text:
Hardy Weinberg problem help!
The three common genotypes at the hemoglobin locus have very different phenotypes: SS individuals suffer from severe anemia, AS individuals have a relatively mild form of anemia but are resistant to malaria, and AA individuals have no anemia but are susceptible to malaria. The frequency of the S allele among the gametes produced by the first generation of a central African population is 0.2.
(a) Assuming that mating occurs at random, what are the frequencies of the three genotypes among zygotes produced by this population?
I know that this is 0.2 for the S allele (q in the hardy weinberg equation)
and 0.8 for the A allele (p in the hardy weinberg equation).
So for the frequencies I got
AA = 0.64
AS = 0.32
SS = 0.04
(b) In this area, no SS individuals survive to adulthood, 70% of the AA individuals survive, and all of the AS individuals survive. What is the frequency of each of the three genotypes among the second generation of adults?
I don't know how to do this! I don't understand what to do! I tried multiplying
0.64 by 0.7 (because only 70% survive), but I know that is wrong answer. I know you have to divide 0.64 x 0.7 by the total that survived, but I don't understand why you have to do that. You didn't have to divide for part a, why do you have to divide for part b?
Also for some reason the frequency of the AS is not 0.32 for the answer. I don't understand why! Please Please help me.
(c) What is the frequency of the S allele among gametes produced by these adults?
I dont know this either!
PLEASE EXPLAIN ALL OF THIS TO ME IN CLEAR STEPS! THANK YOU SO MUCH.

Your answer to a) is correct (standard Hardy-Weinberg equation).
For b) you have to consider that you are calculating proportions of the population, which should sum to 1. Since 30% of the AA individuals and all SS individuals die, this is not the case after selection, which is why you should divide the frequencies by the total proportion that survive (also for the AS genotype), such as:
$$
\begin{array}{c|cccc}
\text{genotype} & \text{freq before} & w_{survival} & \text{freq after selection} & \text{corrected freq}\\
&\text{selection}&&&\text{after selection}\\
\hline
AA & 0.64 & 0.7 & f(AA)\cdot w_{AA}=0.45 & 0.58\\
AS & 0.32 & 1 & f(AS)\cdot w_{AS}=0.32 & 0.42 \\
SS & 0.04 & 0 & f(SS)\cdot w_{SS}=0.0 & 0.0\\
\text{sum} & 1 & & 0.768 & 1
\end{array}
$$
here $w$ is the fitness of genotypes. And for your comment on why you didn't have to divide by the sum of freqencies in a): you could do this, but since the sum of genotype frequencies is 1 it doesn't make a difference.
For c) you use the standard formula for calculating allele frequencies from genotypes, so that $f(A)=f(AA)+f(AS)/2= 0.79$ and $f(S)=f(SS)+f(AS)/2= 0.21$.


text:
The selective pressure of contraceptives
Is it possible that the use of contraceptives will produce evolution humans? Contraceptives can reduce reproductive success, so shouldn't selection favour resistance to them?
In this case it might be useful to think of evolution as a "black box", an information processing mechanism  where only input and output is relevant. From this point of view, we would expect the box to produce an output comparable to the resistance that evolution will produce in a population experiencing a poisoning effect which seriously damages its reproduction mechanism.
The evolutionary "output" from such poisoning  has been studied in great detail. Are there any lessons relevant to future human evolution in these studies?

Well, it seems the subject of contraceptives as an evolutionary factor is not welcome on this website , even if common sense can determine it to be one of the most powerful evolutionary factors determining the future of the human species .  Each person can reach his own  conclution regarding this dissonans...

The topic is certainly welcome. Your question was closed for being unclear rather than off topic. It would have been nice if any of those who voted to close would have explained why. I've editing the grammar a bit and given it some structure.

I think it need works on clarifying a) what you expect to happen if a population of humans has access to contraception b) why you expect that outcome c) why you think it has consequences for human evolution @user3407

@kmm Do you understand the question?

@canadianer Is there any work on novel selective pressures resulting from widespread use of contraceptives and can these selective pressures be modeled on the selective response in the same way as antibiotic resistance or strong truncating selection?

question is very vague and what @kmm rephrases, seems to me, is far from the OP statement, which appears to be looking for opinions

Once you bring choice and selective breeding into the equation, you are pretty much circumventing natural selection. You only need to look at domestication to see how an understanding of cause and effect in breeding can introduce significant phenotypic differences into the population. You could also implicate all of Modern Medicine as circumventing evolution. Children who would have died 1000 years ago prior to reproduction now survive to reproduce. Young adults are kept alive and can go on produce more offspring that would never been a part of the population if NS was not bypassed.

Your choice of words such as "poisoning" and "seriously" reflect that you have a clear bias against contraceptives.

@kmm The question is loaded and isn't really looking for a real answer, it is asked to pose a particular bias against altering human reproduction and introducing choice into the equation. The OP is making a statement in the form of a question. A neutral question, looking for a productive and informative answer would have simply been to ask how does the use of contraception effect evolution and is there evidence that shows that it has introduced new forms of selection. I have a doubt that even a well researched answer would sway the OP. I agree with the original vote to close this question.

There is another point that this question misses, and that is that selection acts on the species. As long as enough of the sapiens species is reproducing, it really doesn't matter evolutionarily what a given individual choses to do. Homo sapiens genes will live on, as Neanderthal genes do in sapiens of European and Asian descent and even if the next species of hominid evolves from sapiens and takes over the Earth and sapiens go extinct.

Relevant, although not a serious answer: http://www.smbc-comics.com/index.php?db=comics&id=2632#comic

Interesting question, but the answer is simpler than you might think.
Antibiotics put selective pressure on bacteria. Bacteria resistant to that antibiotic evolve as only the resistant ones survive. But this is the key, there has to be at least some already resistant bacteria from which the new (resistant) population will emerge.
With contraception, this is not the case. There are no spermatozoids capable of penetrating condoms, for example, and you should also bear in mind that in most cases mild hormonal disbalance is enough to prevent conception. It's a very delicate process, and contraception is basically an overkill.
Even if some spermatozoids could penetrate condoms, that trait would have to be hereditary in order for evolution to occur.
If you'd want to prove that contraception constitutes selective pressure on humans you'd first have to prove that there are spermatozoids and egg cells that can beat contraception, and that it's hereditary.
Evolution doesn't work the way you think it does. If you kill a random person, even if you kill a million people, it's not necessarily selective pressure. There are rules to evolution, and one of them is that it has to be hereditary.
This is not.
It wouldn't even come close to being artificial selection, let alone natural selection.
Besides, there's 7.3 billion of us. More than ever. We can hardly say contraception is reducing the world's population.
You also fail to see one thing, that a person who uses contraception in teenage years still has kids as a young adult. Contraception just delays pregnancy until you're ready. In evolution, there's a concept of "surviving long enough to reproduce". You can both use contraception and be an organism with 10 kids - though not at the same time.

Interesting question. I did not fully understand the entirety of your post so I will answer the question posed in the first sentence, namely:

Does it seem probable that the existence of contraceptives (which has reduced human reproduction to below survival-level in many populations) will be a completely new selective pressure on human evolution?

Yes, the use of contraceptives is a selective pressure. The couples that don't reproduce simply don't pass on their genes so evolution "is favouring" those couples that don't use contraception. This is a bit tricky because if a couple uses contraception for life and doesn't reproduce at all, they are evolutionary dead ends and selective pressure can't act on them because there isn't anything passed to the next generation.
For the couples that use contraception for longer or more often, leading to delayed childbirth or less children born, then the parents would have contributed less genes to the next-generation's gene pool so they may be wiped out more easily. Thus contraception reduces the fitness of humans using it if used often enough to keep the populations using it below replacement levels.

Choice implies that selection is artificial as opposed to natural. Natural selection relies on random changes to the organism and the environment that organism inhabits and favors the organisms fitness to survive in that environment. There are some that would argue that in a society with finite resources, that those who limit their offspring increase the advantage that they give their offspring to thrive, survive, and succeed in passing on the genetic inheritance.

If you keep a population below replacement levels, all genes will be lost regardless of how well you train your offspring. Yes, there is a balance between number and quality of offspring but only if you have enough to propagate the genes forward to the next generation. I.e. there is a lower bound which is around 1.2 or so and some countries are close to this already.

I placed the comment on the original post, but when looking at selection, you have to look at the species as a whole. And as a whole Homo sapiens birth rates far exceed replacement levels.

