as said, the BrainPort (improves tactile-to-vision substitution), but also visual-to-auditory techniques like the vOICe (Striem-Amit et al., 2012). Also don't forget the guide cane, which funnels tactile information to the brain. especially the visual-to-auditory sensory substitution devices require a lot of training (Stronks et al., 2015). You can try the vOICe out yourself on an Android. However, I have tried the BrainPort myself and it is really difficult!
References
- Pascual-Leone et al. Annu Rev Neurosci (2005); 28: 377–401
- Striem-Amit, et al. PLoSONE (2012); 7(3): e33136
- Stronks et al., Brain Res (2015); 1624: 140–52
- Stronks et al., Exp Rev Med Dev (2016); 13(10): 919–31

Fig. 1. The BrainPort converts camera images into a 'grayscale' 400 pixel electrotactile image on the tongue. It partially restores visual function in the blind. Picture source: Midday Daily

Thank you very much for detailed answer! The references also very helpful, I really appreciate it and will check on them. About the definition, I don't really grasp the difference of "the information is simply processed by a sense normally not used for that purpose" and "the information stream is swapped"? Are they not the same? For example in Aural Antennae,2008, they try to create artificial synesthesia by swapping sensation,"by swapping audio sensation for haptic sensation we illustrate one variety of artificial synesthesia"

@raisa_ my pleasure. The definition used in the answer and 'swapping it' seems to imply that tactile information is processed by the visual system. This may not be true. Ultimately, after years of training it may happen, but it doesn't have to. If you need references, let me know. They may be paywalled. The Stronks guy is actually me.

Actually, can I ask one more thing ? If for the same sensor we change the stimuli for example in skin, to gain respond for someone who has less sensitivity with pain (pinch), we change the stimuli into heat instead. Is it still part of sensory substitution then ? Because the sensor doesn't change, the same sensor will process the information, but another stimulus is replacing the original stimulus as the input information.

@raisa_ I guess it is still SS

I couldn't find if there's any other terms related to the condition I asked previously : if the processing sensor is the same and we just replace the stimuli. I thought SS worked with 2 different sensor, so it also fits the condition for 2 different stimuli for the same sensor.  I'm gonna look for some more information on this. Thanks again !

As another analogy that I find heartwarming every time I see it represented, it's a bit like telegraphing a game like some people do for their deaf and blind friends: https://www.youtube.com/watch?v=Xzvdu9u1eUA They are using hand motions to effectively translate the visuals of the game, letting the subject build an internal representation of what's happening out in the world: that's all our senses can do anyways.


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Identify a spider
This spider was making a web on the back porch.
Just wondering what kind of spider it is?

Please tell us about your location and if possible, the weather conditions when the picture was taken.

Did you have a look at my answer?

Seems to be a Barn Spider (Araneus cavaticus).

(photo from here)


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Giga base or Giga byte

"we reported ~2.66- Gb genome sequence of"
"we generated 191.5 Gb high quality reads"

I am very confused with these two quoted lines and I am not sure about giga byte or giga base pair.
and an additional question: How to count base pairs from a FASTQ file?
I have read numbers and length.

This refers to base pairs.
File size has no particular meaning beyond practical considerations, given that it depends on the format. (For example, 2bit files use 2 bits per base, as the name indicates, compared to the 8 bits necessary for each letter in a plain text format like FASTA & derivatives.)
For your additional question, (number of reads * length of each read) gives the total length of sequence contained in the file. It is not really a property of the file format, but a parameter of the sequencing run.


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How many samples to run an association study on B-Cell receptors
We are trying to find biomarkers on the B-Cell receptor VDJ regions. To do this we plan to run Single cell RNA-Seq (using the solution from 10x genomics https://www.10xgenomics.com/solutions/vdj/)  to get the transcripts, then assembling these using VDJ Puzzle: https://www.biorxiv.org/content/early/2017/08/26/181156
The output will be a list of about 100k base pairs per patient per cell sequenced. I will then have clinical information ... how can I compute the number of patients needed to establish a statistically significant association between SNPs and clinical outcomes / disease state?
Furthermore how many cells would we need to sequence per patient?

