text:
Are humans an eusocial species?
In the evolution of sociality among animals, different degrees are acknowledged. Some species present overlapping generations, some division of labor, and the minority present reproductive division. Those that present the three traces above are called "eusocial" (e.g. some wasps, some bees, all ants and termites, and an african mole).
Maybe our own species could be eusocial? After all, homosexuality is present in virtually every culture studied by anthropologists. Some say it may bring an advantage to the group via group selection (not having kids of their own, they could study plants, medicine, weapons, and so on). What do you think? Are we an eusocial species?

I wouldn't go so far as to say homosexuality is eusocial - some still become parents by reproduction.   asexuals might be, but if environmental conditions vary, they might reproduce. habitual sexual practice is not non-reproductive behavior I think.  it might be very low chance of reproduction, but reproduction only needs to happen once really.

Well, some wasps and some Paraponera ants sometimes reproduce, even not being the "queen" in the nest. It doesn't mean there is no reproductive division, though. In our species the "reproductive division" (if that's the case) goes together with our high intelligence, that teaches us to have sex just for fun. But my point is that the lack of sexual attraction for the opposite sex may have evolved similarly as eusociality in other species.

it depends on your definition of eusociality - if eusociality does not mean caste reproduction where some castes cannot reproduce, then by all means call it eusocial.  http://en.wikipedia.org/wiki/Eusociality#In_mammals

Thanks for the link. If we are not eusocial, perhaps something in that sense may have triggered the development of homosexuality, that being so widespread in human societies, asks for an evolutionary explanation.

The question of homosexuality and its role in nepotism is interesting.
According to this wiki article, less than 10% of the population is homosexual. If you consider that homosexuality makes human eusocial because homosexual do not reproduce but help their brothers and sisters to reproduce, then you would have to consider any species where a few percentage of the population produce some kind of altruism to be eusocial. Given that all phenotypic traits theoretically have social impacts, then I would bet that you might call eusocial a lot of species.
It seems wiser to me to limit the definition of eusocial when an important part (maybe 98% minimum) of the population do not reproduce but help others to reproduce. One might also want to consider some other restrictions for a the use of the word "eusocial"
Therefore, using the argument of "reproductive division" I would rather not include Homo sapiens in the list of eusocial species. But it is nothing more than a question of definition. You're free to define your words the way you want and call human eusocial but make sure your interlocutor knows your definitions.
Now, let's say we place the limit to the definition of eusociality at 1%. When more than 1% of the population does not reproduce but help their kin to reproduce, then the species is eusocial. Then, humans would seem to fit in this definition at first sight. But do homosexual in our modern society really help their kin to reproduce? In other words, do siblings of homosexual reproduce more (or have offspring that have a high fitness)? This study investigated the question (as pointed out by @oreotrephes in the comments) and they indeed found some pattern but the difference in reproduction between relatives of homosexual and non-relative of homosexual is is quite weak. But if homosexual don't reproduce and don't help their kin reproducing then, humans is definitely not a eusocial species.
Finally I want to add that individuals from lots of different species have been found to perform homosexual behaviour (see this wiki article). If you want to consider human as eusocial because some homosexuality, then you will have to consider sheeps, labradors and pigeons to be eusocial as well!

Thanks for your comment, Remi.b! I'm using the definition from E.O.Wilson in Sociobiology and other books (The Insect Societies also use the same, if my memory is right). They say nothing about how big is the "sterile caste", only about the 3 traces ocurring together. And if homossexuals change their habits, it doesn't change the reason that behaviour might have evolved in first place - and I think that's the objective within biological reasoning, not to put rules of what we might or not do with ourselves.

Indeed, I have never heard either talking about the number of sterile individuals. But it seems to make sense to me that the whole point of eusociality is that many individuals work for the benefit of one. And therefore, you might see a continuum from some individuals helping some others to many individuals helping one. I guess one would need to define eusociality as an arbitrary threshold along this axis (and some others).

In my last paragraph, I just wanted to say that even if one want to consider that humans were eusocial in the past, he might not be able to say the same for the modern species of human if siblings of homosexual do not have greater fitness than average anymore.

Actually, in social hymenopterans, the queen alone works for the benefit of the worker caste. Because of the genetics of haplodiploidy, when a worker gains a sister, it has a copy of 75% of her DNA. When the queen gains a daughter, it has a copy of only 50% of her DNA. So, no, there's not a "sense" like that "whole point" you mention. Indeed, in different species the logic may vary wildly, according to genetic and/or ecological constraints.

About your last paragraph, I disagree. The cultural time is almost irrelevant close to genetic/evolutionary time. We probably have the same instincts we had 100,000 years ago. Even if homosexuals change their behavior for the next 1000 years (what is highly improbable), this would hardly change the genetics that cause homosexual behaviour. And even if in industrial-western-societies this change happens and is sustained for so long, still there are other societies that would not change alike. That's the reason our cultural behavior are not supposed to define our biological terms. Do you agree?

@Remi.b in regards your last paragraph I think OP is referring to Camperio-Ciani et al 2004 which suggests that female relatives of homosexual men have more offspring than female relatives of heterosexual men.

Nice link, @Oreotrephes! What I mean is: in biology we refer to females as animals that produces big gametes. If a woman has their ovaries removed, would we stop calling her "woman"? Homo sapiens is a biped species, if someone is comatose and cannot walk, would we stop calling him/her "human"? We wouldn't stop being a eusocial species just because of some habit changes in a single century, that's my point, mostly because those changes are usually reversible.

If you call eusocial a species where some individuals help other to reproduce and you find a species where none individuals help others, you cannot call them eusocial because some species cannot reproduce because they evolved in order to help the others. You cannot say that an ant can fly because it evolved ability to fly in its evolutionary history! But anyway, this is just a detail of the last paragraph.

I missed 2 of your comments when post my last comment. Sorry about that. You basically said that culture does not really matter at calling a species eusocial or not, instinct matter at defining species. Well, if you want to. I agree with that but don't think this discussion is biologically relevant. I didn't get your point in your second comment. It seems intuitively coherent that if 0.001 % of the population help a bit their kin to reproduce, then it would be a bit awkward to call this species eusocial. But again, define eusocial the way you want!

You may be right, @Remi.b, but the proportion of homosexuals helping their family is surely much higher than 0.001%.

Yes indeed it is/was probably much higher. probably between 1% and 10%.

I think it depends on the country and the dominant levels of individuality. In the scenario where we evolved, and that still persists in some hunter-gatherer societies, and to a lesser degree in "underdeveloped" countries (i.e. family members count on the support of the others), it's supposed to be much higher.

"some kind of altruism" in your answer is wrong, because the definition of homossexuality is an altruism FROM absence of reproduction. And this is the main point in eusociality.

I'm going to hazard turning my comment into an answer....
Even if the answer might be no, you know this is a good thought and there is something there... lets dig a little.
Eusociality in evolutionary biology is by many like Dawkins and Wilson pointing to the evolution of sterile castes of animals, which are very closely related to the breeding caste.  This is how hymenoptera are famed as examples of the importance of kin selection. Worker ants are entirely dependent upon the queen to reproduce the next generation, but they can do so because the queen is close enough to being them so that ants continue to exist as they do.  Not only is this a reasonable way to exist, but kin selection has produced eusocial animals in every
The application of this definition to mammals has been done, but its not a universally agreed upon definition of eusociality.  To a great extent its because the animals can still breed, even if they are inhibited from doing so by a social structure.  Wolf packs and ape troops where the alpha male sires all the offspring are not eusocial - the other males are only deferring mating (sometimes forever) but they are biologically fertile.  This is not eusocial, just social biology.
But to your question, I think the point to be considered is that the dynamic that allows the evolution of eusociality does shape social structures.  Primates are so rational and their brains are so big that their brains allow them to adapt their social matrix such that we can have different roles in our groups depending on the conditions of environment at any given moment, whereas sterility and castes defined by adaptation will change very slowly, we can change our society in just a generation.  Social animals are eusocial in a way, but they are more adaptable by the use of their social reprogrammability.


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poor RNA quality from zebrafish embryos
Does anyone routinely do RNA isolation from zebrafish embryos?
I have embryos from different stages but all below 24hpf. This is the protocol I follow:

Take 10-20 embryos
Wash once with milliQ water
Treat with 1mg/ml Proteinase-K (5min with gentle shaking) to dechorionate
Wash again with milliQ water
Remove water and add 250 µl Trizol
Homogenize by pippeting
add 750µl more of trizol
Do the standard trizol extraction step (with chlorofom)
Take the aqueous phase and wash again with 200µl chloroform
Precipitate RNA with isopropanol
Wash thrice with 70% ethanol
dissolve in nuclease free water

Despite all this I get a poor A260/A230 : ~0.4
Moreover, this happens consistently in all samples. The RNA bands look fine on the gel.
I have done RNA isolation many times from cell lines and tissues and never faced this problem. Is this common with zebrafish embryos? Is there a way to fix this other than by using kits?

This addition to the protocol worked out and good RNA quality was obtained:
Homogenization

Homogenized the embryos, suspended (and frozen) in trizol by passing through 2ml insulin syringes. (About 10 times).

Washing

Washed 2 times with 500µl 80% Ethanol
Washed 3 times with 500µl 70% Ethanol

Dechorionation was dispensable and Proteinase-K treatment was too harsh on early stage embryos. So I did not dechorionate this time.
I think the number of washes can be reduced (1×80% and 2×70%) but this is what I stuck to (out of superstition :P)

Ah, good to know the solution to this. My guess would also be that the number of washes can be reduced. I wash like this for my tissue samples.

