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Are there lifeforms that have more than 2 sexes?
Are there any lifeforms on earth that have more than male and female biological sexes?
If so, are all three mates required for reproduction or is there something else going on?
If not, why not? There are species that have one sex and there are species with 2 sexes. I get some of the basics of why there are two instead of one, but would those benefits not be even greater if there were three sexes?

NOTE: I am of course only talking about sexual reproduction. I have no intention or desire to talk about transgender or LGBT issues nor am I wanting to make any points on the issue. This is solely a question about sexes in biology and not human social constructs.

Also, I am a computer programmer, not a biologist. Please forgive me for not knowing any of the terminology.

Would social insects, such as ants, qualify as having more than two sexes?

I'm not sure. Could you explain why it would? Again. I am not talking about social structures as much as I am about genetic reproduction. As far as I'm concerned, to have more than 2 genders (let's say three for example), either all three would need to be involved with the reproduction of offspring like we have with male and female humans. [ A + B + C = new life form ] or any of them can mate with any other and still somehow produce offspring [A + B --OR-- B + C --OR-- C + A = new life form].

Do you mean case where it takes 3 individuals for reproduction to happen? Or any two individuals from different sex would do? In the second case, the definition of sex (or gender) might become quite tricky.

Is there precedent for either case?

“There are species that have one sex” — No, by definition. There are sexless species. There are no species with a single sex.

@MakPo Yes, there’s precedent for the three-parent baby but it didn’t evolve naturally.

@KonradRudolph - I just read through the linked article. While it's really cool, it really isn't the same thing. I am really only wanting to know about naturally occurring sexes. In the article, there was one male parent and two female parents. It's really not the same, at least for my purposes.

@KonradRudolph - "There are sexless species. There are no species with a single sex." That brings up an interesting point. What is the difference between asexual and ?mono-sexual (if that's a thing)? There are simple multi-cell organisms that reproduce via mitosis (I think that's right) and there are some creatures where the female is able to produce offspring without a male (parthenogenesis). In in all of the cases of parthenogenesis, the species still have males, they are simply not always involved. Are there cases of species where they are 100% parthenogenesis and 100% females at birth?

@KonradRudolph there are single sex species but they are pretty rare, the new mexico whiptail is an example, it is a hybrid species both parent species have males but they do not, and they cannot reproduce with the males of the parent species. but the are capable of parthenogenesis oddly the females still have to "mate" with each other to trigger ovulation even though no genetic exchange occurs.

There exists something like multiple sexes in fungi, but it's a bit complicated.
First of all fungi don't actually have anything that represents the two classical animal sexes, phenotypically their reproductive cells are all equal (they have isogamic reproduction).
However there can be certain alleles in some fungi species (sometimes multigenic, sometimes not), that restrict sexual reproduction to other fungi with a different variant of that allele, these alleles are therefore called mating types. It is however important to note, that almost all fungi can also reproduce asexually (by basically cloning themselves).
In general all of the mating type systems always require only 2 individuals to (sexually) reproduce, it just can't be 2 individuals with the same type.
In their simplest form mating types resemble the male/female sex we often see in animals: for some fungi (e.g. yeast) there exist exactly 2 forms of the mating type allele (called a and $\alpha$), so basically they have '2 sexes' (though genetically/biologically the difference is MUCH smaller).
There are however also much more complicated mating type systems:
Some species of the Basidiomycota or Agaricomycotina groups have a tetrapolar mating type, which is composed of 2 independent alleles (with 2 variants per allele this would already results in 4 different 'sexes'). Additionally they can have many more than 2 forms for each of the alleles (up to hundreds), which leads to (ten-)thousands of different mating type combinations (or 'sexes').

@KonradRudolph Yeah I was adapting the to the terminology the OP used  - with the changes made to the questions I'll change gender to sex in this answer as well, since that is the better word in this context. Generally though fungi have neither a gender nor a sex, which is why the word mating type is used instead.

It depends on just what you mean by "required", but insects such as bees and ants sort of meet the criteria.
First, the double helix of DNA is inherently binary, so at the lowest level you need two and only two individuals for sexual reproduction.  However, the actual process in the world may require more types.
Take bees for instance.  There are basically three types of individuals in a hive: one female queen, which lays eggs, male drones which fertilize a queen (or try to), and then die, and neuter workers, which feed the queen, raise the eggs & larvae, and determine whether a particular egg will become a new queen or drones.
So for bees, only two types of individuals actually participate in sex, but all three types are required for the hive to survive and reproduce.

That very well just might be what I was looking for. Is the third type biologically different in that it is missing the sex organs of the other two? It's not just a situation where they are not aloud to breed due to enforced celibacy or something? By "neuter workers" are they born able to reproduce but castrated at birth or are they born neutered?

"First, the double helix of DNA is inherently binary, so at the lowest level you need two and only two individuals for sexual reproduction." - I'm not sure I follow. You don't get one DNA strand from your father, and one from your mother... While it seems excessively complex, there's no reason not to have three copies of each chromosome, one from each of three parents.

@gilleain - Why would that be beneficial? It would mean reproduction would take more participants, decreasing the possibility of pregnancy occurring. That is unnecessarily complex when two will do. "You don't get one DNA strand from your father, and one from your mother..." Well, basically kinda you do... You get one chromosome from mother, one from father.

@anongoodnurse I agree it wouldn't be beneficial! It is unnecessarily complex, but there's nothing theoretically binary about it. A chromosome is a double helix (plus chromatin, etc) so you get 2 strands from the mother and 2 strands from the father

@anongoodnurse It’s potentially beneficial in the same way that sexual selection reproduction is beneficial over asexual reproduction, in that it further increases diversity. Furthermore, it may even prevent specific issues with binary sexual reproduction, by decreasing the probability of recessive disease phenotypes. Of course there are diminishing returns and it’s unlikely to offset the vastly increased complexity of the three-way meiosis.

@KonradRudolph - It would not be beneficial if it decreased reproduction rate, which is a mighty important consideration.

@anongoodnurse We agree that on balance it’s probably a terrible idea. But it does have distinct advantages, they’re just outweighed by disadvantages. (Then again, consider that the three-parent baby actually does exist, albeit with a quite different mechanism than discussed here. So under specific circumstances, at least, we happily accept the hardships.)

@gilleain: Multiple copies of chromosomes is a step up from what I meant by DNA being inherently binary.  The molecule is a double helix, and in reproduction it (simplifying considerable) it splits apart and each strand is duplicated.  For chromosomes, having more than two of each (https://en.wikipedia.org/wiki/Polyploidy ) does happen, particularly in plants, where artificially inducing it is one way of breeding stronger varieties.  But there are still two parents...

@jamesqf yes, but the fact that dna has two strands is completely separate from the fact that sexual reproduction involves two parents. you don't get a strand from each parent, polyploidy or otherwise.

@jamesqf - fwiw, a small %age of female worker bees (they are not neuter scientifically speaking, I don't believe) can lay eggs, but only produce male offspring. Only the queen, who has mated, can produce male and female offspring. Tomato/tomahto...

Yes in many different way. No for a species in which all three are required at once.

there are species that have more than one type of male or female, each with drastically different body plans, this is called Alternative mating strategy. (African cichlid fish, cuttlefish)
Bacteria with up to 7 sexs are known to exist, each sex can mate with any of the other 6 but not itself. Tetrahymena thermophila technically these are called mating types.
Worms which have males, females, and hermaphrodites exist. Auanema rhodensis this is probably the closest you will find.

But there are no species that have three sexes that all need to participate. Part of the issue is logistics it is just harder to get three animals together than two, and there are far more ways to split a genome in half than into thirds for exchange and evolution is often a lazy tinkerer. There is also an issue with mitochondria since they mutate faster and differently they do not do as well with genetic exchange than nuclear DNA. it is better for a mating creature to only use mitochondria from one parent, a logistically that makes for two gender one with one without. There is also a statistical issue that three genders are not stable and drift can turn them into two genders rather easily.

I have trouble seeing 1 as different sexes. They are male or female with a different strategy I think. I like the other examples though.

As you describe, needing three sexes comes at an extra cost. And there is no benefit. Evolution makes short work of such a trait.

It depends on how you define sex, Alternative mating strategy is the most common of the options, but I agree it is probably the furthest from consideration.

There are some single celled organism that are considered to have more than 2 sexes but biologist generally call them mating types rather than sexes. One good example is Chlamydomonas. They use flagellas for mating and once their chromosomes is mixed in the fused cell, the cell undergoes meiosis to produce the next generation of haploid daughter cells. (See this Quora post).
A mushroom Schizophillum commune has two mating type genes, with one having over 300 possibilities and the other 64. This leads to a documented 23,328 distinct mating types. A S. commune individual would be capable of reproducing with just under 23,000 of these types. (See this Reddit post for a detailed discussion on this topic).
Clam shrimp have a male as well as two varieties of hermaphrodite, which either self-fertilize or mate with males but cannot mate with each other. The protozoan Tetrahymena thermophila has seven distinct "sexes" that can hook up and swap genes (See here).
See this biology.SE question and this worldbuilding.SE question for more information.


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Tensile strength of collagen?
Really specific question, but what is the average tensile strength of human collagen, type I? I've tried looking for it online, and either my google-fu skills are weak, or I'm just unlucky. Also, is there a specific database for mechanical protien data, or do I just have to look up each protien's tensile strength individually?

Measuring mechanical properties of proteins is REALLY hard, because you either need to measure individual proteins (which is afaik only possible with an atomic force microscope) or you need to assemble purified protein into a larger complex that is normally measureable, however single purified proteins often don't from physiological complexes.

@Nicolai, I'm specifically interested in scleroprotiens, but i don't know if that helps?

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Why telomere shortening slowing down cancer?
I am reading Alternative Lengthening of Telomeres in Mammalian Cells, about how telomeres linked to human cancers.