If contraception helps us to achieve the proximal rewards of sex without reaching one of the ultimate goals (reproductive success), you could say that the availability of contraceptives inhibits reproductive output. But, I don't think that it's as simple as that. The availability of contraception merely means that the desire to have sex no longer automatically leads to the conception of children. Instead, a wish to have children often first needs to get into play. Thus, you would expect a strong fitness reward for individuals who are capable of effectively planning for children and not postponing it indefinitely into the future until they are no longer fertile.
As mentioned in previous answers, you won't get too see condom-tearing supersperm any time soon, but I dare predict that we should expect to see an increase in condom-tearing behavior over the next century or so. Currently, I think there's definitely a shift in selective pressures on behavioral genes related to reproduction.
A caveat is of course that changing behavioral output could also be induces by cultural evolution. Cultures may instill taboos on contraceptives (think of the Catholic Church's attitude towards condoms), or cultures may facilitate child care to stimulate child-bearing at a reproductively healthy age.
An altogether other possibility is that the average age at which the decline of fertility sets in will significantly increase.

Can you provide links that support the selective pressures toward behavioural genes? Also, unless most babies are born thanks to condom-tearing-sperm I don't see how it would be selected for genetically.

Sorry, I should have mentioned that my answer is entirely speculative. Also, I don't mean condom-tearing behavior of sperm. I'm talking of behavior on an whole-organism level.

In principle, contraceptives are a barrier to reproduction, and selection will approximately operate by maximising reproductive. Therefore, one would expect that selection would favour "resistance" to contraceptive methods. However, there is a big difference between selection and adaptation (evolution by selection).
An adaptive response can only evolve if there is heritable variation for the trait, in this case, resistance to contraceptives. For example, imagine we had a pill taken by men which disrupts sperm production as our only contraceptive method. This pill is not 100% successful, as some men still produce viable sperm because they have a gene/allele which prevents the pill from damaging sperm. Given enough time (and assuming no other contraceptive/abortive measures can be taken), then this gene should spread through the population, because carriers will produce more offspring (who in turn are likely to carry the gene).
This hypothetical scenario is similar to that of the evolution of antibiotic resistance in bacteria. We use antibiotics to kill populations of bacteria, but some members of the population have genes that protect them from the effects. The carriers of the resistance genes will then produce the next generation, all of whom carry the resistance gene.
Similarly, you can think of populations where toxic chemicals are more present. In some populations, arsenic is present at high levels. Arsenic is toxic and will decrease reproductive success (because there is a higher tendency die before proper opportunity to reproduce), so consider the environmental arsenic as our "contraceptive" in this scenario. Genetic variance in the ability to metabolise arsenic arose (e.g. by mutation) and spread through a population because of the advantages it gave.
In reality, there is little-to-no genetic resistance to plethora of contraceptive methods we can deploy - the failure of contraceptives is random not genetic. Therefore, we are not going to evolve resistance to contraceptives any time soon.
Furthermore, contraceptives may reduce the rate at which sex leads to reproduction, but it may allow parents to choose when to produce offspring and how many to produce more easily. As such, the children might be provided with better developmental environments or have a lower rate of infant mortality etc. so fitness could be higher in this group compared to those who are resistant to contraception. If so, this could select against contraceptive resistance. It's not reproductive success that matters, but the tricky concept of fitness.

Do you mean that (A) the choice of using contraception is part of the human phenotype and we can study the selection pressures that apply to it or that (B) you consider the absorption of a contraceptive as an external selection pressure and are wondering what evolutionary answer this selection pressure will cause?
If (A):
One can only study the evolutionary pressures applying on the use of contraception under the following conditions:

The choice of using contraceptive is inheritable
People who do use contraceptive have significantly less (or more) kids over their entire life than people who do not

I am not sure any of these conditions is fullfilled.
If (B):
If it was as simple as a "poisoning effect which seriously damages its reproduction mechanism", you could expect the emergence of a resistance allele (for example that would make females insensitive to oestrogens in oral contraceptives).
However I guess that persons who use contraception are likely to choose abortion if pregnant, decreasing the fitness effect of such a potential resistance allele.

I want to upvote the rest of this answer, but can't whilst you generalise people who use contraceptives as people who will readily have an abortion. That statement has no grounding whatsoever.

@GoodGravy As that portion of the answer is speculative, and likely not supported by references, you can edit it to improve the answer.

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text:
How would real-time blood glucose monitoring work?
Is it possible to perform real-time blood glucose monitoring using a wearable non-invasive device (similar to a fitness band measuring heart rate)? I'm aware that there are some devices in the market developed by medical companies but most of them require you to stick a needle in your body and it also requires you to switch needles and reapply it every few days.
How can blood glucose be measured in a non-invasive way?

Mark Arnold and other's have done work on using near infrared spectrophotometry to measure blood glucose non-invasively, but I'm not aware of any clinically approved methods available yet.

NIR spectrometers are relatively big and heavy and not cheap and this has been a hurdle in any wearable device, but perhaps there are MEMS type devices being developed. Luminous Medical, now out of business first proposed a monitor using NIR spectroscopy. But it was targeted for the hyperglycemia of the sick and injured (hospital use) rather than ambulatory diabetics. The cost of the technology is one of the factors that caused the company to fail.

If you browse the on-line patent data bases - either www.uspto.gov or www.freepatentsonline.com for "glucose monitor" you'll find there are at least half a dozen technologies that have been proposed including the most non-invasive technologies such as using light - similar to the pulse oximeters used in hospitals to measure the pulse and PaO2 through the skin to more invasive methods that periodically pump small samples of blood outside the body for chemical or optical analysis. But in terms of accuracy, the best way to measure BG is by some means that can analyze arterial blood in vivo.
Companies that are trying to develop these devices are shooting for accuracies better than 12 mg/dL, but that's very hard to do with the noninvasive methods. There is a very new technology that uses a contact lens as the sensor, measuring from the iris and transmitting to remote electronics for processing, but that's still probably year's away. I believe the best products that are available today may be those developed by Dexcom in San Diego, CA. See their website here: http://www.dexcom.com/
The journal Science just published its year end Breakthroughs and that includes an article that shows hope in restoring the B cells in the pancreas for type I diabetics see http://www.sciencemag.org/content/346/6216/1444.full . This of course is the best solution - a cure. I hold hope scientists are less than 5 years away from that goal.

Those are beta cells (B cells are a type of blood cell), and there are many more T2DM patients than T1DM. Beta-cells would do little for them.

http://news.sciencemag.org/chemistry/2015/01/temporary-tattoo-measures-blood-glucose-levels

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If a gene is located on the X chromosome, does that mean males are never heterozygous for these genes?
As said in the title I am a little confused on the idea of traits located on the sex chromosomes. The example we worked on in class was haemophilia, a recessive trait located on the X chromosome. Does this mean males only have one allele to choose from while females have two? Does this mean that only females have the ability to be heterozygous in sex linked traits?

I guess the terms heterozygous or homozygous are not applicable because there is no homologous chromosome. I think this condition is called hemizygous if I am not wrong.

http://onlinelibrary.wiley.com/doi/10.1111/evo.12224/epdf

There is a specific term for this called hemizygous / hemizygote - meaning that only one allele of the gene is present. Therefore males cannot be heterozygous for genes on the X or Y chromosome (not counting for gene duplication or other chromosome disorders) since they naturally carry only one copy of these chromosomes.

Thanks! I knew there was a term for it when I posted my answer and I couldn't bring it to mind.

Do you mind adding a source that will make the answer complete and will be a good source for users who stumble upon your answer having the same question?

@SanjuktaGhosh Thx, good point well I could link wikipedia for quick fix :) I'll look for better source when I have time (may take a week, i'm quite busy atm).

All of the other answers are basically correct, I just wanted to add that there are some genes which are present in both the X and Y chromosomes, in the pseudoautosomal regions. These genes are inherited in an autosomal manner (hence the name). A male has two copies of each, just as a female would, and can thus be homo- or heterozygous.

In XY sex determination systems the females carry two copies of the X chromosomes, thus can be homo- and heterozygous. Males however, carry one X chromosome, meaning that all loci are hemizygous (excluding those with homologs on the X). Under conditions of complete dosage compensation, often through up-regulation of X linked loci, they are effectively homozygous, as demonstrated here where expression levels of X-linked genes are at a ratio of near 1:1 with autosomally linked genes.
An interesting potential consequence is that males will exhibit more additive genetic variance in X-linked loci.