AS you mentioned before, the problem was I guess homogenization. But insulin syringe is a good tool when you have lots of samples and works better than the hand held homogenizer (in this case) .

I'll keep this in mind.

Usually I had no problems with RNA extractions - from various cultured cells as well as a number of different tissues from mouse. If I look at your protocol this is pretty much the same as the one we used or the one recommended here for zebrafish embryo. This protocol "Purification of RNA Using TRIzol (TRI Reagent)" seems also interesting.
What can happen is a contamination by phenol or carbohydrates, then we usually used the protocol below to clean up the sample. You can also use column based methods, but they are more expensive.

add 1/10 vol of NH4OAc (5M), 2.5 volume 100% cold EtOH (100%) and 10µg
glycogen (for total RNA we usually didn't use any co-precipitation
agents) and mix well
incubate 30 min at -80°C
centrifuge 20 min at 12000g at 4°C and remove the supernatant
wash with 75% ice cold EtOH
centrifuge 5 min at 12000 g at 4°C and remove supernatant
Re-suspend the pellet in RNAse free water (can take some time)

well. I had also tried precipitating with 0.1 vol 5M LiCl + 2.5 vol EtOH.. Still same problem.. If it is a phenolic contamination it should go away in the second chloroform wash. This is persistent.

Are your embryos pigmented?

No.. they are very early embryos.. not pigmented at all..

Ok, this excludes melanin contaminations. This is pretty strange.

i tried without dechorionation.. plus 5 times 70% EtOH wash. Better but still not good enough.. Bands still look quite good on the gel.

What means better in terms of 260/230 ratio?

poor ~0.4, better ~1.2

Thats better. This paper says that the quality is going down when the homogenzation is incomplete and recommends the homogenization of frozen embryos.

Thanks for pointing that out.. now i see where the problem is.. I was homogenizing by pipetting.. most protocols suggest using a homogenizer.. since I have a lot of samples I thought I need to clean the tip every time I run the homogenizer.. Chance of contamination increases.. I do freeze the homogenized embryos in trizol and re-homogenize after thawing, just before RNA isolation. Do you suggest a better technique ?

I stumbled upon it today while I was looking for something else :-) This is the downside of using homogenizers. We usually used a ball mill and frozen tissue samples, there the same problem applies. With a lot of samples this takes much longer, no chance to get around it.

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Sexual selection in cats or other animals
I was wondering if you could answer some of my questions regarding sexual selection in cats (or any other animals). I would like to apologize beforehand for my incorrect term use.

When it comes to mate choice, is mutual choice for both males and females the norm? If not, is it mostly a tomcat or a female cat who does the choosing?
Do female cats always have freedom to choose, or is it more like a rape or consensual sex?
How do cats choose their prospective partners in the wild, what are the mechanics of this process? Does a prospective partner come with the territory or are there any courtship rituals? I am interested in mate availability for female cats and sexual selection from a female cat perspective.

Thank you very much in advance.
P.S. Any other animals will do if they do not live in groups, prides or harems. I am interested in individual choices.

Are you also interested in lions ? (Technically, they are also cats.) I can help you with that , if you are interested.

Yes, thank you, that would be nice to know. Maybe they have the same behavior patterns.

Wilson and Reeder (Mammal Species of the World) count 40 species of Felidae. Most of them are small cats (subfamily Felinae). Lions are in the subfamily Pantherinae, which contains only 6 species, one of them the jaguar, Panthera onca, which is solitary, like the tiger, Panthera tigris. By what I know of small cats, Puma concolor included, and the tiger and the jaguar, it seems that lion social behavior is not typical of felines. (Would add that as a comment, but can't comment with reputation < 50).
EDIT:
Looking for "Felidae sexual selection" or 'Felidae "sexual selection"' in google I have found some links. Look for "sexual selection" or "Felidae" in the text. Though I'm afraid most of them are not exactly what you're looking for, maybe they can open new windows of thought. Hope that helps!
http://www.journals.elsevierhealth.com/periodicals/aaeth/article/0304-3762%2883%2990116-5/
http://www.catsg.org/cheetah/05_library/5_3_publications/E/Eaton_-_The_Evolution_of_Sociality_in_the_Felidae.pdf
http://onlinelibrary.wiley.com/doi/10.1111/j.1095-8312.2010.01520.x/pdf
http://www.jstor.org/discover/10.2307/3544917?uid=26584&uid=3737664&uid=5909624&uid=2&uid=26582&uid=3&uid=67&uid=62&sid=21103320511793
http://en.wikipedia.org/wiki/Machairodontinae
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0048352?utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+plosone%2FPLoSONE+%28PLOS+ONE+Alerts%3A+New+Articles%29
http://books.google.com.br/books?id=FhvmHW972mAC&pg=PA752&lpg=PA752&dq=Felidae+%22sexual+selection%22&source=bl&ots=Ns8iRUQxXW&sig=r5ZEgp-nH9mll5cYgB5GzNaThZs&hl=en&sa=X&ei=FBPQUq63LPDLsQS0m4DAAw&ved=0CDYQ6AEwADgK#v=onepage&q=Felidae%20%22sexual%20selection%22&f=false
http://www.mapoflife.org/topics/topic_203_Baculum-%28penile-bone%29-in-mammals/
http://www.sciencedirect.com/science/article/pii/S0169534703003999

Thank you very much for your comment. If you could provide any links about female cats' sexual selection, I would be very grateful.

it would be great if you can make this more digestible.

Thanks for providing all those links. I will check them out!

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Radiation and "Safe Dose"
I've read about safe doses of radiation, briefly. Why is there such a thing a safe dose? Can't any radiation give you cancer? Why is it more and more dangerous to take in larger and larger doses? Just because the body can't recover as easily? Is there something fundamentally more damaging about larger doses of radiation, as opposed to smaller more frequent doses? I suppose this could go to a health forum, but I don't know of one, and I came about this question via thinking about Physics.

How do I move the question?

flag it with a custom moderator flag, and request a migration.

Great question. It is unfortunate that more people don't understand what "radiation" is and how it affects biology.
Firstly, you must distinguish between ionizing radiation and non-ionizing radiation.
Wikipedia describes the former rather well:

Ionizing (or ionising) radiation is radiation composed of particles that individually carry enough kinetic energy to liberate an electron from an atom or molecule, ionizing it. ...
When ionizing radiation is emitted by or absorbed by an atom, it can liberate an atomic particle (typically an electron, proton, or neutron, but sometimes an entire nucleus) from the atom. Such an event can alter chemical bonds and produce ions, usually in ion-pairs, that are especially chemically reactive.

X-rays, alpha, beta, and gamma radiation are all ionizing forms of radiation. Non-ionizing radiation, as you might guess, is radiation of a sort which lacks enough energy to to strip an electron from an atom. All light is actually "radiation."
The reason why ionizing radiation can be so damaging is because the molecular underpinnings of our cells depend on many very specific chemical bonds. Changing those bonds can damage or even break anything from proteins to strands of DNA itself. Our bodies naturally try to repair damage, but the amount of damage is a crucial factor in how successful our bodies can be. More radiation means more damage; also greater amounts of radiation increases the chances of serious genetic damage to one or more cells. Damaging a cell's rulebook in just the right ways can disable its repair processes and even its fail-safes that keep it from becoming a hazard to the rest of the body (such as growing uncontrollably into a cancerous tumor).
A more in depth explanation of radiation effects can be found at http://www.epa.gov/radiation/understand/health_effects.html#q1

In general, the amount and duration of radiation exposure affects the severity or type of health effect. There are two broad categories of health effects: stochastic and non-stochastic.
Stochastic Health Effects
Stochastic effects are associated with long-term, low-level (chronic) exposure to radiation. ("Stochastic" refers to the likelihood that something will happen.) Increased levels of exposure make these health effects more likely to occur, but do not influence the type or severity of the effect.
Cancer is considered by most people the primary health effect from radiation exposure. Simply put, cancer is the uncontrolled growth of cells. Ordinarily, natural processes control the rate at which cells grow and replace themselves. They also control the body's processes for repairing or replacing damaged tissue. Damage occurring at the cellular or molecular level, can disrupt the control processes, permitting the uncontrolled growth of cells cancer This is why ionizing radiation's ability to break chemical bonds in atoms and molecules makes it such a potent carcinogen.
Other stochastic effects also occur. Radiation can cause changes in DNA, the "blueprints" that ensure cell repair and replacement produces a perfect copy of the original cell. Changes in DNA are called mutations.
Sometimes the body fails to repair these mutations or even creates mutations during repair. The mutations can be teratogenic or genetic. Teratogenic mutations are caused by exposure of the fetus in the uterus and affect only the individual who was exposed. Genetic mutations are passed on to offspring.
Non-Stochastic Health Effects
Non-stochastic effects appear in cases of exposure to high levels of radiation, and become more severe as the exposure increases. Short-term, high-level exposure is referred to as 'acute' exposure.
Many non-cancerous health effects of radiation are non-stochastic. Unlike cancer, health effects from 'acute' exposure to radiation usually appear quickly. Acute health effects include burns and radiation sickness. Radiation sickness is also called 'radiation poisoning.' It can cause premature aging or even death. If the dose is fatal, death usually occurs within two months. The symptoms of radiation sickness include: nausea, weakness, hair loss, skin burns or diminished organ function.

Another thing to understand about why the dose matters is that we are surrounded by ionizing radiation. We always have been. Our bodies have evolved needing to successfully deal with ionizing radiation. You can find a very informative and fun visualization of this fact at https://xkcd.com/radiation/.