Due to the end-replication problem,5,6 the ends of linear chromosomes
  shorten with each round of DNA replication.7 In human somatic cells,
  the progressive telomere shortening that occurs with continued
  proliferation eventually results in the triggering of a replicative
  checkpoint. Telomere shortening and the structural changes that it
  presumably causes, leads to a DNA-damage checkpoint response at the
  telomere and induction of a permanent p53- and Rb-dependent growth
  arrest (i.e., replicative senescence).8-10 Because this limits the
  proliferative capacity of somatic cells, including those that have
  accumulated oncogenic mutations, telomere shortening and replicative
  senescence are a potent tumor suppressor mechanism.

The paragraph states a shorter telomere is a potential suppressor to cancers. Why is that? Why exactly a somatic cell proliferate slower with a shorter telomere DNA sequence?
Conversely, why a longer minority leads to human cancers?

Think about the 24 different linear chromosomes in a diploid human XY cell.  In the absence of active telomerase enzyme to repair the chromosome ends following one round of cell division, then every time that cell divides each end of each chromosome will get a little bit shorter.
If the cell keeps dividing indefinitely, like a tumor cell, the chromosomes are effectively shrinking.  Eventually this chromosome shortening will result in deleting actual genes (at first, 24 chromosomes x 2 chromosome ends = 48 genes).   Not all of those genes are essential for cell viability; and the distance, or length, of DNA between the telomere and the first gene on that end will be variable.  But as soon as the chromosome shortening removes part of an essential gene, then that cell will quickly die.
It would be like erasing the words at both ends of a sentence, one letter at a time.  In the beginning, someone else would still be able to make sense out of your sentence, but eventually they would not be able to fully understand what information you were trying to convey.
Most of the terminally differentiated cells in an adult human are no longer actively dividing, so it is not a problem, they don’t need active telomerase.  However, cancer is a condition of unregulated cell division, and so all cancer cells have to have some mechanism of repairing the ends of their chromosomes.  Reactivation of TERT (Telomerase Reverse Transcriptase, the protein component of the telomerase enzyme) gene expression is extremely common in cancer cells.

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Can cognitive functioning of the human brain change the physical state of the brain?
Can cognitive functioning of the human brain change the physical state of the brain? E.g. does self-awareness, self-reflection change the number of neurons or synapses among neurons? I.e. I am trying to develop self-modifying neural networks as described in my other question https://ai.stackexchange.com/questions/7966/dynamic-self-improving-self-modifying-neural-networks-which-can-simulate-goede and I am interested in the biological process that can be analogues of self-modifying neural networks. What determines the physical structure of the brain - number of neurons and synapses and are the cognitive functions among the determinants? I guess that generally the brains can be less developed matter comparing to the artificial neural networks that humans can invent or that can self-evolve in silica after sufficient period of time and that is why human brain can be more restricted in its self-improving capabilities than in silica ANNetworks. Similar situation is with genetic algorithms which can allow unrestricted number of sexes while biology has at most two sexes.

Your question has loads of unjustified assumptions.

There might be an answerable question buried in here (the title question is somewhat answerable), but it is obfuscated with a bunch of other conjecture that is unsupported and not helpful towards clarifying your question. If your interest is just in ANN, you should stick to ANN and understand that the connections with biology are analogies. If you want to learn about biological neural networks, you should start with a more basic understanding of neuroscience first.

One can invent lot of features for ANN, but I just wanted to be sure if there are analogies with biological world. Although I am not sure about value of such analogies, maybe existence of them gives some reputation to ideas and gives hint that this is path worth exploring.

@TomR Bryan is right; interesting though the metaphor is, the more you learn about machine learning and neuroscience, the more you realise the comparison is almost useless.

Also agree with @BryanKrause. Here is a link to a related answer of mine, although it deals with the case of a single biological neuron at the phenomenological level.

@TomR Biological networks can be motivation for trying new tricks in ANN, but the cost functions are very different for biology versus silica. Some computationally intensive artificial computations are done effortlessly in biology, and some biologically implausible approaches work great in ANN. We're far enough into understanding both that they have diverged: if you want to make a better ANN, study ANN. If you want to learn about biological neural networks, study biology.


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What is the difference between enrichment media and selective media?

Enrichment media
These media are used to suppress commensal bacteria while allowing the pathogen to remain viable and grow.
[Source: Ananthnarayan and Paniker's textbook of Microbiology.]

There is also an example of tetrathionate broth as enrichment media given in the book where tetrathionate inhibits coliforms while allowing typhoid-paratyphoid bacilli to grow.
For selective media it writes:

As in the above case (of enrichment media), if inhibiting substance is added to a solid medium, it enables a greater number of the required bacterium to form colonies than the other bacteria.

For this selective media an example of Deoxycholate Citrate Agar (DCA) for fecal samples is given.
The question:
What's the difference between enrichment media and selective media? Some answers give quite contradictory statements to the statement of the book like stating that "...it is designed to stimulate growth of many different types of bacterial species" for enrichment media.
I am also not able to explain myself as to how selective medium enables a greater number of the required bacterium to form colonies than other bacteria since inhibitory substance is also present in enrichment media?


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Light Hyperoxia
Imagine you're in some lowland way below sea level were the oxygen partial pressure is higher than at sea level but still lower than the 0.5atm limit. Would their be any effect that isn't deadly or harming even if you stay there for weeks but very uncomfortable like the light hypoxia when you're at 3000m and can't do any effort without fainting ?

Well you can imagine anything. But earth's atmosphere has a pretty consistent composition. The largest variation would be much higher humidity at lower altitudes because of lower temperatures at high altitude.


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Muscle layers of pharynx and gi tract
Why does pharynx have an internal longitudinal muscle layer and external circular muscle layer, while oesophagus and the rest of gastrointestinal tract have inner circular and outer longitudinal muscle layer?


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Among primates, is it true that homosexual behavior is extremely unnatural and uncommon?
I was recently reading a book published by some anonymous biologist known as Lynn Saxon, in which she appears to want to refute Christopher Ryan's thesis in Sex at Dawn that prior to the invent of agriculture, humans were presumably far more promiscuous and had sex not just for reproductive purposes.
In order to do this, she then goes on to show how, in the animal world, the great majority of all sexual activity is directed only towards reproduction. Another author, David Barash, says similar things: namely, that "evolution is very much about reproduction—variation in reproductive success is evolution".
However, homosexual behavior is anything but reproductive. Saxon appears to suggest indirectly that all such "non-reproductive" behaviors that are "useless from a evolutionary point of view" are rare and unnatural among primates, who are our closest relatives.
One more biologist, known as Antonio Pardo, says:
"Properly speaking, homosexuality does not exist among animals…. For reasons of survival, the reproductive instinct among animals is always directed towards an individual of the opposite sex. Therefore, an animal can never be homosexual as such."
Is this true? Is homosexuality really uncommon and unnatural among our closest relatives who are primates? Is sex mostly for reproduction?

If you feel like John answered, you can click on the checkmark next to his answer as to classify this question as "answered".

regarding sexuality previous to agriculture, tribal sexual practice and culture varies starkly and heterogeneously per tribe, some tribes are hyper sexual, homo, straight, cannibal, nonviolent, sadistic, spiritual, there is great variety in cultures, just see bhutan vs aztec, hawaiian vs european. ... In human history there is the book of the dead from Babylonian times, the epic of Gilgamesh, the 1001 nights, and the Greek cultural documents, which give a lot of information about early historical orgies and homosexuality. Generally, humans tribes are dominantly heterosexual.

First Antonio Pardo is not a biologist, he is a professor of bioethics and his degrees are in medicine and philosophy.
Second, Clearly he does not know anything about primates, since there is one famous great ape that has sex even more often than humans do, the Bonobo. Bonobo have sex for everything, hello, goodby, conflict resolution, social bonding, ect. Bonobo engage in homosexuality and a hundred other sexual practices, including some things humans can't do, like penis fencing. Bonobos along with chimps are also our closest living relative.
As for other animals there are hundreds of examples of homosexuality in nature. I hate using all these wiki links but this is such general biological knowledge I would need either dozens of links or a link to a textbook.
As for Lynn Saxon, first let me say she does not have a degree in anything, It is possible Lynn Saxon is not even her real name.
Now for her argument, it is true that in nature sex is most often directed towards reproduction (that is why it evolved in the first place* and just consider how many sexual animals have very simple behavior), but as I have pointed out there are notable exceptions one of them our closest relative. And not just homosexuality, masturbation is observed in nature as well. Also consider monogamy is also extremely rare in nature with the exception of birds, arguing humans should behave based on how other animals act will not help their argument. It is also a common fallacy, what is natural and what is ethical are not related, Sanitation, science, religion, medicine and reading are also not natural.
If you want to read more about humans and our relatives I suggest the book (the Third chimpanzee" by Jared Diamond as a t least a good starting book.
"Wild Connection" by Jennifer L. Verdolin is even better, both have actual degrees in biology.
*Of course your legs originally evolved as fins,  so what something starts as is not necessarily what it is used for now.

"As for Lynn Saxon, first let me say she does not have a degree in anything, It is possible Lynn Saxon is not even her real name." How do you know that she doesn't have a degree in anything? And yes, OP said: "book published by some anonymous biologist known as Lynn Saxon", so yes, according to OP she is anonymous and it appears not to be her real name.
As for Bonobos being homosexual. It depends on what you mean by homosexual precisely. See my answer that attempts to clarify this point. Other than, I agree with your answer, and I think the answer is good.

Because she hasn't claimed one, and may not have even be using her real name. Degrees and expertise are not something you get the benefit of the doubt on.

No, degrees are something you either have or you don't. I know many people who don't talk about their degrees despite having one. The fact that they don't mention their degrees doesn't mean they don't have one.

talk about is not the same as publish a book on the subject.Sure it is hypothetically possible she has a degree in something, but the default position and only reasonable way to consider her words has to be she does not unless she demonstrates otherwise.

First, let me say that there are vast amounts of criticism toward the book Sex at Dawn by experts on the topic of the evolution of human sexuality, but generally for reasons other than homosexuality. See here. But that's not what you're really asking about.
I believe there is possibly some miscommunication going on here. Some of the statements in the question, I think, are true and makes sense. Some statements are not totally clear, and the answer depends on how exactly they are interpreted. Others are wrong. Let's see.