I down voted because you say that all loci are hemizygous, which is misleading (see my answer). If you change it to "most loci", or something to that effect, I'll gladly turn that arrow upside down.

@canadianer Good point, edited

Because males only have one X chromosome, they can only have one copy of any gene found on the X chromosome, and therefore only have one allele. This means that in the case of a recessive disorder like hemophilia, should they happen to inherit a recessive allele from their mothers, they will have the recessive (disordered) phenotype because there is no other allele present to give them the dominant phenotype.
"Homozygous recessive" and "homozygous dominant" are perhaps a little misleading here because male individuals aren't homozygous at all, having only one copy of genes present only on the X-chromosome.
But yes, this means only women can be heterozygous for sex-linked traits. Men will have either the dominant or the recessive phenotype, and cannot be carriers.

It sounds like you pretty much have it. Hemophilia is recessive, meaning that a single function copy of the necessary clotting genes will be sufficient to function. So a female can inherit defective genes on one X chromosome and functional genes on the other and be perfectly fine. However, if a male inherits defective genes on one X chromosome he will have the disorder because he does not have another X chromosome to provide the functional genes to compensate.
I realize that you also said you are confused about traits located on sex chromosomes. They are essentially just like any other chromosome and carry genes just like other chromosomes. It just so happens that they also carry genes that are important in sex determination.

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How did life survive in the Snowball Earth theory?
There is this theory that says that the whole Earth was once covered with snow and ice. How was it possible for life to survive this extreme state?

If you refer to ice ages, at that times not the complete earth was covered in ice. Do you have a source for this?

@GerardoFurtado Interesting, I didn't knew that. Always something to learn here :-)


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What are the problems in using an ssDNA or an mRNA for expression instead of using a plasmid?
Let's say you want to do a gene cloning experiment. You have an empty expression vector (mRNA or DNA) and are looking to clone some gene X into it. Why is it you can only buy X already inside a vector (which is in turn often inside a bacterial carrier)?
What is the problem with handling pure mRNA nucleotides of gene X? Or even sscDNA?

Plasmids are vectors. The inserted gene is called a clone or simply an insert that the vector carries.,

@WYSIWYG No, vectors are vectors, plasmids are plasmids, in some cases plasmids are indeed vectors. But literally a plasmid is just a piece of DNA.

I meant the plasmids used in molecular biology, not the natural plasmids.

What is the problem with handling pure mRNA nucleotides of gene X? Or
  even sscDNA?

Problems in directly transfecting a mRNA/ssDNA
mRNAs can be transfected into the cells and is quite frequently done. The problem with transfecting mRNAs directly is that the mRNA gets degraded soon and you will not have sustained expression. This is, however, very useful in certain cases such as creating induced pleuripotent stem cells (iPSCs) where you do not want the cells to continually express the Yamanaka factors (some of which are also oncogenes).
Also, RNAs as such are quite susceptible to degradation. It is much easier to prepare and store DNA solutions for a long time.
Similar problems arise with a ssDNA.

Why is it you can only buy X already inside a vector (which is in turn often inside a bacterial carrier)?

One great advantage with using plasmids is that you can propagate your gene infinitely. If you were instead given a fixed amount of mRNA, then you will run out of it soon. Some vendors do practice such greedy capitalistic policies :P
When you are amplifying a DNA using PCR then cloning it has an additional advantages:

you can sequence the gene using well standardized primers (like T7)
you can make constructs that can express the gene conditionally

You have an empty expression vector (mRNA or DNA) and are looking to
  clone some gene X into it.

You cannot easily clone something inside an RNA. You need specific RNA endonucleases. Moreover a double digestion will be disastrous in this case.

Why vendors don't generally sell a dsDNA insert but rather provide it cloned in a plasmid

A circular dsDNA is more stable
Vendors can keep the stock of the insert for future customers without having to do PCR again
Cloned insert can be amplified via bacterial cultures to obtain very high amounts (maxi/giga preps)

I was thinking from a workflow perspective. When you buy a plasmid (usually double stranded DNA in a bacteria) you need to extract the plasmid first, then cut out the ORF, then amplify and ligate the ORF extract to your own vector. Why don't they just sell vials of ORF?  That should be easy to self-propagate too.

@jiggunjer No you generally don't buy the bacterial culture carrying the plasmid. You just get the plasmid dissolved in Tris-Cl pH 7.5. Linear DNA containing just the ORFs cannot self propagate. You can PCR a piece of DNA but with bacterial cultures you can get a lot of DNA (maxi/giga preps). Circular DNA is relatively more stable too.

Even if one gets pure plasmid, why not pure ORF. I admit the "non-circular is less stable" argument sounds pretty convincing. I know they can't self propagate, but that's why I mentioned the empty vector. So just buy ORF, PCR, and ligate. I'm not very experienced in the lab but I'm trying to get the hang of the protocol, it seems needlessly laborious.

@jiggunjer You do get an empty vector without any insert. Some vendors also sell a pre-digested/linearized vector.

@jiggunjer Vendors don't sell pre-digested inserts for the reason that there is no one standard vector. Different vectors have different expression sites, which require different restriction enzymes to clone. Selling ORFs would mean the vendor would need to keep stock for hundreds of different kinds of sticky end / recombinase end combinations. It's much easier for the end user to PCR the fragment out and subclone it.


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Are there examples of selection on males influencing female phenotypes?
I've been studying selection on female body color in a sexually dimorphic species and am intrigued by the possibility that selection on males, whether it be through sexual or natural selection, may influence the color of females. I think pleiotropic interactions may lead to this, or maybe some sort of genetic linkage.
A hypothetical example may be that selection for red dewlap color in anoles results in more melanic females.
I'm having trouble finding examples of this but I think it's a real phenomenon. Does anybody know examples of this occurring in a sexually dimorphic species?

Selection in one sex can produce a correlated response in the other when there is pleiotropy (or linkage disequilibrium) (see Lynch & Walsh 1998, and Lande 1979 & 1980).
Genes can be considered pleiotropic when they affect more than one trait, for example; the male and female forms of equivalent traits, and this can be seen as covariance between the sexes. Cross-sex covariance is common (see Bonduriansky & Rowe 2005, Poissant et al. 2010, Lewis et al. 2011, Griffin et al. 2013, and Blows et al. 2015 for good examples). This means that selection in one sex will often lead to a response in the other.
The correlated response to selection is captured within Lande's multivariate breeders equation, where the change in a vector of traits ($\Delta \bar{z}$) is a result of the genetic variance-covariance matrix ("G-matrix", $G$) multiplied by a vector of selection on the traits ($\beta$).
$\Delta \bar{z} = G \times \beta$
If covariance is zero (i.e. genes have independent male and female effects) then selection does not produce a correlated response in the unselected sex. However, cross-sex covariance is generally present, so correlated responses to selection should impose constraint on the evolution of sexual dimorphism under sexually antagonistic selection. Note that the within-trait cross-sex covariance is in the diagonal elements of the B-submatrix.
One good example of selection on one sex producing a response in the other is this paper. The authors selected on male mandible size in replicate populations of broad horned flour beetles. The mandible is a male limited secondary sexual trait, but selection on the mandible in males produced changes in female fitness and female traits. Selection for larger (smaller) male mandibles resulted in significantly decreased (increased) female abdomen size, and reduced lifetime reproductive success.

"We find that females from populations selected for larger male
  mandibles have lower fitness, whereas females in small-mandible
  populations have highest fitness, even though females never develop
  exaggerated mandibles."

One thing that is really quite cool about that experiment is that the response came in a non-equivalent trait, i.e. it was not female mandibles but other traits that evolved. There is generally less prior probability that there will be a cross-sex cross-trait covariance unless the traits have clear links.

Thank you very much for the detailed answer! I will definitely check out the papers you suggested. I can't upvote your answer until I gain more reputation, but will when I can.

@Connor I ignored genetic linkage in my answer, generally that is transient (recombination will breakdown the genetic correlation relatively quickly compared to pleiotropic genetic correlations), so is of lesser consequence to evolution in the bigger picture (see Lynch & Walsh).


text:
What does a climax community lead to?
Seral communities modify the environmental conditions in such a way that these are less favourable for itself and more favourable for the next community. Each community acts to end itself.
If the same is applicable to the climax community, what does it lead to?*

Could you please define 'climax community' for the purposes of your question? Dictionary.com gives: "An ecological community in which populations of plants or animals remain stable and exist in balance with each other and their environment. A climax community is the final stage of succession, remaining relatively unchanged until destroyed by an event such as fire or human interference", which suggests an answer by definition to your question: a climax community, without intervention, leads to ongoing climax community.