First of all: Technically speaking there is no such thing as a safe dose in radiation like you can say for drugs or toxins. This is because every single event of radiation can cause damage that can cause cancer.
Besides that, there is no need to panic about low radiation, since you define certain values which are deemed safe, because the likelihood of getting damage from this radiation is so small that it can be neglected. What we use in working with radioactive substances is the so called ALARA principle ("As Low As Reasonably Achievable"), so you try to keep the dose as small as possible, even if you are below the limits.
Taking up larger doses of radiation (or even worse taking up radioactive material) will raise your chances of receiving a harmful dose and damaging cells. A single large dose can cause a damage to your DNA, but this is also true for continued small doses. In both cases there is a certain chance of damage, which is bigger for the larger dose. But since there are more events possible for the continuous small dose, this can be as dangerous as the larger single dose.


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Blood group probability question

My answer ( after rounding off) is 9% -100( 0.75 X 0.25 X 0.5) but the answer given is 22 %
Am I correct ?

I think the quoted answer is correct.
First, the probability of getting a son( and not a daughter) is $P_s=0.5$.
Next, since both the parents are heterozygous, the probability of genotype $hh$ is $P_h=0.25$. This genotype will not produce any antigen precursor, and hence there will be no antigens on RBC. As blood group O is defined by the absence of antigens, this can be classified as blood group O.For the expression of the antigen (dominant at the $H$ locus), the probability is $P_H=0.75$.
Again owing to the heterozygosity of both the parents at $I$ locus, the probability of getting a blood group with genotype $I^oI^o$ is $P_I=0.25$. This is the probability, that if the antigen precursor is made, $75%$% of the times the expressed blood group will be O. Therefore the probability of blood group O due to homozygous $I$ locus and dominant $H$ locus is $P_I\times P_H=3/16$.
Net probability for blood group O=(probability due to homozygous h+probability due to homozygous I and dominant H)*probability of a son.
$$P_{net}=P_s(P_h+P_HP_I)\approx 0.22$$

The blood group without  hh antigen is also known as Bombay Blood group ! One of the rarest type in the world ! Phenotypically O but when O blood transfusion is done, it will create a severe reaction.

@biogirllajja I knew that but I guessed, it was the phenotype of O whose probability was asked.

I realised my mistake of not considering hh as phenotype O when I saw your working. I just wanted to share the information regarding bombay blood group.


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How does fluoride prevent tooth decay?
Fluoride is a common active ingredient in tooth paste to prevent dental caries. It is also added or removed from the water supply in some communities for the same reason, but in children only.
My understanding is that the fluoride in tooth paste reacts with minerals in saliva then bonds to the tooth enamel. The fluoride in water is ingested and is somehow added to the developing bones and teeth of growing children, to the benefit of making decay resistant teeth.
What is the biochemical pathway of each process? A perfect answer will also discuss fluorosis and when that occurs and why.

Your understanding is correct to some extent. Tooth enamel mostly consists of a mineral called hydroxyapatite ($\ce{Ca_{10}(PO4)6(OH)2}$) (Staines et al, 1981).  Though this makes enamel the strongest material in the body, it is susceptible to degradation. In acidic environment, hyrdoxyapatite gets dissolved and leads to cavities (Brown, p. 688). The reaction is:
$\ce{Ca_{10}(PO4)6(OH)2_{(s)}~+~8~H+_{(aq)} -> 10~Ca^{2+}_{(aq)}~+~6~HPO4^{2-}_{(aq)}~+~2~H2O_{(l)}}$
To overcome this, fluoride is added in toothpastes. Fluoride ($\ce{F-}$) reacts with hydroxyapatite of enamel to form fluoroapatite via demineralization and remineralization cycle. The 3 main mechanisms through which it happens are (Rošin-Grget et al, 2013):

Iso-ionic exchange of $\ce{F-}$ for $\ce{OH-}$ in apatite:
$\ce{Ca_{10}(PO4)6(OH)2~+~2~F- -> Ca_{10}(PO4)6F2~+~2~OH-}$

Crystal growth of fluorapatite from a supersaturated solution:
$\ce{10~Ca^{2+ }~+~6~PO4^{3-}~+~2~F- -> Ca_{10}(PO4)6F2}$

Apatite dissolution with $\ce{CaF2}$ formation:
$\ce{Ca_{10}(PO4)6(OH)2~+~20~F- -> 10~CaF2~+~6~PO4^{3-}~+~2~OH-}$

Instead of preventing cavities, fluoride just controls the rate of formation of cavities (i.e. it repairs, not prevents, tooth decay), due to which its repeated exposure on enamel throughout the day is important (Cate et al, 2013). However, the effects of fluoride are minimal once it gets swallowed (Ismail et al, 2008).
Talking about fluorosis, the cause behind it is dissolution of hydroxyapatite due to higher concentration of fluoride (see the 3rd point in mechanisms, it requires higher level of fluoride to occur). Apart from this, formation of fluorohydroxyapatite is also a cause of fluorosis, the reaction being:
$\ce{Ca_{10}(PO4)6(OH)2~+~F- ~+~H+ -> Ca_{10}(PO4)6(OH)F + H2O}$
Dissolution of fluoroapatite causes depletion of enamel layer, causing fluorosis.
References:

M. Staines, W. H. Robinson and J. A. A. Hood (1981). "Spherical indentation of tooth enamel". Journal of Materials Science. 16 (9): 2551–2556. doi:10.1007/bf01113595.

Wikipedia contributors. "Tooth enamel." Wikipedia, The Free Encyclopedia. Wikipedia, The Free Encyclopedia, 25 Apr. 2017. Web. 1 May. 2017.

Rošin-Grget, K; Peroš, K; Sutej, I; Bašić, K (Nov 2013). "The cariostatic mechanisms of fluoride". Acta medica academica. 42 (2): 179–88. doi:10.5644/ama2006-124.85. PMID 24308397. Retrieved 31 March 2014.

ten Cate FM. Contemporary perspective on the use of fluoride products in caries prevention British Dental Journal 214, 161 - 167 (2013) PMID 23429124

Ismail AI, Hasson H; Hasson (2008). "Fluoride supplements, dental caries and fluorosis: a systematic review". J Am Dent Assoc. 139 (11): 1457–68. doi:10.14219/jada.archive.2008.0071.


text:
Identifying mutations in a yeast strain

Cells of a triple-mutant yeast strain (leu- his- trp-) were spread
either on minimal medium or on minimal medium supplemented with
various combinations of histidine, leucine, or tryptophan. The
cultures were grown at either 25C or 37C for 3 days. Colony numbers
in each plate were counted, and the data are listed in the following
table.

What kind of mutation most probably causes the his- phenotype?What
kind of mutation most probably causes the leu- phenotype?
A.Point mutation
B.missense mutation
c.nonsense mutation
d.conditional mutation
e.deletion mutation

My questions : What is the meaning of confluent in this context ? Can anyone give me a hint to solve this question ? I have no clue how to solve this.

For starters, you can just google "confluent".  It means that there are no colonies, but that the cells cover the whole plate.
So when you provide all three amino acids, the cells fill up the whole plate.  If you leave His out, but keep the plate at 25 degrees, the plate still fills up with cells, so the His- allele isn't hurting the cells at all at 25 degrees, but it's pretty nasty at 37 degrees.  That makes it conditional; the mutation only impairs His metabolism at some temperatures.
There is not a single cell which is surviving a lack of Leu, but there are some which are surviving the lack of Trp, and the lack of His at harmful temperatures.  Presumably, those are the small number which are lucky enough to acquire mutations which compensate for the original deleterious alleles, but NO cells were able to overcome the problem with the Leucine metabolism.  This suggests that the Leucine mutation might be a total deletion.

Just to add a useful term to this answer: the rare colonies on the -Trp plates and the -His at 37C are called revertants. Mutation classes (a), (b), (c) and (d) as listed in the question are all capable of reverting. A deletion cannot revert.

@AlanBoyd Why can all the others revert but not deletion ?

Most deletions cannot revert because they represent a large loss of information. A deletion of a single base would cause a frameshift, and that could revert as a result of a compensating insertion (or two more single deletions) that restored a functional reading frame.


text:
Linkage distance calculation

What is the map unit distance between L and S allele ?

My working : If we take the normal ratio :9:3:3:1 , first one should be 9/16 = 0.5625
and then subtract 0.51 from it, we get 0.0525, similarly working we get 0.0525 difference for all 4 and so the distance is 0.0525 X 4 X 100 = 21
Is my working correct ?

I did not get your working and the logic behind it.Can you explain it a bit? But I got exact $20%$ as the answer.

I found out the difference between expected and observed and then added them. Could you tell me what you did ?

With the heterozygous genotype $LlSs$, there are two kinds of linkages possible.
1. Cis=$LS.ls$
2. Trans=$Ls.lS$
All the possible gametes ($LS,lS,Ls,ls$) in both cases are same, but their frequency differs based on the strength of linkage and hence, the distance on the chromosome map. In either case, the frequency of $LS$ and $ls$ will be same, and $Ls$ and $lS$ will be same. This is because, in the Cis linkage, the former pair will constitute the parental linkage and the latter will be the recombinants, but both the gametes within the pair are equally likely to be formed. The same is the case for Trans linkage where the former pair acts as the recombinants.
According to the given table, frequency of $llss$ is $0.01$. $llss$ can only be formed by the combination of two $ls$ gametes. Therefore the probability of an $ls$ gamete will be $\sqrt{(0.01)}=0.1$.
The probability of getting an $ls$ gamete is $0.1$. Therefore, the probability of $LS$ is $0.1$, $lS$ is $0.4$ and $Ls$ is $0.4$.
As $Ls$ and $lS$ are more probable, they are more likely to be linked, and hence the genotype will be in Trans linkage. Then the frequency of recombinants($LS,ls$) is $0.2$. The chromosomal distance is $20 \text{ cM}$ or $20\text{ map units}$.
I am not sure whether my line of arguments are true. If you do find any flaw, please let me know.