In order to do this, she then goes on to show how, in the animal world, the great majority of all sexual activity is directed only towards reproduction.

It is possible that this is true statistically. I'm not sure. However, there is certainly many examples of non-reproductive sexual behavior. See the Wikipedia article: Non-reproductive sexual behavior in animals. One obvious example is the Bonobo.

Another author, David Barash, says similar things: namely, that "evolution is very much about reproduction—variation in reproductive success is evolution".

This statement I think is far more reasonable. It is true, in the ultimate sense, that the main purpose of sex is reproduction. And behavior that increases the probability of reproduction is going to be selected for. (Technically, it would be more true to say that natural/sexual selection is about variation in reproductive success. Evolution contains more than selection, for example drift).
However, homosexual behavior can easily arise naturally in the animal kingdom, especially as a side-effect. One way this can happen is the following: feeling pleasure through sexual stimulation is adaptive, because this increases the probability that individuals engage in sexual behavior, which ultimately leads to more offspring. However, as a side-effect of sex being pleasureable, this means that animals may engage in sexual behavior that is non-reproductive (e.g. homosexuality or masturbation).
As long as non-reproductive sexual behavior is not done to the exclusion of reproductive sexual behavior, there is no reason to suspect that the non-reproductive sexual behavior negatively affects reproductive success (and hence, non-reproductive sexual behavior can perfectly well exist).
Despite the original ultimate reason for sexual behavior is to facilitate procreation, sexual behavior may even possibly become adaptive for reasons other than procreation. For example, it may start facilitating social bonding.
This naturally leads to the following problem, when looking at the following quote:

"Properly speaking, homosexuality does not exist among animals…. For reasons of survival, the reproductive instinct among animals is always directed towards an individual of the opposite sex. Therefore, an animal can never be homosexual as such."

When asking whether homosexuality is common in nature, we need to define precisely what we mean by homosexuality. If a human man says that they're homosexual, that can mean several things. It may be that they are attracted to mostly men, or both men and women, or only men. If they are attracted to only men, they are, what I would call, strictly homosexual. If given free choice they would in a majority of situations prefer to have sex with another man, I would call them primarily homosexual. In this sense, our Bonobo male friends are typically neither strictly homosexual or even primarily homosexual, because a male that engages in homosexual behavior is also willing to engage in heterosexual behavior. Strict homosexuality or primary homosexuality does appear to be quite rare in nature (although there are some examples known. For example, in rams a few percent seem to prefer same-sex even when given the choice). In the quote, when they say 'properly speaking' they may be talking about what I have denoted strict homosexuality. The quote is a bit hard to interpret. If they simply mean homosexual behavior, then no, that is not particularly rare.

Is this true? Is homosexuality really uncommon and unnatural among our closest relatives who are primates?

Strict or primary homosexuality is uncommon, homosexual behavior is fairly common (and therefore clearly not extremely unnatural).

Is sex mostly for reproduction?

In the ultimate sense, the original and most important purpose of sex is reproduction. But as I've detailed out, non-reproductive sex can still easily arise without it negatively affecting fitness. It may even possibly become adaptive (if it is not done to the exclusion of reproductive sexual behavior).

I would hesitate to claim what the most common form homosexuality humans engage in without evidence. research shows such forms of homosexuality are actually very rare, https://www.tandfonline.com/doi/abs/10.1080/15299716.2014.929553?scroll=top&needAccess=true&journalCode=wjbi20 and https://yougov.co.uk/news/2015/08/16/half-young-not-heterosexual/

@John I think you misunderstand what I meant. Perhaps I didn't communicate myself properly. I am not saying that the most common non-heterosexual orientation is strict homosexuality. I am saying that when people say that they're homosexual, they tend to prefer only or mostly their own sex. Otherwise, they tend to use another term ("bisexual", "queer", etc). I completely agree that strict homosexuality is not the most common form of non-heterosexual orientation.

@John Nevertheless, it is also not important for my answer whether which type of homosexuality is the most common. My only reason for making the term 'strict homosexuality' is to make the answer more clear, and to adress the fact that some types of non-reproductive sexual behavior exists and are more common than other types. I have edited my answer to remove emphasis of which type is more common (because it is not necessary for my answer).

And again studies show otherwise people do not identify in those ways consistently or reliably, it is a bad assumption to make.  Additionally strict homosexuality is  mostly irrelevant since it is the quoted authors are not defining homosexuality that way.

@John No, what is irrelevant is how common strict homosexuality is. It still is worthy of clarification. If the authors don't define homosexuality that way, then even better that I clarify exactly what I mean with each term. You don't have to go to strict homosexuality, but just preferred sex. If a man in more than 50% of occasions will prefer to have sex with another man rather than a woman given free choice, you could call him 'primarily homosexual.' Primary homosexuality is also not common in the animal kingdom, although as I discussed there is some evidence for it (in rams, in particular).

To make your life easier you could use the kinsey scale. It is a bit oversimplified but it is also heavily used.


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History of plasmid maps
To create a small history of visual representations in biology, I am seeking the earliest published papers or books that have used plasmid maps as figures ; or strategies to effectively search for these publications.
I have examples like this one (from the 1977 publication presenting pBR322), but as it seems quite modern looking, it may be that earlier examples exist.

I spent an hour trying to follow this one up, without much sucess. My feeling is that, although there must be earlier figures, you are unlikely to find anything for plasmids before 1970, because the advent of restriction enzymes was an important tool in mapping them, because the idea of plasmids emerged only slowly, and because the plasmids from which pBR322 was derived were much larger and more complex. Sorry not to be more constructive.

Thanks for your insight. I think I will follow the restriction enzyme lead, maybe show early restriction maps, then skip to "modern" plasmids.

I imagine you have already considered this, but the switch from genetic maps to physical maps might be worth looking at. There were clearly quite detailed (if incomplete) genetic maps of E. coli, and  I remember in the early 70s that there were genetic maps of E.coli ribosomal RNA genes, that were partly physical, because the sizes of the precursors and mature species could be estimated by sucrose density gradient. The problem with the wild plasmids is that although you could say they contained, e.g. a drug-resistance gene, you couldn't easily map its position with respect to anything else.


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Genotype-Phenotype evolution distinction
I understand the difference between the genotype of an organism and the phenotype of an organism, (genotype being the genetic code, phenotype being the physical expression), however I am unsure about what this figure mean when it says "Selection that takes place in the environment is based on the specific phenotype of an organism-its traits, not the underlying genotype".
(misconceptions about evolution)

I thought the genotype controlled the phenotype, so what does the figure mean exactly when its saying that natural selection isn't based on the genotype?
Thank you!

See my comment on Remi.B’s answer below.  To say that the genotype controls the phenotype is true to a first approximation.  It would be more accurate to say the genotype at one locus influences the organism’s phenotype, because the cumulative affect of the genetic background also influences that phenotype.  Hence, there are people walking around carrying one or perhaps even two alleles of mutations linked to specific diseases, yet these people have no disease symptoms (and may never develop them).  Of course there are other mutant alleles with 100 % penetrance and expressivity.

The difficulty is in the semantic. In the sentence

Selection acts on the genotype because that is what is inherited

it is unclear what is meant by "acts on". The point that the author(s) of this misconception were probably trying to make is that what define the reproductive success of an individual is the phenotype of an individual. In other words, it is the expression of those genes that affect the probability of the genes to be passed on but it is not the actual genetic sequence itself (or at least less directly so).
Let's assume a haploid case where at a given gene, allele A means 'tall' and allele B means 'short' and let's assume that size matters in defining fitness. It is ultimately not whether an individual carry the allele A or B that matters but whether the individual is tall or short. If by some fantastically random event there is an individual with allele B that is tall then this individual will rather have the same fitness as the tall individuals and not the same fitness as the B carrier individuals.

Alleles can have variable penetrance, and variable expressivity.  In a diploid species consider the heterozygous individuals all carrying the same dominant allele, or m/+.  If all of those hets display the mutant phenotype, then it is 100 per cent penetrant.  However, if only some of the hets display the mutant phenotype then the allele has variable penetrance (that you can likely measure).  Similarly, among all of the hets displaying the mutant phenotype, there may be different degrees of severity, so the allele could have variable expressivity.  Same can be said for recessive homozygotes.

Of course. Never did I meant that there is a one-to-one function between genotype and phenotype. I would agree that my answer is a bit poorly phrased. I've had a hard time to write a pleasant to read answer here for some reason!

I almost started my comment with “You probably know this . . . “


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What kind of sieve does one use to extract meiofauna?
Suppose I have a core of sediment, and I want to extract the meiofauna from it, in order to study these organisms. According to the sources I could find, this involves using a very fine (e.g. 45 μm) mesh that will filter out and retain the meiofauna (as they are larger than this e.g. 45 μm that I mentioned earlier, and so, will remain on the mesh).
I have found lots of information on the mesh size, how many μm it should be, etc., but barely anything else about what kind of sieve should be used.
So now, if I want to buy a sieve to use for extracting meiofauna, I don't know anything about what it should look like, except the mesh size. What should I care for besides that, if I want to buy one? Can I just buy any laboratory sieve provided the mesh is of correct size? Or do I need some special kind of sieve to conduct such study?


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Strange insect identification
Tonight I have found this new friend flyng inside my home. First time ever I sea something like this here in the north East of Italy

That is an Oleander Hawk Moth, Daphnis nerii. Order Lepidoptera,family Sphigidae. https://en.wikipedia.org/wiki/Daphnis_nerii


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What confuses me about "homologous gene"
When I first encountered homologous genes I thought those genes are identical because the text book said so, and "homologous" meant the same knowledge.
But as I studied along, it comes out that diploid is a two sets of haploid, each from mom and dad.
This means they are not identical, doesn't it? How could they be "identical" since they are from mom and dad seperately?
If they were identical, crossing over during meiosis loses a point(mixing chromatids is meaningless if they are "same").
Then, when the text book says homologous genes are identical, what identical trait is the text book referring to?