In addition to the comment by @bshane, note that the term climax community is somewhat obsolete, since also late succesional stages (e.g. old-growth forests) are now viewed as much more dynamical systems than previously thought.

As pointed out by @bshane it seems your question is answered by the definition. From the relevant wikipedia articles

"A seral community (or sere) is an intermediate stage found in ecological succession in an ecosystem advancing towards its climax community."

and

"In ecology, climax community, or climatic climax community, is a historic term that expressed a biological community of plants, animals, and fungi which, through the process of ecological succession the development of vegetation in an area over time, had reached a steady state. This equilibrium was thought to occur because the climax community is composed of species best adapted to average conditions in that area."

It doesn't lead anywhere, it is the climax. It is the state a community reaches when there is little change in the biodiversity as it because the community is composed of species at proportions that suit the ecology well.
However, in reality it seems that climax communities are rarely (if ever obtained) and, with increasing climate change and habitat invasion by humans, few communities will be in equilibrium. The adaptive landscape varies in time and space, thus while a community may be well suited to the current environment, it may well be poorly suited to future incarnations of that environment and will be undergoing constant change. As such, the term "climax community" is somewhat obsolete with it generally referring to old or established communities rather than those at a climax.

Yes, and problems with the climax community idea definitely doesn't hinge on human interference. For instance, plant distributions in Europe haven't stabilized since the last glaciation and the dynamics of old-growth boreal forests depend on forest fire dynamics. There are even studies that argue that the diverisity of tropical rainforests (arguably one of the most climax-like habitats there is) are dependent on glacial refugia.

I'm aware of that - just pointing out that habitats change, especially at the moment, so there is little chance that a community can stabilise (because environments are unstable)

It wasn't really citicism, just an addition/clarification to your answer. As a sidenote, I find it amusing that we both independently used the exact wording "somewhat obsolete" to describe the term climax community (see my comment to the Q). Then it must be an accurate description...

haha, weird! must be a very good description of its somewhat obsolete nature

A somewhat vague description of a somewhat obsolete concept.


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Species Identification: Small white maggot/larvae, Missouri USA
I'll try to give as much information as I can, because I don't know which information will be more important.
We woke up this morning to these little white worm/larvae in the house. We are located in the northern portion of southeast Missouri. We live next to some horses and cows. We have 1 inside dog and 1 outside dog. I'd say more of the worms were found in the kitchen (Tile floor) but some were also found in the living room (Hardwood floor).
This is a side view of the worm.
This is a perspective view of the worm. (About a 1/2 inch long)

It's the larvae of an insect - probably a house fly/bluebottle (it looks very similar to the typed used for/bought from fishing suppliers as "maggots")

Try to keep it in a jar and see if becomes an adult, that will be easier to ID.

We've kept one to the side. We'll see what happens. We've also called a pest control in our area to come and look to see what they think about the situation.

What ever became of the specimen you kept? Any adult pictures?

I kept some in a jar, but they all turned hard and brown. I assumed they died. I left them for a while just in case, but they never did anything. I'm kinda hoping they come back. I want to try again!


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Why does evolution not make our life longer?
Why does evolution not make life longer for humans or any other species?
Wouldn't evolution favour a long life?

Your question is a little unclear but are you asking "why do we age?/why hasn't evolution made us live forever?"

@GriffinEvo yes! why evolution not made us live more? Is not goal of evolution to make us better to let human kind live more?

Evolution has no "goal". It is "simply" the survival of the fittest under a given condition. What should be the advantage of living longer? Getting kids (=spreading the own genetic information) is done latest until the mid-40s after that we have not much biological meaning.

@GriffinEvo I'm waiting for your answer!

For the whole species it is advantageous that older individuals die to make more room (and not use up food) from younger generations. Evolution doesn't only work on an individual scale.

In addition to @Chris, not only does evolution not have a "goal," evolution doesn't necessarily mean "make us better!" It's absolutely possible to evolve negative traits.

A longer life span would eventually mean either less reproduction or more overcrowding.  It seems to me that the former would slow down evolution and make us less adaptive as a species, and the latter is simply suicidal.  Of course evolution didn't sit down with Excel and figure all this out.  But evolutionally, immortality isn't all it's cracked up to be.  :)

Related question on "Why do we die?"

I note that the question is incoherent in at least two ways. First, you've used "longer" without saying "than something".  If we replace "longer" with "longer than 100 years", or "longer than elephants", or "longer than lifespan 10000 years ago" we'd get three different answers.  Second, the question presupposes that evolution does not make life longer. Evolution has made life longer for humans than for many other species. Asking "why does X not happen?" when X does happen means the question cannot be sensibly answered. I would clarify your question.

There are a few benefits to aging and death. Firstly, if you have two coexisting (and non-competing) species, one that ages and dies, the other that is immortal and reproduces forever, you'll reach a point where all children of the immortal species die because the large number of adults out compete them. This leaves you with an immortal population with a very slow turnover of individuals and a population that dies of old age with constant genetic fluctuation, much more resilient to change and disease.

I agree with those who think it's not a good question; it sounds like something a creationist would ask, in order to get more arguments why evolution theory is nonsense. The whole premise is wrong: evolution is not a driving force, it's just a description of what happens.

@Chris what you say is true, but how is that relevant to the question? You're also assuming living longer wouldn't increase the number of fertile years, which doesn't have to be so.

@gwho It's a comment, not an answer. Besides that, our muh longer life is occurring only for a very short time period (less than 100 years), so evolutionary we haven't adapted to that. I might happen.

Evolution chooses the best out of available. It can't create best. That can only be a +ve mutation.

If this subject really interests you I would strongly suggest taking a look at the book: The selfish gene by Richard Dawkins. I had a blast reading this and in chapter 2 there is a section specificly answering this question, citing G.C. Williams as does the accepted answer.

@DartFeld Thank you for suggestion! I hope find a free time to give a look at it. :)

@cHao evolution does not care is something is detrimental to the species, gene level selection driving an species extinct is completely consistent with both evolutionary theory and observations.

@John: It is not, however, consistent with some longer-lived species being around to ask the question. :)

@cHao sure it is, it is perfectly possible to a species to drive itself extinct. Some would argue humans are already doing so.

@John: An extinct species wouldn't be around to ask the question. Still waiting for the relevance.