Yes, 20 is right. (My instructor gave us the answer today.)


text:
What is the energy source for adipocytes?
Since adipocytes export fatty acids and glycerol and don't use them as an energy source, what is the main source of energy for adipocytes?

Adipocytes use glucose as an energy source. They express the insulin-responsive glucose transporter GLUT4 just like muscle cells so that when blood glucose levels rise they are primed to take the glucose up for fatty acid biosynthesis, but they also use glucose as a fuel molecule.

Thank you! And in the fasting state, which fuel they use? Glucose too?

In the fasting state blood glucose levels will be maintained by the liver via gluconeogenesis, so yes. During fasting the main function of the adipocytes is fat mobilisation and release of fatty acids (and glycerol, used by the liver as a substrate for gluconeogenesis).

But if adipocyte's GLUT4 recepetors are not being stimulated by insulin in the fasting state, how can they uptake glucose? Does hydrolysis of the ester link between a fatty acid and the glycerol releases energy?

@AlanBoyd, this is an interesting question, do you have any reference for the statement that glucose is the main energy source of (white) adipocytes? They are capable of fatty acid oxidation too (see for example http://www.jlr.org/content/17/5/516.short) but I have not seen any data on the relative importance of glucose vs fatty acids.

@AlanBoyd, also, to my knowledge, human adipose tissue does not synthesize (much) fatty acids from glucose. See for example http://www.ncbi.nlm.nih.gov/pubmed/1113680


text:
What does the (-) in the molecule name mean?
I'm reading some text (purchase request) that has the following line in it.

(-)-Norepinephrine

What does the minus sign mean in front that is in parenthesis? Is this some kind of standard way of describing charge of the molecule or something? Or is this someone's way of representing something else? Or does this mean nothing?

The minus sign in parentheses here indicates the optical rotation, (+) means the molecule rotates linear polarized light clockwise, (-) means it rotates counterclockwise. Typically you would also write exactly which stereoisomer is meant (R or S), which is generally the more useful information.
The following are all valid names for the natural stereoisomer of norepinephrine:

D-norepinephrine
D-(-)-norepinephrine
(R)-norepinephrine
(R)-(-)-norepinephrine

I'd recommend that you take a look at the concept of Chirality if you're not already familiar with it.

And they have the article dextrorotation and levorotation as well.


text:
mouse gene translated to human gene
I have a list of mouse genes, but all our analysis happens for human genes. Is that possible to translate these mouse genes to human genes? and is there any tool that can help me on this?
I am mostly a computer science guy, I am not sure this is even possible. However, according to someone, this could happen, I don't expect a full conversion though.
Thanks.

Your question is a little unclear. Are you trying to find the sequences for the corresponding human genes, or just the name of the human gene?

I would recommend using Biomart from Ensembl. This is basically a Swiss Army Knife for converting gene names into various IDs, getting corresponding locations on the chromosomes and so on. You can upload a list of gene names and convert them into the corresponding gene IDs of other species and the convert these IDs back to gene names.
If you haven't used Biomart yet, you can either start by going on their help page or by having a look on this tutorial for the conversion of IDs.

Yup, use biomart.  When you say you have a list, do you have a list of ensembl gene IDs, or a list of Gene Symbols, or Refseq IDs?  The gene symbol is probably what you want; the name that you will be able to find in both genomes  ("Cdh23" or "ApoE1" are examples).  But of course there will be some mouse genes that aren't in humans, and vice-versa.

Sounds like you are searching for homologs of mouse genes in human genome. BLAST should be able to help you finding that. You might want to find the sequences for the mouse genes on GenBank and run BLAST against it.
However, in this scenario, protein BLAST (BLASTp) will actually helps you more since the protein sequences are conserved better than DNA sequences are between species. In this case, you need to find the proteins coded by the mouse genes, and run BLASTp then.

Depending on how long the list is, you don't want to use Blast. Biomart (once you learned how to use it) is a really good tool here.


text:
Rh factor and dominance of gene

"Formation of Rh  antigen is controlled by dominant gene(R) and its
  absence by recipient gene(r).People having this antigen with genotype
  (RR or Rr) are called Rh positive and those whose blood is devoid of
  it with genotype (rr) are called Rh negative. About 85% in world are
  Europe and 97% human being in India are Rh positive."

My questions are:-
Which factors result into dominance of gene(R) and  absence of recipient gene(r)?
With difference seen in %ratio in India and Europe, can it be concluded that environmental factors affects it.?

You are using the word "dominant" in two very different ways.  I suggest you rewrite your question to avoid that.  I'd say the short answer is that you can't necessarily conclude anything from the relative frequency of genes like that.  It could very well just be luck that the r allele is a little more common in Europe than India.

There are various factors which decide the dominance of one gene over the other. Owing to the complex biochemical pathways it is difficult to predict which gene is dominant unless we know exactly how the gene is translated to protein and how the protein interacts with the body.
These are the few answers that could help:-

What makes a gene dominant or recessive
What determines if an allele is dominant or recessive?

As for your question;
There are two genes:

D- The allele which is dominant
d-The allele which is recessive.

A recessive gene is a gene that is nonfunctional or expresses its characteristic phenotype in presence of an identical allele.
For a person to have Rh negative blood group he must inherit 'd' allele from both the parents as it is a recessive trait.And as @swbarnes2 mentioned in the comments 'd' allele is more common in European countries leading to a wide range of population possessing Rh negative blood groups.

Shouldn't you replace "gene" with "allele"?
For example: "D- The gene which is dominant" into "D- The allele which is dominant"

In this specific case the dominant allele is the presence of a gene (RHD), and the recessive allele is (usually) the absence of that gene. This is why you will see the statement "there is no d gene". There does indeed appear to be an environmental factor which governs the frequency of the various genotypes - Toxoplasma gondii.
I find this topic quite a challenge. Here is a distillation of my research.
It is thought that the RHD gene may have arisen through a duplication of the adjacent RHCE gene. It seems that the possession of this gene (a D allele) confers a selective advantage in individuals suffering from toxoplasmosis (infection by the protozoan Toxoplasma gondii. Toxoplasmosis has an effect upon what is termed psychomotor performance, which is usually measured as reaction time. So, for example, it has been reported that there is an increased incidence of road traffic accidents amongst those suffering from (asymptomatic) toxoplasmosis.
Heterozygosity at RHD seems to reduce this effect of toxoplasmosis. So, the current theory is that the D allele appeared in humans because of the prevalence of toxoplasmosis, with the selective disadvantage of haemolytic disease of the newborn being balanced by the heterozygote advantage (similar to the malaria/sickle cell anaemia interaction). There is currently no biochemical explanation of why the RHD gene product has this effect.
In a region with a very low risk of toxoplasmosis there would be a strong selection for the (ancestral?) dd genotype since these individuals have the best reaction time of all (when not infected). The definitive hosts (i.e. where the parasite reproduces) of Toxoplasma gondii are cats, and these were rare in Europe before the domestication of cats. This could explain why the dd genotype is more frequent in this area.


text:
How does Acetaldehyde accelerate mitosis?
I read that one of the ways alcohol is carcinogenic is via accelerated mitosis due to acetaldehyde, I was wondering what pathway caused this acceleration?

Can you please post where you read this?

I think I was incorrect, can you piece it together for me? This says that alcohol causes cancer from accelerated mitosis:http://en.wikipedia.org/wiki/Carcinogenesis#Non-mutagenic_carcinogens
And then when I looked up how alcohol causes cancer, webpages referenced acetaldehyde.

The wikipedia just states this without giving any source. I will look into it...

First of all Alcohol and Acetaldehyde are both cytotoxic. Along in our development we learned to deal with both substances, which is shown by specific metabolism pathways to break them down (for example alcohol dehydrogenase, acetaldehyde dehydrogenase, Cytochrom P450 and so on).
Alcohol and Acetaldehyde both have a negative effect on mitosis (which explains a good part of the negative effect which alcohol has on developing embryos).
Examples can be the following articles:

Acetaldehyde causes a prolongation of the doubling time and an
increase in the modal volume of cells in culture.
Alcohol inhibits cell mitosis in G2-M phase in cell cycle in a human
lymphocytes in vitro study.
Ethanol induces transient arrest of cell division (G2 + M block)
followed by G0/G1 block: dose effects of short- and longer-term
ethanol exposure on cell cycle and cell functions.
Ethanol induction of sister chromatid exchanges in human cells in
vitro.

Alcohol also has some effect on cancer - probably not by directly causing it, but at least as an additional risk factor. One article I found ("Alcohol and Cancer") mentions the following possibilities:

The mechanisms by which alcohol consumption exerts its carcinogenic
  effect have not been defined fully, although plausible events include:
  a genotoxic effect of acetaldehyde, the main metabolite of ethanol;
  increased oestrogen concentration, which is important for breast
  carcinogenesis; a role as solvent for tobacco carcinogens; production
  of reactive oxygen species and nitrogen species; and changes in folate
  metabolism.