I wonder which textbook would say that homologous genes are identical. They are not. Homology has to do with common ancestry.

Can you please directly cite your textbook. Either your textbook is wrong or you massively misinterpret it.
The concept of homology refers to the concept of shared ancestry. From wikipedia

In biology, homology is the existence of shared ancestry between a pair of structures, or genes, in different taxa. A common example of homologous structures is the forelimbs of vertebrates, where the wings of bats, the arms of primates, the front flippers of whales and the forelegs of dogs and horses are all derived from the same ancestral tetrapod structure.

I would add that a common counter example are bats wings and bird wings (which is an analogy).
Two genes are homologous if they both derive from the same ancestral gene. Of course, as ultimately, all genes are related, the concept only make sense by comparison to other structures that are more distantly related or relative to a time point in time.
For more information, just have a look at any good introductory course or textbook to evolutionary biology (for example evo101 > homology)

The question asks about "homologous genes" but the question body mentions meiosis and chromatids.  The latter suggests you are really referring to the concept of "homologous chromosomes". These two terms are used in different contexts in biology to refer to somewhat different concepts (despite the fact that chromosomes contain genes).
Homologous chromosomes are two chromosomes which, although not identical, are highly similar so that they pair up during meiosis and participate in crossing over.  If the textbook says they are identical, that is incorrect; they are mostly, but not entirely, identical.

I also believe that the OP was referring to homologous chromosomes and not genes since he talks about haploid and diploid.


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Is hydroxyproline an amino acid? (Classification question)
So I know that hydroxyproline is created from proline via hydroxylation as a post-translational modification. I also know that proline is considered an amino acid. However, once you hydroxylize it, you have made a covalent modification to the original amino acid. Can hydroxyproline be correctly considered an amino acid? Or is it simply an amino acid derivative and NOT an amino acid?
Or, a more general question - how much can you change an amino acid and still call it an amino acid?

The other commenter answered correctly that proline is an imminoacid, not an amminoacid. But in biochemistry it is referred to as amminoacid since it basically works like every other amminoacid in any polypeptyde.

how much can you change an amino acid and still call it an amino acid?

Have a look at:

Selenocysteine
Ornitine

As you can see there are some weird modifications of amminoacids in biology. Just like proline/hydroxyproline any amminoacid can be very well modified and be used in proteinogenesis or non-proteinogenesis. Every modification of an amminoacid is allowed, and it will still be considered an amminoacid, even if it doesn't make up a protein. The only parts which can't be changed are the COO- and NH3+ groups, obviosuly, since they give the name of the molecule: "ammino" means that it has a NH group and "acid" means it has a COO- group.


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Please give information about this insects

I took this photo of a small insect which I found near to my house (Maharashtra state, India). What insect is this?

Welcome to Biology.SE! Take the tour to learn about this site and earn your first badge. Also, you have to tell us where and when this photo was taken in order to increase the chances of identifying this insect.

It is definitely a member of Membracidae. A treehopper. Order Hemiptera.

It looks like an insect belonging to the family Cicadidae. Further information is needed to identify this cicada species.

@SachinPrabhu I'm not sure about my answer, where did you find the insect exactly?

In India state Maharashtra where

This isn't a Cicada: it's a treehopper (family Membracidae) but not knowing the Indian fauna of the family I can't go any deeper.


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

He is Shikra (Accipiter badius) in India worldwide he is goshawk

Looks like Butastur indicus, the grey-faced buzzard. The spotted breast and the greyish chin fit well.
A nice picture can for example be seen here


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Why is 450 nm monochromatic light perceived as blue or violet depending on its intensity?
Trying to do some color matching I purchased a 450 nm laser. I expected monochromatic light of this laser to have similar properties to those of all others I've already played with — 808, 640, 520, 405 nm — in that they all cause an unambiguous color sensation.
But when I shined it onto my wall (having removed the lens), I was surprised to see something unusual. In the center, where the intensity is high, it looks as "very blue" — much like those 465 nm blue indicator LEDs we can see everywhere today, only more saturated. But on the sides, where the intensity falls off, the color looks like violet! When I shine this laser on a ceiling obscured by a wall, I see its reflected light as violet. When I move the spot so that the reflected light becomes more intense, I begin to see it as blue again in the intense areas, and still violet in dimmer ones.
I've checked with a spectrometer, and there doesn't appear to be any fluorescence in the light spot to confuse me.
Interestingly, if I increase amount of ambient lighting (white LED lamps + CCFL ones), sensation of blue once again transforms to violet. Also, the "very blue" intense spot looks violet in bright sunlight, although I can make it blue again by focusing into a smaller spot to make it brighter. In a fully dark (apart from the laser) room I still do notice the violet areas on the sides of the spot.
405 nm light also seems a bit silvery-whitish when its intensity is high, unlike at low intensity. Maybe it's the same phenomenon, which I simply didn't notice before because the tint is not that blue in this case.
In both cases of 450 nm and 405 nm the additional color on high intensities is still "shiny" due to the speckles specific to high monochromaticity, so this indeed doesn't look like the result of fluorescence of the objects I shine the light to.
I've asked several people whether they see it the same, and they answered affirmative.
I suppose it's not related to color balance, because I only changed the intensity of ambient light, not the tint to observe the changes in color. Especially it shouldn't be due to color balance since I can simultaneously see different colors in the areas with different intensities.
Interestingly, while I thought the "very blue" color to be the main color of 450 nm, CIE 1931 XYZ value for it, converted to sRGB, appears to be (if we desaturate and normalize to fit in sRGB range) (0.43,0,1), which is purple, not blue.
So, what is going on here? Is it a well-known phenomenon? Could it be due to some fluorescence of the retina itself rather than the objects lit by the laser?

This is a general feature of human perception of blue-white mixtures. It's known as Abney effect. It's not limited to highly monochromatic blue colors (not even to blue colors). We can observe this blue-related phenomenon even with longer wavelength light than 450 nm – e.g. sRGB blue, whose dominant wavelength is about 464 nm. Here's what most people would undoubtedly call blue – in HTML notation #0000ff:

And here's a mixture of 60%† white with 40% blue (in HTML notation #cacaff):

To me, if I haven't stared at shades of truly violet a few moments ago, this mixture seems to have a considerable amount of violet — more than I'd expect looking at the primary blue. Naturally, shorter wavelength light should give even more violet perception, until it becomes violet even in its pure form.

† Percentage is given in linear scale, actual color presented is gamma-corrected to be displayed on sRGB monitors.

Your examples are useless: the first square is not monochromatic if produced by a computer display. It is not laser light.

@Anixx it's not required to be monochromatic. It's good enough to be indistinguishable from monochromatic+{a bit of white}. This perceptual feature is not limited to monochromatic light — I just don't have access to 450 nmD LEDs, but do have 450 nm lasers.

This merely corroborates the experience but is in no way a bioengineering or biology explanation.
If you stare, at arm's length, at any discrete colour 5mm LED of high brightness, it's colour will appear to shift after a few minutes. This is not the (scotopic/photic) night vision effects from Cones to Rods towards blueshift but rather the cone's protective response to the high-density stationary colour indicators and makes that spot less-sensitive.
Also if one often stares at the bright ceiling or street lights for several minutes, then look away, they will see a remanent ghost image with that previously dominant spectrum now suppressed so it will appear in the inverse pastel colour.
It appears as the spectrum has been diminished in that spot,  because it has, by a reduced sensitivity of the cones in the eye for detecting that spot of light. The recovery time is about the same time or a bit more as it takes to react.  The human retina contains about 120 million rod cells and 6 million cones .
This may be safe as long as the light is not held too close to the eye and certainly not looking into a direct laser beam, rather a diffused image.
Even some 5mm LEDs at 20mA can be so intense as to be painful quickly at arm's length with >20,000 millicandella luminous intensity measure by std methods. But it only needs to be as bright as an auditorium ceiling light intensity for this example of color-shift to occur.
 Added
Each depends on the spectrum of dominant and sub dominant peaks in the spectrum that results in the apparent shift in appearance. The 450nmD must  have this sub dominant spectrum in an otherwise monochromatic spectrum for this affect to occur.  Because our eyes are logarithmic yet spectral densities of monochromatic light sources are displayed on linear scale, it is often not reported.  I.e. there must be some red 6xx nmD spectrum for this blue to appear to become purple when our eyes attenuate the blue after a period of intense viewing for several minutes.

I don't think this mechanism is the same as that observed in the OP: the one you're describing relies on an afterimage to distort colors. It'll make a "wrong-color" point or line in the visual field. But the OP is about the light which is not intense enough to make a prominent afterimage. It's easy to look away from the blue part of the 450 nm light spot and see violet in the same part of the visual field (i.e. same part of the retina), without any ghost color spots. So I think that color shift mechanism is different.

I reported both examples which are similar electrochemical responses yet different.  Staring at a  right Yellow LED with some orange red spectrum will shift towards that spectrum because the 592nmD wavelength is attenuated. Or the 420 nmD wavelength is attenuated and the lower level broad spectrum  6xx nmD reddish spectrum becomes purple in the net mix. Each depends on the spectrum of dominant and sub dominant peaks in the spectrum that results in the apparent shift in appearance.

nmD is the dominant wavelength of CIE eye corrected nmP peak wavelength of emitted light. This due to our sensoral bandpass filter slopes spectral response of our eyes is centred around 525nm green and the slope shifts the peak towards green and our brain equalizes these RGB sensors to become a flat white response.

Well, the OP is about a laser, not a LED. The laser I'm testing has FWHM about 2 nm (or less, I'm limited by resolution of my spectrometer). There can't be much difference between nmD and nmP there.

There is ALWAYS a difference nmD vs nmP if it is not green 525nm . Any expert EE in filter analysis understands the effect of spectral peak shift due to bandpass filters. (in this case our eyes)  Also the same effect occurs in yellow (AlInGaAs) LEDs so it is a valid analogy.


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Larva attacking frog ? Guide about this

The above picture was taken in western forest of India where a larva attached itself to a frog neck. What is it and how it will effect the frog?