Why do we age is a classical question in Evolutionary Biology. There are several things to consider when we think of how genes that cause disease, aging, and death to evolve.
One explanation for the evolution of aging is the mutation accumulation (MA) hypothesis. This hypothesis by P. Medawar states that mutations causing late life deleterious (damaging) effects can build up in the genome more than diseases that cause early life disease. This is because selection on late acting mutations is weaker. Mutations that cause early life disease will more severely reduce the fitness of its carrier than late acting mutations. For example, if we said in an imaginary species that all individuals cease to reproduce at 40 years old and a mutation arises that causes a fatal disease at 50 years old then selection can not remove it from the population - carriers will have as many children as those who do not have the gene. Under the mutation accumulation hypothesis it is then possible for mutations to drift through the population.
Another hypothesis which could contribute to aging is the antagonistic pleiotropy (AP) hypothesis of G.C. Williams. Pleiotropy is when genes have more than one effect, such genes tend to cause correlations between traits, height and arm length probably have many of the same genes affecting them, otherwise there would be no correlation between arm length and height (though environment and linkage can also cause these patterns)... Back to AP as an explanation for aging, if a gene improves fitness early in life, but causes late life disease it can spread through the population via selection. The favourable early effect spreads well because of selection and, just as with MA, selection can not "see" the late acting disease.
Under both MA and AP the key point is that selection is less efficient at removing late acting deleterious mutations, and they may spread more rapidly thanks to beneficial early life effects. Also if there is extrinsic mortality (predation etc.) then the effect of selection is also weakened on alleles that affect late life. The same late-life reduction in the efficacy of selection also slows the rate at which alleles increasing lifespan spread.
A third consideration is the disposable-soma model, a description by T. Kirkwood of life-history trade-offs which might explain why aging and earlier death could be favoured. The idea is that individuals have a limited amount of resources available to them - perhaps because of environmental constraints or ability to acquire/allocate the resources. If we then assume that individuals have to use their energy for two things, staying alive via repair and maintenance (somatic-maintenance) and making offspring (reproductive-investment), then any energy devoted to one will take away from the other. If an individual carries a gene that makes it devote all of its energy to somatic maintenance then its fitness will be very low (probably 0!) and that gene will not spread. If the level of maintenance required to live forever costs more energy than an individual can spare without suffering from low fitness (very likely) or can even acquire and efficiently convert in the first place (also very likely) then high-maintenance alleles will not spread (and aging & death will continue to occur).
To go a little further, it is common for sexes to age differently (this is what I work on) and one possible explanation is that the sexes favour different balances of the trade off between somatic-maintenance and reproductive investment, this can lead to conflict over the evolution of genes affecting this balance and slow the rates of evolution to sex specific optima. This paper provides a good review of the area.
To summarise, evolution has not managed to get rid of death via genetic disease etc. (intrinsic mortality) because the effect is only weakly selected against, and those alleles may provide some early life benefit, and resource limitation may also reduce the potential to increase lifespan due to trade-offs with reproductive effort. Adaptive evolution is not about the survival of the fittest but the reproduction of the fittest - the fittest allele is the one which spreads the most effectively.
EDIT: Thanks to Remi.b for also pointing out some other considerations.
Another thought is that of altruistic aging - aging for the good of the population (the population is likely to contain related individuals, you are related to all other humans to some degree). In this model aging is an adaptive process (unlike in MA where it is just a consequence of weak selection). By dying an individual makes space for it's offspring/relatives to survive (because resources are then less likely to limit populations). This will stop excessive population growth which could lead to crashes in the population and so, by dying earlier, an individual promotes the likelihood that its progeny will survive. Arguments of altruistic sacrifice are often hard to promote but recent work suggests that this is a more plausible model than once thought.
Evolvabilty theories also suggest that aging is an adaptive process. These suggest that populations, composed of a mixture of young and old, have biases in how well adapted the members of the population are - where younger individuals are better adapted (because they were produced more recently it is likely that the environment is similar to the environment they are favoured in). Thus by removing the less well adapted individuals from a population via senescence and freeing up resources for younger better adapted individuals, a population evolves more rapidly towards it optimal state.

+1 I bet I would never have got 5 upvotes to my answer if you'd had posted your answer earlier $\ddot \smile$ . You don't talk about some hypotheses of the kind "Because our body is not so flexible (most cells are specialized (not very totipotent anymore)) we can't heal from many damages. The population where old individuals free places (by dying) for the younger individuals which are more fit will thrive compared to populations that don't do this (lineage selection)". You may not be so far from giving an exhaustive list of hypotheses that would definitely would make your answer perfect!

Regarding your third consideration; there are 3 things that an organism can spend its resources on: reproducing, growing and maintaining. The third consideration only works if growing is cheaper than maintaining (since if an old organism reproduces and dies a new organism must grow to replace it).

On the other hand, living a bit longer than reproducing can also be good for fitness because then you can help your offspring along until they are old enough to live on their own. (So your 40/50 year example gene might still have a bit of negative selection.)

@RichardTingle I would include both growth and maintenance in somatic maintenance - this is how it is regarded in the literature on the subject

@PaŭloEbermann yes, some kin/group selection arguments would reduce the negative effect of living long but it requires some social structure and group selection is generally weak so I chose not to delve to far in to that subject, but yes, if by living longer an individual increases the fitness of its offspring then there is a positive effect of long life via indirect selection

@GriffinEvo it seems strange to group them together.  If (for example) growth =10 units/year. Maintainance = 5 units/year then (other consideration aside) immortality becomes the optimum choice, whatever the cost of reproduction, since every year an old organism lives you have a net 5 extra units to spend in reproduction.  On the other hand if growth=5 units/year and maintenance=10 units/year (seems unlikely; although perhaps repairing a damaged organ could be more complex than building a new one from scratch) then a finite age makes sense

@richardtingle  your example doesn't give the full picture, it needs more info. if, within a population, the average individual takes up 10 units of energy which it can spend in its life, reproduction events cost 1 unit of energy per offspring produced, and the repair and growth costs 3 units of energy per reproductive cycle then the optimal strategy is to to neglect somatic maintenance (growth AND repair) and have seven offspring in one reproductive event - it's the way to pass the most copies of its genes with its limited budget

The evolvability ideas would suggest that, in a stable environment, lifetimes (and reproduction window) will get longer and longer. But we're not seeing this in any lifeforms at all, even in the most stable environments. So, there must be the other factors involved, i.e. that from some point it's easier to build from scratch than to repair, for the same reason that old buildings from the sixties are knocked down instead of being refurbished. About the last sentence: it evolves more rapidly towards a local optimum state. Evolution cannot find global optima in general.

@evgenisergeev evolvability is in my eyes a weak argument to the adaptive spread of aging - at best I'd suggest it can offer very weak influences on selection. Like you, I think other factors play a larger roll in shaping the evolution of aging, but many of these above are not mutually exclusive ideas. *and nor do I necessarily agree with the ideas, but this site is about answers based on science, not my opinions :)

Do we know why exactly does a bacteria or eukaryotic cell, seen by itself, die of old age? Are its protein structures all crumbling? Is its membrane all wrinkly? Are its organelles cluttered with debris and have bits broken off? If that's so, then the only way an animal can live indefinitely is if it replaces all its cells every so often. And how many animals do you know that can do that?

@evgenisergeev RE the last sentence - you may have misinterpreted what I said, to clarify -  if we compare two populations, where the resources (inc. space) are limited and the rates of evolution are high such that young are better adapted than old. If in one population we remove the oldest individuals and in the other we remove at random (but equal rate) then (according to evolvability hypothesis) the selectively altered population should be better adapted after time has passed

@GriffinEvo I'm not sure I understand this concept of energy/lifetime. Why is an organisms total energy capped? As opposed to its energy/year. If we are getting free radical damage into the equation thats a reason for non infinite age but thats a seperate issue and something evolutions would try to overcome

@RichardTingle energy will be capped by the energy content of food, efficiency of energy conversion, ability to find and consume food (spatial and temporal limitations, including spending time doing other things like sleep and reproduction), resource competition... You can ignore the thought of free radicals in regards to this question, it is more why aging evolves (ultimate question) rather than why we age (on a mechanistic level)

@GriffinEvo Yes but that is all a cap/year not a cap/lifetime. If it takes 10 years (and 100 units of energy - 10/year) to bring an organism to sexual maturity and 5 units/year to maintain it and 5 units to reproduce. An organism is 10 years old, its total spend is 100 units and its got 10 to spend this year. It can (a) have 2 childern and die or (b) have 1 child and live to next year. If it chooses option (a) it will have 2 children; neither of which will reproduce for 10 years (and 100 units will be effectively thrown away). If it chooses (b) it can keep having 1 child a year indefinately

So in a decade from now there will be 2 sexually mature organisms either way. Option (a) it’s the two children and in Option (b) it’s the original organism and the first child. But in option (b) there are also children at ages 9 through 1. Of course all this breaks down if you’ll probably be dead in a year anyway (which in nature probably isn’t an unreasonable assumption).

Won't Individuals who are fittest get to reproduce more? If someone lives upto 40 and have 5 children vs if someone lives upto 500 and have 400 children...isn't 2nd one at advantage. Secondly, many life forms seem to live their whole lives without aging much...and i know of one that is actually biologically immortal...aging is no problem to it. Where is error accumulation in them?. I agree with the theory that for a group with limited resources natural selection would favor formula where weak gets replaced by stronger ones..However, more favorable group would be in which no one gets weak.

@RichardTingle The disposable soma model is a TRADEOFF scenario - in your example that does not happen (individuals have enough resources to reach 10 years regardless of strategy). The idea is that an individual can not secure the resources necessary to both produce the most number of offspring per reproductive episode and maintain/grow indefinitely.

@MuhammadUmer See above - the disposable soma is a TRADEOFF, an individual can either prioritise reproduction or maintenance because it is resource limited so it is not as simple as your example. As for biological immortality, it does appear in some species (lobsters is one example) and rate of aging varies between species. Immortality is probably not ubiquitous because it likely requires complex cellular machinery and species where it occurs could boom and collapse due to over-population/resource depletion.