Using Pubmed you can find more articles on that topic.


text:
Carcinogens, how do they work?
The easiest carcinogenic thing for me to grasp is radiation, as it directly messes with DNA. Then it seems there are other compounds that simply mimic hormones, but these shouldn't necessarily cause cancer, right? Then there are things that can accelerate mitosis or mess with other processes, which can inadvertently mess with DNA. So my question is, in general, how many different flavors of carcinogens are there? I know there are a lot, but can someone list a good few? Maybe some examples? I'm most interested in how plastics and things like smoke cause cancer. I think a few examples would be best in aiding my understanding. Thank you!
Edit: I also just realized this is not the Chemistry Stack Exchange, I think I am more interested in the chemistry side of this question, but it might need to be migrated.

Have you read the WP article on carcinogens? Do you have any specific questions that aren't answered there or by a google search?

More Wikipedia articles to peruse: mechanism of carcinogenic behavior of tobacco smoke components (primarily by mutating DNA); Possible mechanisms of asbestos carcinogenicity. In general, my strategy is to look at the list of common carcinogens and follow the links to the carcinogen pages, and look to see if there is any info there on the mechanism of carcinogenicity.

Another interesting mechanism that can contribute to carcinogenicity via disruption of the DNA's structure and subsequent reading of the DNA is DNA intercalation.

The user wants the question to be migrated to Chemistry SE

this is not a chemistry question.. this is a biological question but a broad question. It should not be migrated to ChemistrySE. The OP can narrow down the question and add some details- it is perfectly on topic

"So my question is, in general, how many different flavors of carcinogens are there?"
As mentioned in the comments, almost all carcinogens act by damaging DNA.  In general there are three ways to do this:
Alkylation, a good example is pyridine.  These compounds covalently modify the DNA and either cause a mutation by misincorporation during DNA replication (where the wrong base is incorporated across from the alkylated base), or by generation of double strand breaks during DNA replication that result in a mutations during the repair process (the details of which are not in-scope here).
Intercalation, my favourite example being ethidium bromide.  These compounds literally insert themselves between the bases of the double helix, where they cause "fork collapse" during DNA replication, and the ensuing repair process mutates the DNA.
Ionization through radicals.  Yes, carcinogens can generate radicals that will generate DNA damage.  A good example is doxorubicin, which is a highly effective chemotherapeutic, but also a carcinogen in its own right.  Some heavy metals can also generate radicals under the right circumstances.  These compounds typically oxidize the bases of DNA, and result in broad misincorporation during DNA replication.  Radicals can also result in breakage of the phosphodiester backbone, which cause mutations during repair. This mechanism is taken advantage of in some methods for studying the primary and secondary structure of RNA molecules, and in "foot printing" methods.  Incidentally, it is this mechanism of carcinogenesis that causes antioxidants to be associated with the prevention of cancer.  Compounds like vitamin C soak up the radicals generated by the carcinogen (or radiation), thereby preventing the damage from occurring.
An interesting point: pyrimidine dimers, which are generated whenever you get a sunburn, are a carcinogenic form of DNA damage somewhere between the ionization and alkylation mechanisms.  UV light induces a redox reaction that results in covalent linkage of two neighboring pyrimidines.  A dedicated repair process can cause a mutation at the site of the dimer.
However, the take home point is that the DNA damage itself is not usually the mechanism of mutation!  Mutation occurs when the damage is repaired, either as part of a dedicated repair process, or by (non)homologous recombination after a stall in DNA replication.
I hope this answers your question.  It is a complicated subject, and I doubt I covered everything here.

There are no papers available which prove a carcinogenic effect of ethidium bromide. It is clearly mutagen and teratogen because of its ability to interact with DNA. It is used as a cure for trypanosoma in cattle. The dangers of EtBr are widely exaggerated.

They are indeed widely exaggerated!  However, it is an intercalator.  Nonetheless, intercalation is a mechanism for inducing mutations.  For example, coal dust is carcinogenic due to this mechanism.

But you have to differentiate between a mutagen and a cancerogen. Mutagens have indirect effects via hampering around with gene expression, while cancerogens act directly.

Doesn't get a little existential though?  I mean the actual carcinogen by your definition is a repair polymerase that slams in the wrong base.  I agree that it is important to point out what compounds are dangerous, and which are not, but at the end of the day, an intercalator is a potential mutagen, and everything else is context.

You are probably right.


text:
How does your body ultimately recover from a cold?
Is it the eradication of the virus (assuming rhinovirus) by white blood cells? Or does your body somehow adapt to presence of the virus?

Great question.
Rhino Virus
For the rhinovirus in particular, it is eradicated.
Integrase
However for some of the retroviruses and other virus that contain an enzyme called 'integrase', they actually integrate their DNA with yours. That way as your cells go about their business, they make the virus genes too. However, you have some white blood cells called CD8 T Cells that mark these 'compromised cells' for death.
Evading
Some viruses though can remain cleverly hidden and don't turn on their own genes in your genome until the immune response goes down, or you stop taking anti-retroviral drugs.  HIV is a great example of a virus you can also 'live' with but never actually eradicate. The medicines you take can kill all the circulating virus down to a non detectable level. However, when you stop taking your meds, the DNA integrated in your genome will start making the virus again, thus you will always 'live' and can never eradicate it.


text:
What are the lifetimes of cellular components on organelle or molecular level?
I was thinking that even though I know how generally the cell works, I don't really have a feeling of how volatile it is.
I want to know what is the lifetime/turnover rate of different constituents of the cell.
On the molecular level what are the lifetimes for various proteins, for ribosome, lipids, carbohydrates, DNA and RNA. What about aminoacids, nucleotides?
On the organelle level what are the lifetimes of the mitochondria, golgi apparatus. Does nucleus or ER ever change if not during meiosis.
I understand that the lifetime depends on the context. For example, for DNA, cells that replicate, half-life is about one replication as a whole new strand is generated. In neurons, that don't replicate for decades it's not the case. But the DNA can't just sit there. It is constantly unraveled, transcribed, damaged and repaired. So it has a different time constant.
I am still very interested to know any specific numbers.

Your question has several parts to it so I will attempt to address them one-by-one.
In terms of protein stability and turnover, this is a nice paper describing how human cell (HeLa) line, although this is a cancerous cell line, is used to measure the turnover of proteins (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3316722/?report=classic). They have used labelled amino acid technique and mass spectrometry (SILAC) to make measurements of protein turnover. It is concluded that on average the turnover is 20 hours, which is correct in my experience when doing gene knockdowns in Drosophila (S2) cells using RNAis as we incubate the RNAi with cells for 72 hours to ensure most proteins that we targeting are degraded and we can see the desired effects in cells.
Now getting to your questions regarding organelle turnover, you have to consider that cellular organells are very precious to the cells as most of them consume a lot of energy to build hence they are maintained unless they suffer critical damage, and they would become detrimental to the cellular integrity. In that case organells such as mitochondria undergo a specific type of degradation called mitophagy, which is a subtype of autophagy. Now I'm sure there are specific average times for the so called turn-over of cellular organelle under "normal" conditions but thats a slightly misleading view since the turnover can be tipped through reactive oxygen species (ROS) or ageing leading to less efficient cellular maintenance and buildup of toxic aggregated proteins or ROS.
Now just to clarify the use of the word half-life in you last paragraph, half-life normally refers to the time it takes for half the molecules in a given system to degrade (or to be more correct Half-life is the amount of time required for a quantity to fall to half its value as measured at the beginning of the time period) so I do not agree with your use of the word half-life in the last paragraph of above question although human DNA does have a replication limit (Hayflick limit) of roughly 40-60 due to telomer shortening and afterwards the cells (due to the DNA) that no longer replicates will enter senescence and eventually die.
Now getting to non-replicating, highly differentiated cells such as neurons, it still remains a mystery as to how neuronal DNA remains so highly stable (although DNA is a highly stable molecule (compared to RNA) and its further stabilised through histones), while undergoing many dynamic processes such as transcription (since if anything goes wrong the cells cannot be replaced at least in CNS) and how axons of some neurone that can reach over a meter in length are maintained so well for decades. There is a lively argument amongst the scientific community about this, which you can find out about if you simply search for axonal maintenance in a search engine.
Hope this answers some of your questions.

I agree that the DNA doesn't degrade per se, so in that sense half-life is the wrong word. What I meant was some temporal metric of its change from the original. If we look on one DNA, during replication it looses one half and a new one is attached. In that sense half of the DNA is no longer the same. So half of it has changed in one replication. After the second replication we will either with probability one half exchange the second old half, or the new one. I have calculated and on average it takes 3 divisions for the DNA to change.

In PCR based plasmid replication it is different, and more in line with your description, since primers are used and after annealing and amplification, you get denaturation, and the cycle continues so the original strand gets matched against new ones many times so you get a dilution effect of the original stand v.s the newly synthesised strands.

I am pretty confused now. http://en.wikipedia.org/wiki/DNA_replication#mediaviewer/File:DNA_replication_en.svg             Doesn't this show that DNA stays with its new strand?

Apologies, my bad. You are correct, it is a semi-conservative replication in cells so I see your point!

I was thinking of RNA pol and I confused myself and you. Sorry.


text:
Topology of protein

The domain structure of protein Z, which is composed of 180 amino
  acids, is shown in the upper part of the figure below. Protein Z is
  palmitoylated at a cysteine residue (the third amino acid) through the
  mechanism shown in the box.

Which of the following diagrams shows the correct topology of protein
  Z in the plasma membrane?

I think the second diagram is correct because cytoplasmic side has reducing environment and so SH will not be allowed to react this way. Am I right ?