Maybe an Epomis larva? Just based on the fact that it's attacking a frog. It is not supposed to exist in India, but it does range as far east as Tajikistan, so maybe it's plausible.

Actually it seems there have been two records of Epomis in India.


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Examples of plant families that contain species that are safe for human consumption and species that are poisonous to humans?
I am trying to make a point to someone that just because two plants share a family and one plant is safe for human consumption, it does not follow that the other plant also is safe for human consumption. Can anyone provide an example I can use as proof?

Well, given that often enough a plant is considered "edible", while parts of THE SAME PLANT are already poisonous (see the potato), it stands to reason that the definition of "safe for human consumption" is far too lax of a term to even allow for a clear "no there aren't any". [Also there's a ton of counterexamples, like Byans below]

"family" in itself is such a borad term, that even a pure explanation to what a plant family is accidentallly provided an answer to your question:
https://www.maximumyield.com/definition/785/plant-family
[it's the nightshades again though, but this shows how valid your point is]

The most classic example if you want to win this argument would be the family Solanaceae.
Also referred to as the Nightshade family, it includes the deadly nightshade or Atropa belladonna and many other plants not safe to eat.
Other members of the family are tomatoes, peppers, potatoes, and more.
Plant families can be massively diverse, and toxicity doesn't really have much relationship to family. Most of the compounds that are found in plants that are toxic are found in other non-toxic plants as well: dose is crucial.

Potato is also an example of a plant that is considered non-toxic, but parts of the plant are toxic and - even worse - the tubers can become toxic.  The green parts (leaves, stems, etc) contain a poisonous alkaloid.   If a potato in storage starts to sprout, the sprouts and eyes are often toxic.   If the potato itself enlarges while sprouting, it will also typically have elevated toxicity.

@Peter: Another common example is rhubarb.  The stems are edible (at least when cooked), but the leaves are toxic due to concentrations of oxalic acid.

I believe that if the potato tuber is exposed to sunlight as the plant grows, it will also become green and poisonous, like the leaves.

Indeed, not just potatoes - tomatoes are toxic as well (leaves, unripe fruit...), and arguably, so are peppers (not "deadly" toxic, but the capsaicin is definitely another thing "designed" to make mammals avoid eating the fruit; it's not spicy to birds, who are the primary dispersers of pepper seeds) and eggplant (though that one has been pretty effectively domesticated to be safe as long as it's not raw). But it still definitely counts as "safe for human consumption" as long as you avoid the poisonous parts.

Mmmmm...fried green tomatoes! So cooking eliminates the toxicity of unripe tomato fruits, @Luaan?

@DennisWilliamson It doesn't seem to - even deep frying isn't enough to destroy the solanine (and tomatine, while also an alkaloid, doesn't seem to be dangerous to humans); you'd need 10-20 minutes at ~210 °C to decrease the content significantly. Most likely, there simply isn't enough of the toxin to do any significant damage (far less than in potatoes). All I could find is one death from tomato poisoning, from a tea made out of tomato leaves. You'd probably need to make a salad out of tomato leaves to be in significant danger.

The Apiaceae family has many edible plants including carrot, parsley, fennel, celery, and parsnip, and has toxic plants such as poison hemlock, fool's parsley, and giant hogweed.

Both the cashew and poison ivy are members of the Anacardiaceae family.

For what it's worth, part of the cashew plant is actually lethally toxic as well.

@AustinHemmelgarn which parts are toxic? Any sources?

The shell of the nut itself,, which is why they're almost always sold with the shells already removed..  Just like poison ivy, it has oils that cause contact dermatitis, and if ingested can cause potentially lethal internal reactions in the digestive tract.  Also like poison ivy,, the smoke from burning the shells is really dangerous because the oils don't completely combust.

The poison ivy, oak, and sumac all used to be in the genus Rhus alon gwith edible sumac used as a spice.

Fungi are not plants and you've tagged this as botany, so this is perhaps off-topic, but I feel like it might help you make your point: the genus Amanita contains extremely toxic species (A. phalloides), highly regarded edible ones (A. caesarea) as well as psychoactive ones (A. muscaria).

While all the other answers have described one plant family having both edible species as well as poisonous species, I am compiling all the families in one answer.

Anacardiaceae

Mangos (Mangifera indica) and Cashews (Anacardium occidentale) belong to Anacardiaceae, and also the poisonous Sumacs (Rhus spp.).

Apiaceae

Carrots (Daucus carrota), Parsnips (Pastinica sativa), Dill (Anethum graveolens) and the poisonous Poison Hemlock (Conium maculatum), and Water Hemlock (Cicuta spp.)

Apocynaceae

Milkweed (Asclepias spp.) and the poisonous Dogbane (Apocynum spp.) is commonly known as the poisonous relative of Milkweed.

Ranunculaceae

Marsh Marigold (Caltha palustrus) and the poisonous Buttercups (Ranunculus spp.)

Solanaceae

Food crops like Potatoes and Tomatoes and deadly poisons like Deadly Nightshade (Atropa belladonna), Jimson Weed (Datura spp.) etc.
References

https://survivalcache.com/5-poisonous-plant-families-the-survivalist-should-know/
http://www.botanyeveryday.com/online-classes/2013-plant-talk-8-poisonous-plant-families
http://mentalfloss.com/article/69254/8-edible-plants-potentially-deadly-doppelgangers

This would be better as a community answer.

See Prunus Dulcis: bitter almond vs. sweet almond – contains enough cyanide that "approximately 50 bitter almonds" will kill an adult and "5–10 bitter almonds may be fatal" for children.

Many common names are reused for different plants. This is true for "buttercup" which is also used for daffodils and pink evening primrose. Thanks for including the binomial.


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What's the decomposition rate of a mammal at -20 Celsius?
Is there any where to predict it without thawing? In terms of measuring it.
What if the body was immersed in sugar prior to freezing?

What do you mean by decomposition rate, if you mean rot then the answer is none, if you are talking about other effects that would fall under taphonomy and it will be extremely slow.

Cell apoptosis.

Zero, apoptosis is programmed cell death, it does not occur in frozen tissue, do you necrosis?

Does necrosis happen then?

At -20,chemical reactions and biological activity of microbes is nearly static. The mammal can get dehydrated if the ambient humidity is low, they freeze dry animals in cold temperature, If the animal is protected from humidity fluctuations, the DNA can last 100,000 years. They just revived nematodes found frozen in ice for 40,000 years, they are multicellular.

@com.prehensible Thanks for the answer but this should not be right, i ve spoken with a specialist and was told that cell still undergo apoptosis because they are starved to death. The cells that survived being frozen.

Take a look at the frozen carcasses of mammoths and dire wolves found in the permafrost regions of Siberia... Freezer burn happens quite frequently... the outer layers of soft tissue will start drying out.
Some even say that mammoth meat was eaten at a conference in 1951
If this is true or not... A mammal carcass preserved at -20 degrees can last long... very long.
I recently thawed a crocodile, which was frozen at -20 degrees since 1986... Except some freezer burn and shrinkage of the meat within the hard and partly ossified skin, you wouldn't even think that it was frozen for such a long time.
Adding sugar decreases the freezing temperature of water and the freezing process will take longer. Given the fact, that you have -20 degrees during this step, too - nothing will happen with the carcass.
So: no rotting, no necrosis, but: long time freezer burn

Thanks for the answer but this should not be right, i ve spoken with a specialist and was told that cell still undergo apoptosis because they are starved to death. The cells that survived being frozen.

Apoptosis is not decomposition. you said Decomposition rate. the answer is - virtually no decomposition. If you want to ask about apoptosis of the cells at -20, write a new question. The cells wouldn't undergo apoptosis because they starve. they don't consume any energy at -20 so they don't respire and starve. if they cells survive they don't decompose.

com.prehensible is absolutely right. Apoptosis is not decomposition. You asked about decomposition - I answered the question about decomposition. Please tell me where my answer is incorrect regarding your question about decomposition of a body at - 20 degrees

@JulPal For some reason I don't get notified when I get a reply. I thought that decomposition includes apoptosis.


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Can anyone identify this spider? Found in Italy
My cousin found this spider at his place. He lives near Milan, Italy, in a small town. It's a humid region, around there the are a lot of fields but it is a 15 km from the city. It's still hot in these days. He told me that in the picture it seems a little bit too yellow. In reality it is more of an orange shade. He has never seen anything like that around there. Any clues?

Is there a spider somewhere on the second picture? I can't see it!

No, it's just to give a rough idea of the dimensions

Oh ok! You might want to just state something like about 6cm in diameter (legs included) or something.

@Gitana Yes please give a number, we don't know the size of your hand.

Judging by the photo and the web it may be an orb-weaver spider of the family Araneidae.  Orb-weaver spiders get their name from the circular webs they spin.  It's possibly an Araniella cucurbitina, also known as a Cucumber spider, which are commonly observed hanging head down in it's web.  Several photos can be found at eurospiders.com.

If I understand well, the Araniella cucurbitina seems smaller than my cousin's spider. I read that it measures at most 1 cm, whereas the spider he found is several centimetres long

@Gitana Is your cousin maybe exaggerating a bit for dramatic effect? The perspective of the picture might be a bit confusing but "several cm" might be closer to 2 cm, with the body about 1 cm.

It looks like marbled spider. Araneus marmoreus, commonly called the marbled orb-weaver, is a species of spider belonging to the family Araneidae. It is sometimes also called the pumpkin spider from the resemblance of the female's inflated abdomen to an orange pumpkin.[2] It has a Holarctic distribution.


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How can biologists rule out multiple early organisms that went through conjugation?
The current idea is that all life evolved from a single cell. Analysis indicates the probability of two different origins being very unlikely, given shared DNA. However, why couldn't numerous organisms have evolved and then conjugated, with a few lineages surviving? It would vastly increase the odds of modern organisms sharing the DNA that they do.