@Griffin Under my example I'm assuming an animal does not become reproductively active until 10 years, what you're saying makes sense if you could have 1 child ever or live forever, but I don't see the mistake in my maths where you can trade off halving reproduction per year to increase life by 1 year (each year - so effectively half rate for immortality). The avoidance of boom and bust makes sense however

This is a very good question.
There is a big ongoing field of research called "evolution of aging/senescence" that tackles this question. I won't give you a complete overview of the different hypothesis the could explain why we age but here is a fundamental concept that is to know.
We'll assume that there is some extrinsic mortality, mortality against which a lineage won't ever be able to escape and I think it is not an assumption that is hard to meet. Therefore, an allele that has age-specific effect such as decreasing the fecundity at age 3 will undergo a higher selection pressure and will faster get eliminated from the population than another allele causing the same decrease in fecundity but at age 4 because some individuals would have died between age 3 and age 4. In other words, natural selection is more efficient at lower age than at higher age. Now, imagine in humans an allele that increases the reproductive success of an individual at age 20 by decreasing the survival at age 78. This allele will easily spread in the population. Such alleles are said to have age-specific antagonist pleiotropic effect. And empirical studies have shown that alleles that have antagonist age-specific antagonist pleiotropic exist.
In short, it is because there is some extrinsic mortality that natural selection acts with a different strength at different ages allowing some deleterious allele at old age to fix in the population especially if those alleles have age-specific antagonist pleiotropic effect. You'll find in this book mathematical formulation and more complete discussion of this effect
Other hypotheses exist which are based on lineage selection, group selection or on the mutation-selection balance.

Actually, genetically, there is no reason for animals to continue to exist after they have procreated.
If you look at salmon, they die immediately after procreating, which is probably the most efficient way to carry the best genes to the next generation.
In the case of mammals, they need to teach their offspring where to find food, where to find water and how to avoid dangers.
In the case of humans, that goes into the third generation, so most humans know their parents and their grandparents, and even they live with them in some cultures, since their experiences and ideas are taken as very important.
So maybe the question should be the opposite, why do we live to see our grandchildren grow?
Taking your same question to the opposite: why do people die? Why don't they live forever instead of reproducing? I can think of various reasons for this. Imagine a race that lives forever and another race who have a lot of children early on and then die. Now imagine a contagious disease that spreads among both populations. Which race has the most probability of survival?
Of course, the race that reproduces rapidly has a better chance.
And also, evolution works wonders for the race that reproduces rapidly instead of the race that lives forever. Meaning the number of years a species live has carefully been "designed out" by evolution.
Evolution would not work if it didn't stabilize around the best genes. And that's exactly what happens with humans. Most humans have the same traits: live around the same number of years, and have more or less the same abilities, most differences are almost irrelevant.

Another example for this line of argument: http://www.wired.com/2014/05/absurd-creature-of-the-week-this-marsupial-has-marathon-sex-until-it-goes-blind-and-drops-dead/

There is an exception to the statement that animals dont need to live after they have procreated, and that's in most social mammal groups, the older patriarchs or matriarchs use their memory to guide the group away from danger and towards food. Especially with humans, where the oldest naturally occuring individuals are about 80-90 that help to guide the group, see native american tribes for example. In other social animal groups, the oldest individuals often have a role to play in guiding travel,i.e. elephants.

I get what you're saying, but I must first object to "reason for animals to continue". This language is hard to avoid, but it does imbue a certain paradigm or assumption that genes are the purpose (there is no purpose in evolution), while the phenotype and the boday are carriers. It's a useful paradigm to analyze the essence of evolution, which are the genes, but that wording confounds and obfuscates clear thinking, which is necessary to tackle questions like these.

Animals after reproducing can have a "purpose" if they reproduce more. having multiple kids. If they can extend their fertile years, that would be reproductively advantageous, and help with those genes surviving. This is naturally assumed when anyone asks "why don't we live longer" with some awareness of evolution. If we live longer, they are also assuming fertile years be longer as well.

Here is an idea: if animals lived long past their fertile years, they would take up resources (less food, safe ground, etc), and leave less for the offspring which do/can reproduce. (Species may not compete for resources with vastly different species, but they certainly do compete with members of their own species.) Having a bunch of old, non-reproducing individuals would put a damper of the chances of survivability of their offspring. This is only one isolated effect to be superimposed with other effects which may take precedence or overshadow this effect.

Because evolution isn't about individuals: it's about species. What matters to natural selection isn't how long you live, but how many grandchildren you have. A long lifespan can be an evolutionary advantage, but like any trait, it's only an advantage to the extent that allows you to reproduce more.
It would seem that a longer lifespan would be advantageous anyway, because it would give you more time to reproduce. However, for reasons we don't yet fully understand, it doesn't seem to work out that way in practice. Most organisms (assuming they live long enough) eventually reach an age where they stop reproducing. Even humans do this, and although we've managed to increase the average lifespan quite a bit over the course of recorded human history (to say nothing of the millennia before that), the average age at which people stop reproducing apparently hasn't changed very much.
Why not? What makes this an evolutionary advantage over having more reproductive years? This is one of those things that we haven't really figured out yet. There are a number of competing theories, and the other answers here go into some of them. But the most direct way to answer your question is fairly simple: longer lifespans (and/or reproductive years) haven't given us, or our children, any more success at reproducing. Thus, there is no pressure on the species to live longer, and so it doesn't happen.

longer lifespans haven't given us more success at reproducing why do you say that?

Technically, evolution isn't even about species, but about aleles. Something can be an advantage to a gene, even if it provides no advantage to the species; for example retroviruses.

@MuhammadUmer: It's interesting, just because it seems so counterintuitive, but if you look at the period over which human lifespans have been increasing, the birthrates have actually gone down, not up. Nowadays, many of the nations with the longest life expectancies actually have some of the lowest birthrates, and vice versa. There probably isn't a direct causal link here -that is to say, the birthrate probably isn't dropping because people are living longer- but the fact remains that lifespans are going up in some parts of the world, but where that's happening, birthrates aren't going up.

First i don't think this effect among humans, that countries with highest expectancy have lowest birth rate, is the result of evolution. But could be a hint as to why it may happen in Evolution. Shorter the lifespan in the country the poorer the population..The reason recent study discovered that poor like to have many children while richer parents often opt for 1 or 2 max, is because value of the Amount of wealth that gets divided among children goes very high as parents get richer...

...on the other hand poor man can have 10 children and they would still be relatively as rich as only 2 would have been. For rich the effect multiplies...if you were going to inherit 10 million if you were only one child...but if you had 9 other siblings you'd get only 1 million. Loss of 9 million. If you were poor, then instead of inheriting $5000.   you get $500 Both won't last more than a month.

@MuhammadUmer: I think you're right. It's not the result of evolution, but it may explain why evolution isn't going the way that the original question was asking about. It's just like you say: having fewer children is a good economic strategy if you are rich, because it means that you don't have to divide your wealth as much. But it is a bad evolutionary strategy (whether or not you're rich), because you can't get your genes out into the wider species unless you have many children. And so even though economic factors are helping people live longer, we don't evolve along those lines.

Wow, you should work in politics or PR. You've done a wonderful job of repeating the question without answering it, in a very eloquent way, giving the impression that you've said something smart or worthwhile.
Also, you start off by saying evolution isn't about the individual, and then directly contradict yourself, saying living longer would help you reproduce more. Of course it will help you reproduce more if you have more fertile years, barring other linked genes. Yes, it's about the individual. The individual shares genes with others, also making it about the species. It's both, not one.

@gwho: I did not contradict myself. I said that it seems like living longer ought to help a person reproduce more, but in practice, it hasn't worked out that way (i.e. that living longer actually hasn't helped people reproduce more). There is no contradiction there: it's a simple difference between what's intuitive -such as the original question's reasoning, which is why I mentioned it- and what works out. The question wasn't about the evolution of the aging process, but why evolution hasn't given us longer lifespans, and so I even answered that. Your attacks on me are uncalled for.

One factual inaccuracy here: Most organisms (assuming they live long enough) eventually reach an age where they stop reproducing. This simply is not true. It is true that fecundity decreases with age, but it is not true that it goes to zero in most species in the wild. Rather, humans are quite unusual in that human females go through menopause.

I think you're right. The true evolutionary stable strategy has people able to never get too old to reproduce. If a mutant woman who reproduces asexually and happened to have the right genome arose, her clones would outcompete the rest of humanity. After that, if another mutant woman who's like a hydra and could had a rate of death that remains constant at 1/3000 years under laboratory conditions and can keep reproducing until she dies, her clones would outcompete humanity. After they spread, they would have a rate of death by competition that remains constant at 1/30 years.