I think you're right - disulfide bonds don't usually occur in cytoplasmic proteins either for that reason.

I don't think there's any oxidation or reduction going on in this reaction; certainly there is no net reduction or involvement of NADH cofactor or anything like that. Furthermore, I think that it isn't too hard (esp. since these are enzyme-catalyzed reactions) to imagine that the mechanism is simple: nucleophilic attack of the carbon of the thioester by the cysteine, forming a thioketal intermediate, resulting in ejecting the CoASH as a leaving group. No reduction or oxidation.
Instead of oxidation or reduction, I would think about where exactly are the components of each reaction present. In order for the palmitoylation reaction to occur, you need: the protein Z N terminus, palmitoyl-CoA, and protein acyltransferase. Where are these components more likely to be present, inside or outside of the cell? Especially given that CoASH has several negatively charged phosphate groups.

I would say - inside the cell because of the enzymes and the substrates required. But how is negative charge connected with this ?

This review (http://bio.ijs.si/~krizaj/group/Predavanja%202011/Biochemistry%20Lipids%20Lipoproteins%20and%20Membranes/02.pdf) indicates that thioacylation of the type depicted in the question is indeed a cytoplasmic process.

@biogirllajja, a common strategy for keeping cofactors inside the cell is to give them net charge, particularly negative charge since phosphate is the most common charged species around that can be easily added to molecules. The net charge prevents the diffusion of the cofactor across the plasma membrane. For example, one of the main reasons glucose is rapidly converted to UDP-glucose upon entering the cell is to prevent its passive diffusion out of the cell.


text:
Do humans have enough biological differences to be grouped into races or subspecies?
After my online research on the subject, I learnt that, biologically speaking, many scientists believe that there is no such thing as a race. Homo sapiens as a species is only 200,000 years old, which has not allowed for any significant genetic diversification yet, and our DNA is 99.99% similar. I've read statements that there can be more genetic variation inside a racial group than between different racial groups, meaning that, for example, two individuals from the same "race" can have less in common with each other than with an individual from another "race".
Wikipedia on Race (human classification) quote:

Scientists consider biological essentialism obsolete, and generally discourage racial explanations for collective differentiation in both physical and behavioral traits

Q1: If Homo sapiens has no races (according to biologists), why are we so different morphologically? (hair/eyes/skin colour and even athletic performance seem to differ between human populations)
Q2: Is it common for other species too, when genetically close populations have very different morphological traits? Are there any other mammal or animal species that exhibit biological diversity comparable to human diversity, and how do taxonomists treat these species? (excluding intentionally bred domestic species to keep the comparison fair)

The question has been paraphrased to emphasize that it is the biological debate that is in question, not the sociopolitical. I.e., why is there no consensus in evidence and opinions of scientists?

Why did you remove "to the point that we cannot tell an individual of one racial background from another based on a DNA sample" from the question? This makes the first sentence in the answer obsolete.

You have to note that taxonomy is artificial

Here a recent paper that mixes philosophy and population genetics that is probably of interest. I haven't read it though.

See also Does it make sense to classify all humans in a single species?

Some random googling gives this article on the topic (more searching might give other articles with different conclusions; I haven't made any comprehensive effort) which finds that ...human races/continental groups or clusters have no natural meaning or objective biological reality.

Firstly, it's not true that you can't tell racial background from DNA. You most certainly can; it's quite possible to give fairly accurate phenotypic reconstruction of the features we choose as racial markers from DNA samples alone and also possible to identify real geographic ancestral populations from suitable markers.
The reason that human races aren't useful is that they're actually only looking at a couple of phenotypic markers and (a) these phenotypes don't map well to underlying genetics and (b) don't usefully model the underlying populations. The big thing that racial typing is based on is skin colour, but skin colour is controlled by only a small number of alleles. On the basis of skin colour you'd think the big division in human diversity is (and I simplify) between white Europeans and black Africans. However, there is vastly more genetic diversity within Africa than there is anywhere else. Two randomly chosen Africans will be, on average, more diverse from each other than two randomly chosen Europeans. What's more Europeans are no more genetically distinct overall from a randomly chosen African than two randomly chosen Africans are from each other.
This makes perfectly decent sense if you consider the deep roots of diversity within Africa (where humans originally evolved) to the more recent separation of Europeans from an African sub-population.
It's also worth noting that the phenotypic markers of race don't actually tell you much about underlying heredity; for example there's a famous photo of twin daughters one of whom is completely fair skinned, the other of whom is completely dark skinned; yet these two are sisters. This is, of course, an extreme example but it should tell you something about the usefulness of skin colour as a real genetic marker.

Yahoo answers say you can't tell race from DNA... that's why I mentioned it. I also never heard this in crime investigations or detective stories... are you sure we can? Just double-checking, by no means I imply that my sources are credible.
Regarding skin colour, we can also consider that the skin colour of a Caucasian can vary from pale-white to red to dark-brown at different levels of UV exposure. These changes are only in the phenotype, not in the genotype.
What about athletic performance though? It's something more than just skin tinge. It must be related to organ systems, muscles, etc.

It depends what you mean by race; because race isn't actually meaningful you obviously can't reconstruct it. However, given a DNA sample it is possible to make a good approximation of the appearance of the person the sample is from. I don't think such a reconstruction would be reliable enough for law enforcement purposes, but it's pretty good none-the-less.

@Herman Suppose that in some sport it is an advantage to be very tall. Then because all genetic variation of humans is in Africa, you would expect the tallest people of the world to be in Africa. But you would also expect the smallest people in the world to be an African people. Similarly, in Africa you would find those who can sprint fastest. But you would also find in Africa those which are the slowest runners. So expect all variation to be on that continent. Also remember that those Africans who were deported to the Americas as slaves, all came from a small area on the west coast of Africa.

I think you mean to illuminate variable expressivity in the last paragraph.

does Europeans are no more genetically distinct overall from a randomly chosen African than two randomly chosen Europeans are from each other ?

@Qbik, yes, I believe it is, and I mentioned this information in the question too. I suggest you go to this part of Wikipeida's article on Fixation Index. There are also two links there to original studies, if you won't to go even further.

@Jack Aidley, how do "deep roots" of African populations and "more recent separation of Europeans" explain higher genetic diversity in Africa? Sorry, it doesn't make "perfectly decent sense" to me. Europeans inherited these deep roots too when separated, no?
From my ecology background I know that there are theories that claim that evolution occurs faster in the tropics, but I never thought about it in the context of human populations. That could explain your point, but I don't think that's what you meant.

@Jack Aidley, as to your first paragraph, have a look at this question. If you learn something new and change your opinion, you might want to edit your answer a little.

@Herman, from the answer to the question you link "So to sum up, DNA analysis can tell the gender, skin color, and eye color of the suspect, but very little about height and weight, and virtually nothing about age."

@Herman: Evolution follows a branching, hierarchical structure (broadly, it's more complicated than that) and Europeans group within the various African populations, i.e., they're essentially a subpopulation of a particular African population.

@JackAidley, do you mean the founder effect? A subset of the original African population that founded European nations did not represent the whole genetic pool of the original African population, is it right?

@Herman: No, although that can also be a factor. Have a look at this image - http://bit.ly/1iHOMss - and note how there is no clade that includes both Africans but not the Europeans. This is because the European population is a subpopulation of the African population. The two African populations shown are as different from each other as the European population can be from the first African population. In reality, there are many more distinct African populations than shown here.

let us continue this discussion in chat

I'm not sure skin color is a good example of characteristic that is used to classify people into race. In an ordinary life yes, race mostly equals skin color, but it seems that 20th century racial scientists relied more on skull measurements and facial features.

Well, that's just it, we don't actually have much phenotypic variation. For example, compare this:

to this:

or this:

Or this:

to this:

This is phenotypic variation:

So, as I hope is clear from the images above, phenotypic variation among humans is tiny compared to other species. We just notice small differences much more because, well, it's us so little differences are much more noticeable.

This ridiculously obvious illustration somehow put the issue in a totally different perspective for me. Quite an eye-opener. I think this is a brilliant answer, thank you for the effort.

Hmm... I'm not sure how useful comparing natural variation (human phenotypes) to artificial variation (dogs, cats and pigs) really is. Are you humans really less phenotypically variable than wild animal species? I guess ring species might make a good comparison?

@JackAidley birds of paradise are "natural" as far as that goes. In any case, the point is moot, whether the observed variation has been affected by humans or not, it is clear that the human species shows relatively little variation compared to what can be seen in others.

@terdon: The bird of paradise are not a species, as you note in your answer and I don't think it's clear - at all - that humans show relatively little phenotypic variation. I would say that humans are probably on the high side (likely due to the huge range that humans occupy).

@JackAidley the statement is one I remember from university. Anecdotal evidence like that presented in my answer seems to confirm it and I was tought it years ago. I'll see if I can find a proper reference but it certainly looks to me like we have far far less variation than other species.

Dogs are deliberately hybridized.

I also think it is misleading to compare human phenotypical variation and phenotypical variation that is the outcome of artificial breeding. To make this argument you would have to place human phenotypic variation within the range of phenotypic variation from a large number of "natural/wild" species. And comparing variation in birds of paradise (family Paradisaeidae) would only be valid if compared to Hominidae, i.e. including chimps, orangutans, extinct Hominini etc (still ignoring that taxonomic families cannot really be considered equal).

"excluding intentionally bred species to keep the comparison fair"

@Rodrigo yes, that was added after I posted this answer.