I don't know about the number of cells per patient, but there is a vast literature on power calculation for association studies. Power depends on several parameters. This tool developed by Goncalo Abecasis' group might be of help in exploring power while changing several parameters: http://csg.sph.umich.edu/abecasis/gas_power_calculator/index.html


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Most sensitive hearing human ever measured?
The Fletcher Munsen curve shows the lowest spl that humana can hear is -6db around 4 KHz.I assume this curve is average obtained from measuring many people.
My question is,what is the most extreme hearing in terms of threshold spl ever measured? What person holds the record for most sensitive hearing?


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Hematuria due to Nitric Oxide

Drug interactions between properly dosed NO and other medications are not expected, but side effects may include noisy breathing, hematuria, or possibly atelectasis. (pg.no:577; Goodman and Gilman Pharmacology 13e)

What is the basis for this hematuria?  Is it because of platelet inhibiting activity of Nitric Oxide?


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qPCR : Cross-contamination while sealing plate
I'm trying to do realtime PCR on a plasmid and I have my positive and negative controls close to each other along with a no-template control. I add 1 ul of my template last into the 96 well plates (on the side wall of the well, to be precise) and I seal the plate with optical adhesive seal (applying pressure with hand) and centrifuge afterwards.
While sealing I have noticed that the template drop I add on the side of the wells is being wicked up and is likely spreading into the neighboring wells. I notice amplification even in wells where I added water instead of the template
Has anybody notice the same or has any suggestions for how to avoid this? Do you add template into the liquid in the well or onto the side wall?

I can't say this happened to me before (but also don't do qPCR all the time).
In principle it should be fine to add the template to the side of the well, since this also lets you visually confirm that you did add the template. However, if you are having problems do consider adding the template to the liquid.
As another way to avoid this problem I would try to first put the adhesive foil lightly on top and then push it down/fix it with something sturdy that has a straight edge (there are special plastic things for this, but a tip-box can also work).

Thanks for the answer. I found a plastic applicator to seal plates in the lab. I will try it and see of it improves the result.

I have tried now sealing with a straight edge and it definitely does not wick the samples or cross-contaminate them. Thanks for the advice!


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Identify Bronze Coloured Beetle
Spotted this beetle on Morfa Nefyn, a beach in North Wales, UK. The beach is a mixture of sand and stone, with large sandy cliff faces and rocky outcrops.

The beetle was about 3 to 5 mm or so long, running around on the rocks at the edge of a rock pool (not in the water though!), on a warm sunny day. It was moving are quickly, but not really fast, maybe around 1cm per second.
I've seen them on the beach before and sure I know what they were called but can't for the life of me remember.

I'm reasonably sure you have a Ground Beetle (family Carabidae) here, but I don't know the British complement of that group, so going deeper isn't an option for me.

Amara aenea (Common Sun Beetle)

Welcome to Biology.SE! For identification questions inclusion of an uploaded image for comparison will help you get a more favorable response to your posting.  If you can provide details (ideally with references) for what characters led you to this identification that would be even better. ——— You may also wish to take the tour: biology.stackexchange.com/tour and then consult the help pages on the standards for how to effectively provide answers — see: biology.stackexchange.com/help/how-to-answer. Thanks!


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What is this plant with hardened fruits on the beach in Mozambique?
We saw these near the Barra and Tofinho beaches in the Inhambane province in Mozambique, in July. They were hard and leathery and dry to the touch, long past something resembling edible fruit.
Anybody have an idea what they might be? (just curious)

Edited: Here is some context around the tree.

I will take a guess that it is Ficus racemosa which is found in that area. More info. If you have pictures of the rest of the tree that would be helpful.

Thanks for the suggestion. I added a context image, and one can see that they are indeed clustered around a trunk, as with Ficus racemosa.

Interesting.  Looks to be a very small specimen or one that is broke-off and making its last stand (my first thought was "where is the rest of the tree?).  These can be very large trees but maybe it is in an exposed area and relatively small or young.