If you take the line of "The Selfish Gene - Richard Dawkins". Evolution doesn't care about individuals, it cares about genes. So as long as the genes are passed along reliably into the future, evolution may do it with 4 generations per 100 years or 100 generations per 100 years.

Lifeforms that we know tend to have a mature state towards which they rapidly develop, and then live for a while after that. What about a hypothetical lifeform, such that the longer an individual survived, the more successful it became? Suppose its tool of choice was intelligence, and it was a a whale with four human hands, and its brain kept growing and it became smarter and smarter every year... I guess there is still a limit at which it can't improve... But this thought experiment shows that if a lifeform can find a way to develop further during its life, its life expectancy will grow.

The evolutionary drive works on preferential survival of children. So in such a species such as you suggest, the children of older members would have to be preferentially selected over the offspring of younger members.

We can arrange that. Just as in countries with higher IQ, the life expectancy is longer, because they can organise better healthcare for themselves, perhaps the growing brain will improve the medical skills of this hypothetical animal, and it would preferentially provide medical help to its own children first. (Assuming it's a universally benevolent species; if it's partially or fully malevolent, you can also imagine how the cleverer older individuals' children will be better off.)

This then becomes involved in politics and the organisation of healthcare.

@user6571 I just commented OP to take a look at this book before even seeing your answer. Extremely good book on the subject.

I agree with your first principle of the replication/survival of the genes. However, your conclusion is unclear. What do you mean by "doesn't care about individuals"? Are you saying the individual life span is irrelevant to the gene replication/survival? That is a strong claim without proof. In fact, I contend thos is a priori wrong. If the life span of the individual improves the replication/survival of the gene, there will be the tendency for the gene to increase the individual life span.

To an extent it does; in that we live longer than our mouse-like ancestors. So the question becomes: why not keep extending it to immortality.
The key thing is that evolution cares only about the survival of your genes; so if you live for 1000 years or if 10 generations of your family have 1 individual's worth of your genes in each generation (each living for 100 years) this is equivalently successful.
But this assumes it's either-or that an organism can reproduce or live a long time, could it not do both? In principle it could but the resources of a particular niche are limited so in order to avoid mass starvation the reproductive rate must reduce as the average age of the individuals go up.
So this suggests having very long lived individuals is no better than having short lived individuals, but is it at least equal? Sadly not, if fewer new individuals are born then the rate of evolution of that species is reduced. A very long lived species is less able to respond to environmental changes. As such over an evolutionary timescale an extraordinarily long lived animal is likely to be outcompeted by a shorter lived species.
Of course there is a natural breakeven point; there is a considerable cost in bringing an individual from infant to reproductive adult so once they've got there it makes sense to keep them around for a while, but not indefinitely.

There is no selection mechanism that would favor high age.
By the time it's apparent whether or not an individual can reach a high age healthily, they'll have ceased all reproductive activity.
Conversely, people who get cancer at 45 will have likely reproduced already.

This assumes an organism becomes long lived while still stopping reproducing early rather than the whole of life extending.

but shouldn't genetic variations result in individuals that are of higher age than average age at which they cease all reproductivity. Thus being at advantage..then why that advantage hasn't been represented among humans?..to me this conclusion is flawed.

I am assuming that by longer life, you mean slower aging, because evolution can do little if a mountain falls on a person!
So, why don’t organisms have slower, or better, zero rate of aging?
The theory I am describing is based upon life history theory. Life history theory assumes that:

Resources available to any organism are limited,
Life processes like ‘reproduction’ and ‘repair and maintenance of the body’ are costly with respect to resource consumption, and resources directed towards one life process must be directed away from the other. Hence a trade off mechanism between the different life processes must exist.

Based on this data, one can infer that given a specie with a given death rate of extrinsic causes (causes beyond that of aging, like getting eaten), one can use a little mathematics to find the average life span of the organism if the organism does not ages. Simple…?
Now, given that the average life span of the non-aging specie is limited, do you really think that the optimum life strategy of the specie would be zero aging? Remember that to not to get old one needs to spend energy, and that all the energy gone in maintaining health will certainly be wasted in the form of dead bodies once the organism dies.
Hence, given a mechanism through which trade off of resources between life processes is possible, the organisms must invest a little more towards reproduction and a little less towards repair and maintenance? Why? Just to reduce the loss of resources in the form of dead bodies and to increase reproductive success, which is what gets counted in the end!
So, indeed, having zero rate of aging has disadvantages! It would be more advantageous if organisms age with a fixed specie specific rate.
Now, time to make few points clear:

This theory assumes Life history theory to be correct. I am not saying- “hello there- this is the correct reason of aging!” I am saying- “This is the correct theory of aging if life history theory is correct!” So, if you do not believe in life history theory, then get busy trying to prove it wrong. The theory I have discussed stands on the shoulder of a giant. On the other hand, if you believe that the theory I discuss does not follows from Life History theory, then lets hear your argument.
This theory also assumes that aging happens due to lack of repair and maintenance of constantly occurring body damages. The special thing about this theory is that it gives a non-altruistic mechanism through which aging can directly benefit the organism. Hence, this theory makes it easier for us to explain why aging got natural selection- because it has benefits!

I found this theory on this SE question, where the question has now been put on hold due to dubious reasons. Also, the OP mentions this book- Modern Biological theory and experiments on Celibacy, which, I think, was one of the reasons why the question was put on hold!


text:
Why even if all requirements for natural selection are met, it may not happen?
In the book written by John Endler Natural Selection in the Wild p. 4
it says that even if condition a, b and c are met, evolution by natural selection might occur,

[...] , but not necessarily, [...]

See last paragraph of the image.
Endler, J. A. 1986. Natural Selection in the Wild. Princeton University Press.
I’m wondering in which case it’s possible that everything is in place for natural selection to occur, but is not having any effect.
It seems to me that if every condition of natural selection are met, there will absolutely a change in the phenotypic distribution? Why does the text say evolution is not guaranteed to occur?

if all the living things are killed for instance there is no natural selection.  if the environment does not affect the outcome of reproduction, i suppose that natural selection is not occurring, but its hard to imagine such a situation

Hi @mbeausoleil - could you respond to the comments under remi.b's answer - we could do with clarity

What does the sentence below mean?

As a result of this process, but not necessarily, the trait distribution may change in a predictable way.

To my understanding, but not necessarily means that other processes than natural selection can affect the trait distribution in a predictable way.
Other than natural selection, what affects the trait distribution in a predictable way?
I am not trying to make an exhaustive list but I am just providing here two obvious examples.

An intense gene flow (migration) from a nearby population will also cause the trait distribution in a local population to change in a predictable way.
Genetic drift, will reduce genetic variance and therefore reduce the variance of the trait distribution. While the change of the mean of the trait distribution is not predictable under genetic drift, its change in variance is predictable.

Note that the book has been published in 1986 and the vocabulary and science is probably slightly outdated. If you are learning about evolutionary biology, you can probably find better source of knowledge. For example Understanding Evolution is a free online introduction to evolutionary biology. There are many textbooks that offer very good introductions to evolutionary biology.

I'd add genetic correlations - selection on one trait (a) may oppose the selection on another genetically correlated trait (b), so when studying a all conditions would be met but no change (or lesser than expected, or opposite to expectation, change) occurs

Sure I could add that. However, as you said, this is NOT an example of when something else than natural selection can affect the trait distribution in a predictable way. It is an example of when selection is counteracted by something else.

Upon reading the question again, I think the user is asking why evolution doesn't always occur (in the predicted way) if the conditions for natural selection are satisfied. A question of why doesn't selection always give a response, rather than how else can predictable evolutionary change occur.

Hum... indeed. However, there is contradiction in the sense of the question between the actual question and the citation that the question is supposed to tackle. As a consequence the post would deserve being closed as unclear.

Agreed, need the OP to come back!

Actually, the answer of @Remi.b is clear and is in relation to what I asked. If you want to go deeper, you can ask the question: is it possible if all the conditions (a, b and c) are met that natural selection, regardless of other processes considering that they have no effect, is not changing the trait distribution?
In other words, if the conditions a, b and c are present, is the trait distribution changing all the time?