Maybe it's just me, but I'm having a hard time estimating any objective scalar value of the variation here. Nevertheless, it seems like humans still are on the top of the league regarding phenotypic variation. Look at the western jackdaw for example, four different subspecies identified mostly on the base of some slight colouring variations.

@Alex I'm normally a stickler for quantification, but I think the point is made quite well qualitatively. Your rebuttal is neat -- the jackdaw has similar variation to us. But that itself is justification for ignoring the subspecies divisions in jackdaws as much as imposing subspecies labels in humans! @bshane offered a great summary of subspecies here that demonstrates how arbitrary a term "subspecies" is.

All pictures exhibit some degree of phenotypic variation, and if you see all these people in person and close up, you'll notice yet more variation than with isolated faces. Even the smell is different (but how have we lost our smell senses recently!). So your answer is considered good because you used beautiful pictures, though your reason is completely subjective.

@Rodrigo of course there's some phenotypic variation. And of course you, as a human whose eyes and entire social structure are centered around the necessity of differentiating between the different members of your tribe, would see variation. That, however, does not mean that humans exhibit a lot of phenotypic variation. That said, no, this isn't a very good answer and yes, of course you'd need some hard, quantitative data to be able to answer correctly.

You say: What is race? "a lot of phenotypic variation". Seeing 29 upvotes in this answer reminds me of the fact that Homo spp are about 80% vision, but much less reason.

@Rodrigo what? I never said that race is a lot pf phenotypic variation. This answer is just pointing out that humans have far less phenotypic variation than other species. In any case, I'd appreciate it if you'd stop now. You first commented on this question in 2014, so just downvote it and walk away.

By the way, races of dog are really races? To me they seem only a few genetic loci that can control a limited range of morphological and behavioral traits. They're probably not the kind of "general genetic diversity" that some have been proposing for us humans.

Your example cannot show how less phenotypic variation, actually. The pathways between genes and morphology are far from linear. And we should not walk away from questions that bother us, should we?

@Rodrigo this isn't a discussion forum. If you disagree with an answer, you can downvote and you can leave a comment explaining, if you like. But engaging in long discussions in the comments is against the rules. I also have no interest in defending this answer from your accusations given that I dont' make the claims you think I'm making. So if you insist on badgering me, at least take it to [chat] where it belongs. Ideally, just downvote, express your disagreement and leave me alone though.

Sorry, but I think this is of relevance to anybody following this page. If we need to go to chat, the message appears automatically, like "Please avoid extended discussions in comments. Would you like to automatically move this discussion to chat?"

Let us continue this discussion in chat.

Human Fst is comparable to cats' Fst: https://emilkirkegaard.dk/en/?p=7753

I decided to summarize a competing hypothesis to make our answers more balanced. I also tried to address the question about the degree of human morphological diversity compared to other animals.

According to Woodley (2010), it is plausible that H. sapiens does not belong to one species and subspecies (i.e. is polytypic). Some of the data he uses to support this hypothesis could be useful for answering our question. He claims that H. sapiens, which is often considered monotypic, posses higher levels of morphological diversity, genetic heterozygosity and differentiation than many animal species which are considered polytypic.
Woodley cites a study by Sarich and Miele, who claimed that morphological differences between humans, on average, are equal to the differences among species within other mammalian genera (excluding species bred for domestic purposes), and are typically more strongly marked than in other animals.
However, morphological differences are known to be caused by little genetic differences too, like in the case of domestic dogs, which are still considered to be one species. Therefore, Woodley presented further evidence that looked on these inconsistencies in classification using allele frequencies and genetic diversity.
He presented data from a wide range of studies, which compares genetic diversity of various mammalian species based on heterozygosity (H), which is a common indicator for genetic diversity, and describes whether both alleles are the same or not on a studied locus. According to this data (which you can find in the linked paper):

Chimpanzees exhibited H of 0.63-0.73, which is very similar to H found in humans (0.588 - 0.807), however, chimpanzees are divided into four subspecies.
Some species like the grey wolf even exhibited a lower H (corresponding to lower genetic diversity) than humans (0.528 vs 0.588 - 0.807), while the grey wolf has been divided into as many as 37 subspecies.

This data suggests that humans are more diverse both morphologically and genetically than some of the other mammalian species that have been divided into subspecies.
References:
Woodley, M. A. (2010). Is Homo sapiens polytypic? Human taxonomic diversity and its implications, Medical Hypotheses, 74, 195-201. doi:10.1016/j.mehy.2009.07.046 (full-text PDF)

It's a political question. They think (or pretend?) they're fighting racism denying human races. At the same time, a country with more species and subspecies receive more funds for conservational programs (see my answer).

How would that translate into multiple species? From my uninformed perspective it looks like a species with a high but uniform heterozygosity is possible, so that there would be absolutely no clear cluster or even that any attempt to build clusters based on this would lead to weird effects such as people ending up into a different species than their siblings.

Bias
When you say phenotype you mostly mean "skin color", "size of the nose", "hair color", "shape of the eyes", "height", and some others. All these traits that we manage to find to explain population structure among humans. But you forget all the rest of the phenotypic diversity. If you would choose 1000 randomly chosen traits (external morphology and other stuff) and make a PCA. Will the main axes explain much of the inter-subpopulation (or inter-racial) diversity? I am not sure about that. One cannot use one subset of the total phenotypic or genetic variance and use it in order to define several species within what was previously thought to be one. It is not because two genes are associated with the same population structure that one can define two different species.
scientific observations vs biased intuitions
You say:

[..] is it reasonable to use a genetic approach to races and claim that biological races do not exist, while it seems to be a poor indicator, when it comes to comparison of phenotypes of human populations.

Similarly, one could say

Bats look like birds. We consider them as being mammals just because that is what scientific observations (genetic data or in-depth observation of the phenotypic variance) says. Should we follow scientific explanations when my personal bias intuition tells me that these observations are poor indicators?

The answer is yes if you want to increase your knowledge and no if you just want to be comforted into what you think you already know.
I have to confess though that I don't know much about phenotypic or morphological variations among humans. And I'd be curious if someone could give some words about that and whether or not much of the phenotypic and morphological variance is explained by what we consider being racial groups. It might be possible that very little of the total phenotypic variance is explained by racial groups but quite a lot of the face morphological variance is explained by racial groups.
Concept of species
For species that can reproduce exclusively with sex, we tend to use the concept of reproduction isolation to define a species and I really don't think that there is a pair of racial groups are sexually incompatible (however you delimit the racial groups). Eventually, there might have some slight inbreeding depression but I am not sure.
You might want to have a look at this answer to understand the semantic difficulties behind the concept of species

I would be very, very surprised to find out that any two racial groups cannot reproduce: not only we are one species, we are also one subspecies, and we share over 99.9% of the same genome. The world would be a totally different place if this was true, from the sociopolitical perspective. It might happen one day though. I hope collectively we'll be much wiser when and if it does happen.

Yes, that would be immensely surprising indeed! But I don't think any study ever reviewed cases of reproduction between all "considered social groups".

On the other hand, it also means that no one has ever noticed any suspicious trends in child mortalities from cross-racial parents to think about such a survey.
I also believe that gentlemen from the Third Reich would be very interested in this question, and they conceivably could do some research, which wasn't published because the results were negative. It's just my guess though, and I'm no specialist in history.

Remi, sorry, I'm not familiar with PCA, and the Wikipedia page is intimidating. Was your first point that we share so much traits in common that the ones that distinguish us from each other are statistically non-significant?

"For species that can reproduce exclusively with sex, we tend to use the concept of reproduction isolation to define species and I really don't think that there is a pair of racial groups are sexually incompatible" But this reproductive isolation is not only due to genetic incapability, but to purely practical geographic isolation as well, right?

But other animal races are only defined genetically? Or is it (or has been for millennia) more a biogeographic concept? Or, for any species where there is no genetic data, we just can't say anything about races?

It seems to me that many answers to this question suffer from the nasty habit of "political correctness". As a zoologist, I never heard of somebody sequencing the whole DNA of any species to decide when to use or not the term "race". If a group of animals comes from a side of a river, and the other comes from the other side, and they have one or a few distinctive features (color of chest pelage, tuffs of hair in the sides of head, etc), that's enough to call them both different races (or even subspecies). Of course some geographical isolation has taken place, although it hasn't been long enough to divide the two (or more) populations into full species. The same logic should be used to humans, right? Maybe some folks believe that, pretending there are no human races, then the question of racism is "solved"? Bad logic, to me.
Look at http://www.worldbirdnames.org: they cite 10,518 extant species of birds and 20,976 subspecies. About 2 subspecies per species. How do they do that? (No DNA for most of them.) Subspecies/races are usually from different regions (like human races), their vocalizations are usually different (like human races) and their colors sometimes vary (not as much as in human races). My point is: there is NO SCIENTIFIC REASON to say there are no human races, if we're using zoological reasoning. (Unless we are not animals anymore!)
For mammals, http://www.catalogueoflife.org/col/browse/classification/kingdom/Animalia/phylum/Chordata/class/Mammalia/match/1 cite: 4,843 species, 2,998 infraspecific taxa. Again, if someone show me they did complex DNA analysis for most of those infraspecific taxa, and those analysis showed that variation inside races is smaller than between races, THEN I will be forced to agree with them.

Maybe, but the "why?" question is beyond our scope here, I asked the "is it?" question, which is purely biological. If you improved your answer by expanding on your experience as a zoologist when it comes to defining subspecies and removed the "why?" question of your own -- I, personally, would like your answer much more :-)

I just inverted your question: "If human populations have several distinct phenotypes, why (they say) there are no human races?" Or, from other point of view, I questioned your first "If" in the title. It's not just a biological question, to me it seems much more a political one. How many biological races have been described? Or subspecies? Take a look at IUCN Redlist, for instance, or Zoological Records in many universities. Do you really think they scanned their DNA in depth? There's no biological reason for a different approach on human beings. As I said, it's just politics.