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Identify this bug
So we found this bug and it wasn't in our software for a change. Any help identifying it is appreciated. The bug was found in Cambridge, Massachusetts.
Three of the pictures are over 2MB, (and 2 of them are useful, I think), so I can't post them here, but I can give a link to the album: https://photos.app.goo.gl/DK7NBqZtfCaXi8BS8

I'll try to fix the links.

Well, it's a fly. Possibly a Robber fly (Asilidae) or Thick-headed fly (Conopidae)

How do you know it's a fly?

Agreeing with @RHA that you have a fly here (the fourth photo shows a haltere [AKA balancer] just above the hind leg/just below the wing, which is what Diptera have instead of hind wings); I believe that it's a Soldier Fly (Family Stratiomyidae), but would like other photos (if possible) before comitting myself to that level of precision.

@theresawalrus bugs should have their front wings hardened to wing-cases callers elytra. They are covering the remaining hind wings. Your specimen doesn't show that.

@ArthurJFrost there are more pictures on the google drive album if you need more.

@theresawalrus ... sorry about the tardy reply: one of the album photos was a great almost: the one with the specimen against a solid background might have helped if it hadn't lost resolution when zooming in.  If you still have the specimen and can get an in-focus extreme closeup of one wing, that would help immensely in confirming or denying my guess.

@ArthurJFrost Sorry, we put it out of its misery because it couldn't fly well anymore. It would try, but could no longer generate enough lift so would just glide down.


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Does the ratio between M and L cone cells vary in one indiviual?
Wikipedia says:

The ratio of M and L cones varies greatly among different people with regular vision (e.g. values of 75.8% L with 20.0% M versus 50.6% L with 44.2% M in two male subjects).

This made me wonder if other people then can perceive colors more or less green/red than me. But then I asked myself why do I perceive all colors similarly for both objects on my sightline and at sides (except 90+° from my sightline horizontally). Is that because the ratio of cone cells is similar on the whole retina (in one individual)?

The wavelength of light that appears unique yellow is surprisingly consistent across people even though the ratio of middle (M) to long (L) wavelength sensitive cones is strikingly variable.
Source: https://jov.arvojournals.org/article.aspx?articleid=2531368


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Could an 150 pound human have flown on the back of some species of pterodactyl (assuming they still existed)?
I'm curious if any type of flying animal that ever existed would have been able to carry your average 150 pound man.

Assuming that the heaviest pterosaurs (Quetzalcoatlus, Hategopteryx) probably weighed around 200 kilograms... No. This extra load would have required a huge amount of extra muscles and the forces acting on the wing bones (which are the distal phalanges of the 4th finger) would be too high.
The biggest bird was Teratornis incredibilis with an estimated weight of around 25 kilograms... This should answer your question.

I assume you mean biggest flight capable bird, given modern ostriches typically reach weights of over 150kg (adult males). In any case, the extinct flighted bird Argentavis is estimated to have weighed in excess of 70kg.

Thanks for adding this! I'm no native speaker... So sorry for my confusing English. You are totally right with Argentavis but even this bird wouldn't carry a human


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Identify this organism I found in my food
I found this thing floating in my orange juice this morning.
I pulled it out and it appears to be some sort of protozoa or something. It's about a quarter the size of my pinky nail. Was not moving at all.
Should I be worried about this? Either way I will be notifying the store. Location is Okinawa, Japan.

A flatworm (Planaria) perhaps?

This appears to be the same organism, and is (also) unanswered.

See my comment on this question

See this SO question for an answer to a related question, which points to Chironomous egg masses.


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What is the meaning of Sequestered germline?
What is the meaning of Sequestered germline. I understand the meaning of Sequestered in English but what is its meaning in context of germline.
For eg-"  female germ cells are Sequestered early in development ".

"The germ line cells are sequestered" means "the germ line cells are separated from the non-germ line (somatic) cells."


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Wasp? Wicked looking bug
Saw this bug this morning in Colorado. Looks like a giant wasp.

That is a horntail, family Siricidae. https://www.insectimages.org/browse/taxthumb.cfm?fam=455
They are a family of sawflies. Not technically wasps, but they are Hymenoptera.