Because they would not use the same DNA codons. Codons are extremely conserved across life, with only minor variations, there is no reason this should be the case unless those codons are inherited from a common ancestor. This is contingent on what you mean by organism, prior to the incorporation of ribosomes it would be more possible.
If what you suggest had occurred it would drastically DECREASE the odds modern organism would share the same DNA.

How many different collections of codons would be useful for encoding genetic information in an environment in which life evolved?

Another thought: if different systems of codons existed in different lineages, wouldn't that decrease the probability of conjugation so that if any cells did go through early conjugation, they were likely with similar codon systems?

they would have to have identical codons to fuse, the likelihood of separate lineages ending up with identical codons is close to nil. multiple codon lineages could and likely did existed but only one of the contributed to existing life.

Could you provide some data to that effect? Again, how many different systems of codons function reasonably well in the environment in which abiogenesis likely occurred?

Also, are you talking about the codons or the nucleotides themselves?

codons although it could also apply to nucleotides. Codons are arbitrary so any of them would work, but they would not be compatible, organism with different codons could exchange DNA but they would be complete gobbledygook to each other. https://link.springer.com/article/10.1023/B:BIPH.0000024412.82219.a6

Not all organisms do share the same codon configuration. And "gobbledygook" might not necessarily be detrimental, so it could be added in as a plasmid, and eventually come to serve a function. I'm just not convinced that the codon argument is sufficient, but I do appreciate the answer. Thank you.

could and at all likely are different things, very few things can ruled out entirely.


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Who are Ursprungliche Eukaryoten?
The school textbook of my daughter (the textbook is written in German) describes the five kingdoms of life: prokaryota, plants, fungi, animals and "Ursprungliche Eukaryoten". These are defined as "single cell organisms with real nucleus and other specialized organoids, both autotrophs and heterotrophs". No Latin name is given.
I am somewhat confused, as I know that there are both multi and single cell varieties between algae, and these used to belong to even particular taxon within algae (a single cell Rhodella, for instance, not just belongs to plants but also specifically belongs to red algae). Also, there are unicellular fungi like yeast that used to be fungi (and, OK, protists used to be a separate group that probably also belongs to "Ursprungliche Eukaryoten"). Are they all pulled out of they groups into this new kingdom in this system?
The summary of the proposed classification schemes over history can be found at https://en.wikipedia.org/wiki/Kingdom_(biology)#Summary . Which scheme, if any does this taxon correspond? Is something missing in that table?
The textbook is Training Gymnasium - Biologie Mittelstufe Band 1, Harald Steinhofer (2013), ISBN 978-3-86668-709-7, seen here. The description in question is on the page 16.

It is natural to be confused because the consensus has changed over the years and is still not settled.  In part this is because knowledge has been gained but remains incomplete, and in part it is a matter of opinion and aesthetics about what is best for usefulness at various levels of detail and understanding.
The system put forth in the textbook seems to best match the system Whittaker put forward in 1969.  His Monera is the text's Prokaryota, and his Protista corresponds to the text's Ursprungliche Eukaryoten.  Essentially Protista/Ursprungliche Eukaryoten is a catch-all for all Eukaryotes not included among the Plants, Animals, and Fungi.  There may be some variations in which of the eukaryotic algae are included among the Plants versus the Protista/Ursprungliche Eukaryoten.
It should be noted that in most or all systems of "Kingdoms", at least some of the kingdom groups are not monophyletic, that is, do not include all descendants of a common ancestor, and so do not exactly reflect a true tree of descent.  The Wikipedia Kingdom article notes:

Some recent classifications based on modern cladistics have explicitly abandoned the term "kingdom", noting that the traditional kingdoms are not monophyletic, i.e., do not consist of all the descendants of a common ancestor.


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Is it theoretically possible to safely eliminate most viruses in the atmosphere, hence preemptively cure all the viral diseases?
Could we create a genetically modified virus or bacteria (with inability to mutate into something dangerous for animals) that would quickly spread all over the planet and selectively kill most of the viruses that we train it against?
Are there any other potential methods we could use to do it safely (without any danger to living creatures)?
Is that something we could actually do with a few billions of dollars?

(1) Dollar is not a good benchmark of costs (gold-gram is better); (2) not all viruses spread through atmosphere; (3) Viruses are ecologically important; (4) beware of unintended consequences; (5) the most dangerous viruses (from human perspective) are those not adapted to humans: don't eat bats, don't work in slaughterhouses; (6) immunization is a viable (pun not intended) anti-viral strategy; (7) i can imagine air-cleaning (bio-)nano-robots scooping up viral particles . . . but not until the robotization of vacuum cleaners advances a bit (pun intended).

No (or a bit more scientifically: very very unlikely)
There a couple of reasons why your idea would not work:
Viruses are not alive, so you can't really kill them. The only ways to get rid of all airborne viruses at once would be to either:

A) UV-sterilize the whole atmosphere (bad idea, good xkcd what-if question though) or
B) fill the whole atmosphere with something that replicates itself and consumes very small particles of biological material (oops, we released grey goo).

It's also not possible to create bacteria or viruses that can both spread quickly (which means it need to be able to grow / self-replicate) and is physically unable to mutate.
Mutations arise from errors in DNA replication, and DNA replication is never 100% accurate, you can reduce the error rate, but it will never reach 0, so mutations will always be possible. It's also impossible to predict the 'direction' of mutations so you can't exclude that they will be dangerous for humans either.
As other comments have already mentioned there are even more problems with the idea itself:

not all viruses are airborne, many reside in animal hosts, so getting rid of the airborne ones will not do much
many viruses are not pathogenic for humans but ecologically important, you will get an unknown amount of ecological impact

@Nicolai A baseball thrown near the speed of light should do it.

@BryanKrause A baseball thrown near the speed of light would flash-vaporize and burn up in the atmosphere, thoroughly obliterating anything in its path for its arguably short existence.

@user1258361 That's the joke; Nicolai was talking about sterilizing the atmosphere and referred to XKCD's "what-if" series; the first in that series was titled "relativistic baseball" https://what-if.xkcd.com/1/


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What happens in a brain of a person suffering with apathy?
According to this article

Apathy is a profound loss of motivation not attributed to decreased
  level of consciousness, cognitive impairment, or emotional distress.
  Apathy refers to a set of behavioral, emotional, and cognitive
  features such reduced interest and participation of activities of
  daily life. Another prime characteristic is lack of initiative or an
  absence of responsiveness to stimuli as demonstrated by a lack of self
  initiated action.

Could you describe what happens in a brain (on the level
of neuroreceptors) of a person suffering with a lack of
motivation (or apathy)? And how does it look in the healthy
brain?

Could you explain why you think a lack of motivation is not healthy?  And why there should be some physical difference?  I'd think it'd be like asking whether there's a difference in your computer when it's playing computer games vs running a computational modelling program...

@jamesqf apathy is a disease, similar to depression, but there are differences

Why do you think this?

Apathy is not unhealthy.

Plus 1 from me. You donated time and effort from the apathy and created a bounty. Also interesting to me.

Starting your comment, first, apathy in itself is not a disease; it's not categorized as such by any medical or psychiatric organization. It is part of the symptoms of some disorders, including depression, schizophrenia and Alzheimer's.
Furthermore, apathy is not a simple symptom, but rather a constellation. That also makes it more difficult to address its brain correlates. From a review,  Moretti & Signori (2016):

Apathy is an uncertain nosographical entity, which includes reduced motivation, abulia, decreased empathy, and lack of emotional involvement; it is an important and heavy-burden clinical condition which strongly impacts in everyday life events, affects the common daily living abilities, reduced the inner goal directed behavior, and gives the heaviest burden on caregivers. Is a quite common comorbidity of many neurological disease. [...] As a general observation, the occurrence of apathy is connected to damage of prefrontal cortex (PFC) and basal ganglia; “emotional affective” apathy may be related to the orbitomedial PFC and ventral striatum; “cognitive apathy” may be associated with dysfunction of lateral PFC and dorsal caudate nuclei; deficit of “autoactivation” may be due to bilateral lesions of the internal portion of globus pallidus, bilateral paramedian thalamic lesions, or the dorsomedial portion of PFC. On the other hand, apathy severity has been connected to neurofibrillary tangles density in the anterior cingulate gyrus and to gray matter atrophy in the anterior cingulate (ACC) and in the left medial frontal cortex, confirmed by functional imaging studies. These neural networks are linked to projects, judjing and planning, execution and selection common actions, and through the basolateral amygdala and nucleus accumbens projects to the frontostriatal and to the dorsolateral prefrontal cortex. Therefore, an alteration of these circuitry caused a lack of insight, a reduction of decision-making strategies, and a reduced speedness in action decision, major responsible for apathy. Emergent role concerns also the parietal cortex, with its direct action motivation control.


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Once neurotransmitters bind to its receptors, how does the post synaptic neuron "know" when to start a new action potential?
My textbook seems to gloss over this subject. Once the post-synaptic receptors are activated, do they cause particular ion channels to open, letting positive charge into the cell and inching the neuron closer to the AP threshold?
Also, does the action potential start in the dendrites or the axon? Does the cell body experience membrane voltage? If so, how does the charge get past all the miscellaneous organelles in the cell body? Does it have like a special charge pipe to go down? Or do the ions just float past the organelles?

Welcome - does this answer your question?

Yeah, mostly. Although I'm having trouble figuring out exactly what an ESPS is, Wikipedia is mostly helpful. Thanks!


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Is it logical for someone to be allergic to the water molecule, but be perfectly fine with drinking milk since it's only 87% water molecules?
Recently this article got into the tabloids. The comments were disabled very quickly. Strange.
The authos says she has Aquagenic Urticaria but it is a skin condition not an allergy, and hence wouldn't cause an internal reaction like she says. She claims that drinking milk does not cause her mouth and throat to blister.
If she is truly allergic to the water molecule as she claims, does it make sense that water with fats and sugars dissolved in it doesn't cause a reaction and she also doesn't have a constant reaction to her internal bodily water?
I've come across at least a dozen cases of women claiming they are allergic to the water molecule and die if they drink water so they drink milk/tea/diet cola instead.
So here we have yet another supposed case of someone having antibodies against the water molecule and being 100% healthy as long as they do not drink water. Does this match up to reality or medical science?