I think you make a fair point... I might paraphrase my question. Why paraphrasing? Although intuitively I agree with you that it might have something to do with politics, it's not really something that I wanted to discuss, and it's probably not even allowed to be discussed on Biology SE. If we do, someone will ask: "Well, how do you know that it's all just politics", and here we go, it becomes a debate with no science behind it, just opinions.

Rodrigo, ok, most of subspecies and "races" in zoology don't have DNA analyzed but are still considered to be separate. However, in the case of humans it is analyzed, so it would make sense to apply this information if it indicates that humans cannot be grouped in races, wouldn't it? (whether that's what our DNA indicates or not is another, not mentioned by you, question)

What is the definition of race? Is it the same as subspecies or semispecies? http://www.ucl.ac.uk/taxome/jim/Sp/Sub-semi.pdf By this article, what human DNA says is that human races are not human semispecies nor subspecies. According to Mayr definition (http://en.wikipedia.org/wiki/Race_%28biology%29), "races" is a concept that requires less genetic divergence than subspecies.

@Rodrigo However, generally, I would argue that when classifying non-human animals into races we either know or imply a very low level of gene flow between races/subspecies. We know that this is not the case for humans.

While I see your point about there being races, I very much doubt you'll be able to support the use of the term as it tends to be used today. With the criteria you state, the Scots and the English would be different races, for example. If we take variations in vocalizations and geography as indications of race, each country will represent a race of its own. So while your argument does indeed support the existence of human races, it does not support the idea that those races are defined by color alone.

Well, all this should be properly studied. I just don't agree with the "findings" that "there are no human races".

Couldn't you also phrase this as "genetic diversity of most animal species is probably overstated, because morphological differences which aren't sufficient to establish the existence of subspecies in humans are used to claim the existence of subspecies in other animals" -- or in other words "look at how there aren't human races -- therefore there probably aren't  as many animal races in most cases where we assume that there are animal races". I don't understand how your answer shows that there are human races, in other words. It just seems to show that zoological reasoning is bad.

@Will Actually I'm asking: What is the present definition of race? Is it the same definition we used 30 years ago?

Oh OK that makes sense

You claimed that vocalizations & hair/skin coloration are evidence of substantial genetic differences between races; but this is flawed. Fair-skinned individuals, if exposed to UV radiation develop darker skin. While this isn't permanent for them, the fact that the change can happen within an individual's lifetime indicates that it is not a dramatic difference in genetic / evolutionary terms.
Human vocalization is dependent on the environment. If you adopted an infant of another race and raised it, it would speak in your language & accent; not that of its biological parents.

@Kent.Green people who lived in cold climates for millennia developed a white skin, and those who lived in warm climates for millennia developed a dark skin. Both are well adapted to their environments. That's the biological definition of race, not the amount of DNA involved in the adaptation.

That's exactly my point, while superficially races appear very different; the amount of DNA involved in the distinction is relatively small, which is the reason that "race" does not make sense as a classification on the level of species or subspecies. Moreover, you still haven't addressed the differences in "vocalizations" which are even more contingent on environmental conditions than skin pigmentation.

@Kent.Green Races are indeed less "discrete" entities than subspecies. I just want to know how much DNA divergence people want to use as part of their definition, since I've not seen such "objective" definition anywhere, just a systematic denial of the existence of human races (motivated by some kind of "political correctness" it seems). About human vocalization, you're right, it's not the best trait, but it does show that human populations remained isolated for long periods. That's the general definition of "geographic races" used in zoology, or I've been learning it wrong for so many years?

Here is a source that might be what you're looking for: "The biological definition of race is a geographically isolated breeding population that shares certain characteristics in higher frequencies than other populations of that species, but has not become reproductively isolated from other populations of the same species."

http://www.biologyreference.com/Ar-Bi/Biology-of-Race.html#ixzz4dVXjcmSb

Not objective at all. Skin color, hair type, nose format... those already are "certain characteristics". By this definition there are human races.

This is a bad answer, opinion-based and apparently driven by some kind of political views, and proposes an incorrect definition of 'race' or 'subspecies. People in the past didn't use genetics to identify subspecies, but they do now, and for good reason. Take a read of this paper to educate yourself.

@user438383 Thanks for the link. Dog races are called dog subspecies?

First you can take a look at this diagram:

You can make a google image search for "Cavalli Sforza" and get a lot of similar diagrams. This diagram is using a concept known as genetic distance by fixation index. This is a way to measure how different different ethnic groups are genetically.
Basically what you do is you compare how many differences there are on average between two humans from the same population and between two humans from two different populations. The same method can be applied to animals. There is no "threshold value" where you can say that two groups of people or animals have become different enough that they can be defined as "different races".
Traits such as skin colour are regulated by a very small handfull of genes so even if we have different skin colours that does not mean that we differ much genetically speaking.
Lions and Leopards can have fertile offspring and live basically in the same habitat in Africa. I do not know if crossbreeding is known to have occured in the wild. Probably a hybrid has lower fitness than the original species.

So, what's your point about human races?

I would say focus on the actual differences instead of the name. Differences as far as Fst, IQ etc. goes. "These are the differences between group A and group B". I like the term "ancestral group", nobody can really deny that they have an ancestry.

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


text:
Events after Endothelial interruption
What are the physiological events that occur after there is endothelial interruption in the blood vessel?
What does endothelial interruption mean here? And what could be the physiological events?

Are you sure it is endothelial interruption ? Do you mean injury ?

Our teacher gave us this question as an assignment so, i think i should ask him about "endothelial interruption". Thanks


text:
How does sequence independent single primer amplification work?
I'm having difficulty finding an explanation of how single primer amplification of DNA works in the literature available to me, can anyone explain the methodology and what it accomplishes?

This process is called sequence-independent single primer amplification (or in short SISPA). Its used to amplify unknown sequences for amplification, for example in unknown viruses.
The primers used for this process contain random sequences which should bind to the DNA to be amplified and also known sequences, which can be used a adapters. In the first rounds of PCR only the random primers give rise to specific products, which are amplified exponentially in the later rounds of PCR since the primers fit perfectly then. This is described in detail in this publication:"Random priming PCR strategy to amplify and clone trace amounts of DNA"
Another interesting paper describing the method is:"Sequence-independent, single-primer amplification (SISPA) of complex DNA populations."

single primer amplification is used to find unknown regions of DNA if you have no idea what to use as a primer further upstream. It works on the idea that any primer given a certain temperature will misprime. That it, it will anneal to a non specific location. So it is PCR, but at this temperature, the five prime region primer will bind specifically to it's known location. On the three prime end up to 3500 bases away, the low annealing temperature will allow this specific primer to bind to something resembling its complementary sequence but not exactly. This way you will still get a successful PCR reaction. Then as the cycles continue, the 3' end binds specifically to your one primer and you can raise the temperature to make it more specific. The primer design and temperatures have to be considered very carefully.
Sources
Roth Lab


text:
Why are genes expressed as proteins rather than other types of bio-molecules?
I guess, we could infer that the structure of an amino acid has the same functional units as RNA is used to synthesise it. Therefore, from a logical point of view it would make sense that genes are expressed as proteins.
However, why is this the case; why are genes expressed as proteins rather than any other type of bio molecules? Also, from what are other bio molecules expressed if not for genes?

Wow - like a biophilosophy question! The answer lies in in building up the largest diversity with minimal subunits. Efficiency if you will. In this case we are talking about amino acids. We only need 20 of them to approach unfathomable numbers of diversity.
The protein acts as a messenger, as an enzyme, a carrier and it's own building unit. If you wanted that kind of range out of any other known biomolecules, you would need a gene to code for each of them, and itself a gene a completely different mechanism to build them which we can't even fathom. It's so much simpler to code for a protein, which can act as an enzyme to build other biomolecules.
However if you are asking about why the central dogma of molecular biology is the way it is...well then, it seems to be axiomatic.

No, in fact I wasn't intending for it to be a "bio-philosophy" question. I just couldn't think of a better way to explain it, than touching on points that I already know.

No I like it. Don't misinterpret. Life is so complicated though so its a very real possibility that the our central dogma of molecular biology could of been completely different.

The fact that genes are expressed as proteins and no other type of molecules is because it is one of the oldest remnants from evolutionary history and it was so successful that it has carried on throughout the eons and is now present in every known living organism. It is so old that most biologists would say that it has been present since life first began.
Scientists conclude that it is one of the oldest because the genetic code is universal. That means the gene that codes for a specific protein can be inserted into a completely different organism and that organism will begin synthesizing that protein. There are very few exceptions to this rule and this is how scientists can culture bacteria to produce human enzymes such as insulin.
Genes do not code for any other molecules because there has been no selective pressure for it (if that can actually apply here) and proteins are quite diverse in structure and function for having so relatively few building blocks. There really are no other macromolecules quite like them.
I am unaware of any non-protein molecules being expressed from genes. You might say that RNA is, but you have to skew the definition of "expressed". Ribozymes are a good example to make this case. But there is a reason the creation of RNA is called "transcription", meaning the RNA is not coded from the DNA, rather it is analogous to it, while the creation of proteins is called "translation", meaning that there is a code involved to get the correct result. It is also obviously clear that RNA serves for protein synthesis and is far less dynamic than proteins.