Yeah, she looks dangerous doesn't she. However, the 'stinger' is used for ovispositing eggs in wood. These wasps do not sting.
This species is called Pigeon Tremex Horntail, Tremex Columba.
Nice pictures and very interesting information on the website below, however the images have copyrights, so I can't include them here.
http://bugeric.blogspot.com/2012/09/wasp-wednesday-pigeon-tremex-horntail.html?m=1

I haven't formally asked for a species identification (maybe I should?), but you may find this of interest and potentially amenable to an additional answer: Why do wasps have "wasp waists"? What's been optimized?

Yes, beautiful tremex!


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Is there a publically available database of microbes that details what their wastes and food sources are
Is there a publically available database of microbes that contains what their wastes and chemical food sources are in addition to other traits.
So that I could do like a sorted search for microbes that eat Ammonia or excrete sulfuric acid?
Cant seem to Google this one.

You could try to look into the kegg database. It's main purpose is to describe biochemical pathways, but it also has information on which species actually have these pathways (not sure how well this annotation is for bacteria though).
You should be able to pinpoint a few key pathways that start on free ammonia or have sulphuric acid as a sink/endpoint and then check for all annotated species. I wouldnt expect such lists to be comprehensive, but it should give you at least a starting point.
As an example the Nitrification and Anammox sub-pathways of the Nitrogen-metabolism page show direct usage/incorporation of free ammonia. If you click on some of the enzymes/genes (the boxes with numbers) and follow through to the 'taxonomy' box under genes, you'll get a list of some bacteria species each.

Make a list of all named bacterial species (Bacteria I. Taxonomy: Genera and Species) and search the Internet with the names of the species and the keyword(s) of your interest. Alternatively, collect all descriptions of the bacterial species by following the links in Bacteria I. Taxonomy: Genera and Species, and search the descriptions for the keyword(s) of your interest.
Note that there are more than 16,095 named bacterial species . . . I am building a database of the descriptions of bacterial species, but it is a mammoth (multi-year) undertaking and I started only few months ago. Meanwhile, if you can get access to Bergey's Manual of Systematic Bacteriology, there you can find the descriptions of many (but not all) bacterial species.

Right, I never thought anyone would have a complete database, I was looking more for ecosystem building purposes. Trying to cobble together a system based on inputs and outputs (granted I know theres a lot more to them like conditions, etc, etc, gotta start somwehere). but thanks for the attempt

To get the big picture, you can start at higher hierarchical levels: phyla and classes: http://bacteria.martinklvana.com/book3.htm (Unlike the descriptions of genera and species, the descriptions of most phyla and classes are not in publicly available papers but in the Bergey's Manual of Systematic Bacteriology.)


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Why does the iron content differ in different species on seeds?
Iron can be affected by pH of the soil but why does each species actually have a different iron content. What causes it? What genes cause it?

I don't think there is some single omnipresent gene in plants that says what the iron content of their seeds are. I think different genes in different species plays a role as well as environment.

Why would you expect different species to have the same iron content?  Or anything else, FTM.


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How to grow bacteria?
We have this science experiment on how to grow a bacteria, our teacher told us to use gelatin, beef stock, and sugar as an alternative for agar. I am confused on  why we need gelatin, beef stock, and sugar in growing a bacteria. What ingredient is in those 3 materials that can aid in growing bacteria?

There are several requirements for bacteria to grow.

A carbon source - Sugar
A nitrogen / amino acids source - Beef stock
Gelatin is there to hold everything in place, it doesn't provide any nutrients.

The list is incomplete.

Everything that lives needs food to grow. That food may be as simple as nutrients needed to build parts to more complex tasks like storing and/or converting energy.
Different bacteria require different things. A nutrient source like beef stock contains lots of amino acids and proteins which can feed a large spectrum of bacteria.
Sugar is a densely packed energy store that many bacteria can use for powering biologic processes.
Gelatin is a mixture of peptides and proteins which adds even more nutrients to the system. More importantly, its thick gelatinous structure acts as a binding agent/ substrate which keeps everything from sloshing around in the dish (which can be very inconvenient when moving it around).
In short the simple petri dish is about providing a wide variety of nutrients so that it can support the growth of a wide variety of microbes.

"Converting" rather than "producing" energy.

You know you could just edit it for a point that small

i only edit my own answers.