Please don't ask the same question twice.

Short answer
Aquagenic urticaria is though to be caused by dissolved allergens in water and not by water per se.
background
Aquagenic urticaria is a rare condition in which urticaria (hives) develop rapidly after the skin comes in contact with water, regardless of its temperature.
Water allergy in itself is obviously a ridicule, as up to 60% of the human adult body is water. In fact, water is essential to our very existence (Fig. 1). Auto-immune responses to water would be disastrous, as pretty much all of our body would be attacked, likely resulting in anaphylaxis — a potentially life-threatening emergency. Further, small molecules typically are non-allergenic. Examples of allergens are, e.g.., chitine (a large polymer), drugs and even macrostructures such as pollen, all of them a lot bigger molecules than water.
Instead, Aquagenic urticaria is thought to be caused by a substance dissolved in water that enters the skin and triggers an immune response. In this theory, the hives are not caused by water, specifically, but rather an allergen in the water. What also may be the cause is an interaction between water and a substance found in or on the skin generates a toxic material, which leads to the development of hives (Park et al., 2011).
Reference
- Park et al., Ann Dermatol (2011); 23(3): S371–S4.

Fig. 1. Water is essential for a lot of processes. source: USCGS

How does aquagenic urticaria explain these particular cases going into anaphylaxis if they drink just a mouthful or sip of water?

Allergens dissolved in the water - see above :)

Are there also allergens in milk? The first girl claims she only survives on 4 150 ml glasses of whole milk a day, so it's implied she still reacts, but not as bad as rainwater or tap water in her mouth/throat.  She avoids watery foods and lives on cereal without milk and biscuits,  She also reacted to a drip because it was water based.

Yes there are allergens in milk, but other ones. The allergens the girl is responding too are present on her skin.

But she goes into anaphylaxis if she drinks water. So it's something different than just something on her skin because her internal body has a more severe reaction compared to water on the skin

This answer is unlikely to be helpful to the poster, who seems to have some sort of obsession with this question. It's unclear what she's trying to get out of asking it. It is not an answer.

I'd note, this is not the first time a user (possibly the same individual) has repeatedly cross posted this same question.

@DeNovo thanks for pointing this out; I didn't know. It actually looked like a rather well-researched question to me at first glance.

Small molecules can be allergenic if they bind to protein: https://biology.stackexchange.com/questions/7905/what-is-the-smallest-molecule-that-can-present-as-an-antigen-to-the-immune-syste


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What kind of bug is this one?
We are trying to figure out what kind of bug this is? It appears to have larvae on its back it is not dust and debris.

It is some sort of Neuroptera

Karl's answer is about as far as we can go without size and locality information, and by the way, that is debris on the animal's back ...

It looks like an earwig to me, they're great parents too, lugging all their young around with them.

This is a kind of neuroptera larva https://www.google.com/search?q=neuroptera+larva.
The smooth jaws discard an antlion https://en.wikipedia.org/wiki/Antlion.
Is more like a chyrsopidae https://www.google.com/search?tbm=isch&q=neuroptera+larva&chips=q:neuroptera+larvae,g_1:chrysopidae:qWI0Ngq4zAQ%3D. They like to camouflage with debris found around them.

i cant really tell but, the op's photo doesn't look like it has hair on its leg, antlion definitely has hair on its legs. But you know cant really tell


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How does a glucose molecule enter the cell from blood vessel?
The transporters in the plasma membrane of the cells promote the entry of glucose molecules from the extracellular matrix to the cytosol of the cell. Could someone explain how does the nutrient molecule enter the extracellular space from the blood vessel?
For instance, in the context of the pancreas, the walls of the blood vessel is fenestrated. The literature also provides evidence for the presence of connexon in the endothelium of the capillaries.
My doubt is, the nutrient molecule that diffuses from the blood vessel reaches the cytosol of the cell through

Diffusing through connexon ?(or)
Does it reach the interstitial matrix(the fluid surrounding the cells) and then uptaken by the transporters present in the plasma membrane of the cell?

Connexons form gap junctions right? I am not sure because right now I don't have any appropriate literature to site for good answer but doesn't glucose transport involve solely GLUT? I mean if connexons were the option then why would diabetes even happen?Please do rectify me if I am going wrong.

@user33690 Yes, connexons form gap junctions.  GLUT transporters are involved in the active transport of glucose molecules from the extracellular space. For example, in the liver, the capillaries(sinusoids) are surrounded by the perisinusoidal space, the cells are found adjacent to the perisinusoidal space. Likewise, is there a layer, surrounding the fenestrated capillaries, from which the nutrients can enter the cell? My question is, which is the region in the pancreas that supplies nutrients to the surface of the cells? Any further thoughts?

I think I understand your question, Natasha. In short, your own answer #2 is correct.
There are 3 spaces, and 2 pathways for glucose to pass from one to the next:

intracapillary plasma
extracellular fluid
the cytosol.

Ways glucose gets into the cell:

(2->3) To get from the ECF to the cytosol , glucose always needs a transport protein. These are the GLUTs. In two cases, the small intestine and kidney, these are part of a secondary active transport system based on the Na/K-ATPase. In the pancreas, it's GLUT2.

(1->2) To get from the capillary plasma to the ECF requires filtration, the process of applying hydrostatic pressure to the plasma and literally squeezing it like a sponge. The boundary of the "blood sponge" is the basement membrane. The membrane holds in the proteins, and lets anything dissolved in the watery serum (like glucose) through.

The Filtration Constant Kf is proportional to the percentage of the BM that is exposed in a given capillary, which varies by the type and other factors like histamine release.

Type 1 (continuous) has the lowest exposure of the BM (only the intercellular clefts). Type 2 (fenestrated)has the clefts and the fenestrations to expose the BM. Type 3 (sinusoids) have huge gaps between the cells, and importantly, an incompetent BM that allows proteins and cells through along with the watery serum.
Dynamic factors that change filtration rates:

Histamine causes the post-capillary venule's endothelial cells to contract, and exposes more of the BM allowing more serum filtration, but it also allows neutrophil extravasation, during which the neutrophils punch holes in the BM through which white cells can squeeze, which is why you get a proteinaceous exudate in Type I hypersensitivity.

Increase in blood flow Like a water balloon increasing its surface area with more blood flow, skeletal muscle capillary beds (Type I) increase their volume and surface area when engorged with blood during exercise. This doesn't change the Kf (the only exit for serum is still the intercellular clefts, but they're bigger now).

P.S. A 1985 morphometric study of pancreatic capillaries shows that the idea that endocrine glands need a boatload of bloodflow (high serum filtration) is valid. Even within a single capillary that feeds both an exocrine acinus and and endocrine islet, the side facing the endocrine islet had more fenestrae.

From what I understand from the above explanation, the BM covers the endothelial layer .When the plasma is filtered out of the pores in the endothelial layer of the fenestrated capillary, how does it cross the BM? Will there be pores in the BM too?

Could you please provide references of studies that measure the Starling forces in the capillaries of the endocrine glands of the pancreas, if you have come across these studies in the past? I could only find the measurements of hydrostatic pressure and osmotic pressure in the intestine of cat.I have been looking for these measurements in the capillaries that pass through islets.

Terms to understand filtration. Blood = cells + plasma. Plasma = proteins + serum. Serum = water + ions + small-molecule solutes. Due to the transmural pressure in the capillary, the blood gets squeezed. Stuff that is too big to make it across the filtration barrier gets left inside (cells + proteins). The plasma gets filtered, like spaghetti in a colander. The proteins/spaghetti stay inside, and the watery serum gets through because it's small enough. The BM is made of Type IV and other collagens, laminins, and other adhesion PROTEINS. (more in next comment, ran out of room)

All proteins get their 3-d shape because they are dissolved in water. It is everywhere in the body. It surrounds each protein, and fills the space between them unless adjacent proteins have hydrophobic pockets for protein-protein interactions. So, even though there aren't pores you can see on EM, there are gaps to accomodate bulk flow (called convective flow). To answer your second question, that's a pretty specific study you're asking for, and I haven't read it. Have you tried a PubMed search?

+1 "The plasma gets filtered, like spaghetti in a colander".Couldn't have explained it better!! If my understanding is correct, in a fenestrated capillary, there is convection in the inner channel, filtration across the inner channel, and convection in the space between the inner channel and the BM.A silly doubt, is the fluid between the inner channel and BM referred to as the interstitial fluid? How do the cells get in contact with this fluid?

I tried a PubMed search and found values of pressure reported in the literature(a ref.).I'm yet to find a reference that provides measurements of the pressure gradient across the capillary channel.I could only find absolute values termed Capillary Blood Pressure or Hydrostatic blood pressure. I'm confused with these terminologies? Is the capillary blood pressure same as hydrostatic blood pressure?Could you please explain?

First, to your question about "capillary blood pressure" versus "hydrostatic blood pressure." Unless there is some very specific context in which the former is being used weirdly, I would take them to be synonyms if you are talking about intracapillary blood. You can also talk about hydrostatic BP in veins and arteries. The pressure gradient you talk about is the transmural pressure, a critical concept and part of the driving force for filtration explained well and briefly by the link I gave in my original answer at CVPhysiology.com. [1/3]

The wall (Latin: mura) of the capillary divides the blood from the tissue interstitial fluid (L: inter=between + statum=standing), the "fluid standing between the cells of the tissue." Since the fluid in the intercellular clefts between the endothelial cells is inside the BM wall, it's still plasma. Remember, the lack of albumin in the ISF makes it chemically distinct from the plasma in those clefts. [2/3]

I'm not sure what you mean by "inner channel." I infer that you mean the capillary lumen, as defined by the endothelium, because that's the only way I can understand your statements about convection and filtration. As stated in this book chapter on filtration, the BM has long been thought of as the filtration barrier, though studies released in 2010 suggest that it might be the glycocalyx of the endothelium. At a teaching level, it doesn't change the equations we use, as described in the first link I provided.[3/3]

Sorry for not using the appropriate terminology. By inner channel, as you rightly inferred, I was referring to the capillary lumen.Thanks a lot for the detailed explanations.


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What kind of bug is this? I found it on my Cleome plant in Atlanta Georgia

This bug was on my cleome plant in Atlanta Georgia

It is an immature from the order Hemiptera. I am sure of that, but cannot help further.

@KarlKjer If you want to take the time, I think it might be worth posting a canonical immature hemiptera post with some identifying characteristics and any particularly interesting individual examples (you seem to be the most active arthropod ID answerer lately), then we can close and direct people there; although this is the only one I recall recently, I feel like since I've been here there have been a lot of questions on them, especially with the spread of certain shield bugs.

This is an instar (nymph) of a shield or stink  bug (order Hemiptera, family Pentatomidae).
Specifically, it appears quite similar to a later juvenile stage (~4th instar) of Chinavia hilaris, the Green Stink Bug.

 4th instar; Source: Oregon Dept of Agriculture

 4th instar; Source: UF IFAS; Credit: Herb Pilcher, USDA-ARS, Bugwood.org.
Alain Hogue also captured a wonderful picture of this species at bugguide.net
From UF IFAS:

Distribution
The green stink bug occurs in most of eastern North America, from Quebec and New England west through southern Canada and the northern U.S. to the Pacific Coast, and southwest from Florida though California. This is the most commonly encountered stink bug species in North America.


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Identification of Jumping Spider Species
I found this jumping spider (Salticidae family) in Pune/India. Most common species of jumpers in my region is heavy-bodied jumper (Hyllus semicupreus), but this is different species by observing body size and blue colored patch under eyes. Its size was about 7mm-8mm.


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How are elements like iron recognized and routed to the right places for use in the body?
I asked this in Chemistry and it was suggested to ask it here. I wondered how the genome, which afaik does not contain iron or calcium as "reference" copies, nonetheless produces an organism that uses certain elements. If it create proteins which bind preferentially to iron or calcium, how then are such elements routed to sites where they can be bound? Are there proteins in addition to those which bind to elements that are responsible for routing? I should mention that I am a software developer and imagine mechanisms analogous to computer code.

Hi and welcome to Biology.SE! It's unclear to me whether you're wondering about iron uptake into blood from consumed food or iron uptake by cells from blood. Or are you asking how individual iron ions reach binding sites on iron-binding proteins? Chemically, proteins that bind ions are no different from proteins that bind other organic molecules, and the genome contains codes for proteins that specifically bind almost every class of chemicals out there. You can get some basics re:iron here: https://en.wikipedia.org/wiki/Human_iron_metabolism#Mechanisms_of_iron_regulation

We welcome new users to SE Biology, but unfortunately your question has problems which will be apparent when you take time to read the introductory tour and the help. First, you really have to show evidence of your own research before posting a question. if you had done this you would see the second problem, that your question is much too broad. Different elements are handled in different ways. You seem to think there is a general problem here in relation to the elemental composition of the genome, but I see none. Please explain further.

@com.prehensible please refrain from answering in the comments. Please turn this into an answer. I'll delete your comment shortly. Problem is that answers in disguise demotivates others from writing quality answers.

As another software developer, I should point out that analogies between computer hardware or software and biological systems can be misleading sometimes. What do you mean by "reference copies" in the genome?

A wikipedia source gives you general informations and precise details about the locations and methods of absorption and distribution. Reading the page is well recommended, I will add the quote to save others time:
en.wikipedia.org/wiki/Human_iron_metabolism#Dietary_iron_uptake :

Like most mineral nutrients, the majority of the iron absorbed from
  digested food or supplements is absorbed in the duodenum by
  enterocytes of the duodenal lining. These cells have special molecules
  that allow them to move iron into the body. To be absorbed, dietary
  iron can be absorbed as part of a protein such as heme protein or iron
  must be in its ferrous Fe2+ form.
A ferric reductase enzyme on the enterocytes’ brush border, duodenal
  cytochrome B (Dcytb), reduces ferric Fe3+ to Fe2+.[9]
A protein called divalent metal transporter 1 (DMT1), which can
  transport several divalent metals across the plasma membrane, then
  transports iron across the enterocyte’s cell membrane into the cell.
These intestinal lining cells can then either store the iron as
  ferritin, which is accomplished by Fe3+ binding to apoferritin (in
  which case the iron will leave the body when the cell dies and is
  sloughed off into feces), or the cell can release it into the body via
  the only known iron exporter in mammals, ferroportin.
Hephaestin, a ferroxidase that can oxidize Fe2+ to Fe3+ and is found
  mainly in the small intestine, helps ferroportin transfer iron across
  the basolateral end of the intestine cells. In contrast, ferroportin
  is post-translationally repressed by hepcidin, a 25-amino acid peptide
  hormone.
The body regulates iron levels by regulating each of these steps. For
  instance, enterocytes synthesize more Dcytb, DMT1 and ferroportin in
  response to iron deficiency anemia.[10] Iron absorption from diet is
  enhanced in the presence of vitamin C and diminished by excess
  calcium, zinc, or manganese.

The fundamental question is, how can an element be "recognized" without any sample to compare it to? How are proteins able to bind iron from among any number of things that might be encountered?

Enzyms have specificity, a lock and key method, a preferential fit method. The DNA keeps information on millions of external constructs, it is only a code, so it can code anything, not only mineral specific enzymes, it can code about 146 heptillion different enzymes, which change randomly and are selected by evolution or equivalent purpose(for enzymes). If the enzymes are randomly generated to begin with, the coding/cell memory structure doesn't need to have a "reference" copy of the mineral. it's quite a complicated deep theory, you can embark on readings about enzyme specificity/history.

By the way, nobody knows the precise science of enzyme binding and evolution, it's one of the most complex things in biology. you can learn lots of theories, dozens of well written research, about enzyme binding and evolution, for example here: http://www.plantphysiol.org/content/125/1/54 there's another website with all 10,000 or so enzymes known to science, and apparently 75k enzymes are expected in the human body, and a lot more proteins. So, in computing there is no parallel, and computers are good at simple biomimicry, but advanced copying of nature is generally too disorderly for pc's.


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What does this biomass measurement mean and how to translate it to volume
This is probably a softball question but because of the nature of the term, it's difficult to Google.  I am not a biologist, I am a web developer.  :-)
What does this measurement mean (it is a measurement of biomass production): 50 g m-2 d-1
I believe it means 50 grams per square meter per day - but not sure why there are '-' signs in there.
And perhaps more complicated, it is possible to translate this measurement to volume (either cubic meters or ideally cubic feet)?

Look for negative exponents to learn about the minus signs in the unit.

Could you please make clear, what you want to achieve? Turn "50 grams per square meter per day" to "XY cubic feet" or to "XY cubic feet per square meter per day"?

Thank you, @Marzipanherz.  Appreciate the Wikipedia link.  I was hoping to gather something like this: "50 grams per square meter per day" to "X grams per cubic foot" but based on Bryan's answer below, I see now this isn't a reasonable expectation.

50 g m-2 d-1 translates to "50 grams per square meter per day": the negative signs are negative exponents (check a math textbook). This is equivalent to writing
((50 g)/m2)/day
You cannot transform this into volume, doing so would lose the meaning: if you are talking about biomass growth of 50 grams per square meter per day, you are saying that there is 50 grams of new biological material produced within a square meter of land (say, a patch of grassland or forest). Talking about it in terms of volume doesn't make sense because the "height" coordinate doesn't produce additional biomass, since the source of energy is the sun.

Thank you, Bryan -- exactly what I was looking for.  This makes perfect sense now.


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What is the name of this spider and is it poisonous?

We found it between Palm trees in the backyard of a home in West Palm Beach Florida.

Ah, that would be the spiny orb weaver. You can see an almost exact same picture here. To make a guess on the species, its maybe Gasteracantha cancriformis as its said in that webpage I have tagged. They are generally harmless. Here's the wikipedia page.


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What flower is this grown in Southern China
It is grown in Tropical Southern China. It is not wild.

Google image search, first result, thinks that your photo is a mexican petunia. I find the color fairly specific, and the leaves fairly dark, so i tried a google image search: https://www.google.fr/search?q=mexican+petunia&num=100&source=lnms&tbm=isch&sa=X&ved=0ahUKEwiwm8vigNjdAhVjc98KHeOiAgQQ_AUIDigB&biw=898&bih=461#imgdii=DDoju-SfrCdmOM:&imgrc=xC36dN7qAGPh0M:

Google images sais that it's a mexican petunia, I think it's right due to the good focus of your image, and the different attributes of the photo.
http://www.gardenality.com/ImageViewer/?id=2116&IUID=3&RID=88#imageId=2116


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Environment requirement for human life
I was wondering, what are the humans needs to fulfill to achieve a human colonisation on mars ?
Let me explain, this is for role play game in a futuristic world where humans colonized mars.
That creates questions that needs answers for background purposes.
I saw like each another some scifi, read novels etc. But I'd like to know scientifically what could help us achieve that.
If this post doesnt have it's place here, do not hesitate to remove it.
In my mind :
breath
eat
drink
dont take radiations (at least not to much)
stay at the right pressure and temperature
any gravity issue on our body ?
try to avoid wandering naked in space
Any help is appreciated
thanks guys :)

This would be more appropriate someplace like Worldbuilding.SE, it isn't really about biology per se. From a biology standpoint, it is under researched for the standards of Biology.SE.

Here is a good write-up for NASA of human needs in space, which applies to other planets, too.
Here is a table of contents with links to chapters that discuss relevant information for you.
The source is described so:

Space Settlements: A Design Study, provides information on space
  settlement development and education and assists teachers and students
  in the NASA Ames Space Settlement Design Contest. The design study was
  the result of a 10 week program in engineering systems design held at
  Stanford University and Ames Research Center in the summer of 1975.
  Participants included professors, technical directors and students in
  a variety of disciplines from physical science and architecture to
  engineering and social science. The goal (see preface) was to
  construct a vision of how people might sustain life in space in a
  large colony.