Evolution, a change in the trait distribution of a population, occurs by four mechanisms; drift, mutation, migration, and selection. E.g. These mechanisms cause a change in the mean of trait, or variance in a trait etc.. Just to summarise the conditions you gave:
a) Trait $i$ has variation
b) Trait $i$ covaries with fitness ($\omega$)
c) Trait $i$ is heritable from parent to offspring
Genetic drift is the random loss of genetic variance from the population by stochastic processes. Mutation (generally) generates new genetic variation within populations. Migration can lead to loss (emigration) or gain (immigration) of genetic variation from a population, as variants come or go from a population.
Selection is mechanism underlying adaptation. This is what is in condition b of the conditions you gave. We can predict the response to selection using some simple quantitative genetics in the form of the (multivariate) breeders equation.
$\Delta z = G\beta$
Where $\Delta z$ is the response in the trait, $G$ is the genetic (co)variance matrix, and $\beta$ is the selection.
In a simple toy example we could look at a single trait, $i$. We allow $i$ to satisfy all of the above conditions. This means that both $G$ and $\beta$ are non-zero, and therefore, $\Delta z_i$ will also be non-zero. Just putting some random numbers in to the equation to make it clear, if $G = 0.5$ and $\beta = 0.8$ then;
$\Delta z_i = 0.5 \times 0.8 = 0.4$
Mutation, drift, and migration could all oppose or distort the effect of selection. In other words, they can cause the actual and predicted response to be different from one another (i.e. $\Delta z_i \neq 0.4$), and there will not necessarily be a change in the phenotypic distribution.
However, selection is also factor that could cause a difference between the predicted and actual response to selection in trait $i$. This is because genetic correlations can arise among traits, either by linkage (close proximity in the DNA) or pleiotropy (when one gene affects more than one trait). For example, we may see no response at all in $i$ ($\Delta z_i = 0$) when both $G_i$ and $\beta_i$ are non-zero, if selection on a second unmeasured trait, $j$, opposes selection on $i$ ($\beta_i = -\beta_j$), and trait $j$ has equal variance ($G_i = G_j$) and is perfectly covarying with $i$, $cov_{i,j} 1$. Approximately this would be;
$\Delta z_i = (G_i \times \beta_i) +  (G_{i,j} \times \beta_j$)
$\Delta z_i = (0.5 \times 0.8) + (0.5 \times -0.8) = 0$
This is a major issue in the study of evolutionary biology. Genetic correlations can cause severe disparity between the actual and predicted response to selection and univariate methods are insufficient as a result. More studies adopt multivariate methods these days, though these are generally limited to just a handful of traits so its still not perfect. In reality methodological and logistical constraints present a huge obstacle to being able to predict $\Delta z_i$.


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Why does vitamin D need to be exogenous?
Vitamin D is a either a hormone or a precursor to hormones. It is very unlike any other vitamins, which are either cofactors or antioxidants, or may be other chemicals necessarily performing catalytic function, just like transitional metal.
But in all sources I found so far it says that Vitamin D doesn't really do anything chemistry-bound, but rather just works as a hormone matching some arbitrary protein receptors or something. E.g. it signals something to the body. But what? And if nothing, then why does not evolution not select out Vitamin D in favor of endogenous chemical or nothing at all?

Vitamin D is vitally important for the uptake of calcium, iron, magnesium, phosphate, and zinc, as well as for bone maintenance:

Vitamin D promotes calcium absorption in the gut and maintains adequate serum calcium and phosphate concentrations to enable normal mineralization of bone and to prevent hypocalcemic tetany. It is also needed for bone growth and bone remodeling by osteoblasts and osteoclasts. Without sufficient vitamin D, bones can become thin, brittle, or misshapen. Vitamin D sufficiency prevents rickets in children and osteomalacia in adults. Together with calcium, vitamin D also helps protect older adults from osteoporosis.

It also acts as a hormone, binding to the Vitamin D receptor in the nucleus of target cells which then acts as a transcription factor for genes related to multiple processes:

Vitamin D has other roles in the body, including modulation of cell growth, neuromuscular and immune function, and reduction of inflammation [1,3,4]. Many genes encoding proteins that regulate cell proliferation, differentiation, and apoptosis are modulated in part by vitamin D. Many cells have vitamin D receptors, and some convert 25(OH)D [an inactive form] to 1,25(OH)2D [an active form].

So, the truth is far from your statement that "Vitamin D doesn't really do anything chemistry-bound, but rather just works as a hormone matching some arbitrary protein receptors or something." In fact, a cursory reading of the first couple of Google results for "Vitamin D" shows that it is broadly involved across the body in many different processes ranging from inflammation and cancer to bone maintenance and mineral absorption.
Sources:

Vitamin D - Fact Sheet for Health Professionals. NIH Office of Dietary Supplements. November 2014.
Vitamin D Wikipedia
Effectiveness and safety of vitamin D in relation to bone health. A Cranney, T Horsley, S O'Donnell, et al. Evid Rep Technol Assess (Full Rep). 2007 Aug;(158):1-235.
Vitamin D WebMD

I'm going to answer your question as asked.
It doesn't need to be exogenous. In fact, it's often not exogenous at all. The truth is, vitamin D can be (and is) be synthesized de novo in adequate amounts by most mammals exposed to sufficient sunlight.[1]
Now, obviously, the presence of the correct wavelength of UVB simply allows the reaction to proceed at a reasonable rate. But the first misunderstanding is that calling "cholecalciferol" a vitamin is simply a misnomer. In reality it is not an essential dietary factor. As you allude to, it's better to consider it a hormone.
You next question is "why does not evolution not select out Vitamin D in favor of endogenous chemical or nothing at all?" Again, answering this question:
It doesn't.
Vitamin D is an endogenous chemical!
It has been in many organisms for millions of years! And very useful too. Ergosterol, previtamin D2, and its photoproducts could have acted as an ideal UVB sunscreen since they could absorb UVB radiation and dissipate its energy by the rearrangement of the double bonds.
Of course, the photochemistry of vitamin D is important and the synthesis in the body is very dependent on a variety of factors. Firstly, environment and the incidence of solar radiation with wavelengths of 290–315 nm on the skin. Other factors include the zenith angle; nitrous oxide, ozone sulphur dioxide pollution, altitude, sunscreen, skin pigment, aging, latitude, season, etc.[2]
It's vital for maintaining the skeletal calcium balance by promoting calcium absorption in the intestines, promoting bone resorption by increasing osteoclast number, maintaining calcium and phosphate levels for bone formation, and allowing proper functioning of parathyroid hormone to maintain serum calcium levels. 1,25-dihydroxyvitamin D influences a large number of biologic pathways. Hence rickets, etc.
One thing to be aware of is that vitamin D either from endogenous synthesis or the diet must be biologically activated through enzymatic hydroxylation in the liver and kidney.


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Is there a term for when a detrimental gene can be positively selected for because of linkage to a very fit gene?
Let's say that some piece of DNA would be subject to extreme negative selection if it were independently inherited, but it is very closely linked to an extraordinarily fit gene, and so the complex it belongs to is positively selected for.
Is there a term for this phenomenon?

related http://biology.stackexchange.com/questions/44946/infer-gene-frequency-within-a-species-over-time/45004#45004

Genetic hitchhiking / genetic draft
From wikipedia

Genetic hitchhiking, also called genetic draft or the hitchhiking effect, is when an allele changes frequency not because it itself is under natural selection, but because it is near another gene on the same chromosome that is undergoing a selective sweep.

The term "selective sweep" is used improperly in the wikipedia definition. One should replace the last sentence by [..] but because it is near another allele on the same chromosome that is undergoing positive selection or if we want to reuse the term "sweep", once could say [..] but because it is near another allele on the same chromosome that is sweeping to high frequency
Selective sweep
From wikipedia

A selective sweep is the reduction or elimination of variation among the nucleotides in neighboring DNA of a mutation as the result of recent and strong positive natural selection.

(For the direct answer to your question skip to the end!)
Genetic linkage can affect the spread of other genes. The degree of linkage, affected by the rate of recombination between the point (nucleotide, gene etc.) directly under selection and the other point. If the rate of recombination between to given points is low then linkage between them is high and occurs either because the region has low rates of recombination (rates of recombination can vary across a genome) and/or because the two points are physically very close. When two loci are associated by linkage such that they are more often associated with one another than would be expected under random conditions, they are said to be in linkage disequilibrium.
Selection on linked loci relates to a number of key terms:
Selective Sweep
When a new beneficial mutation arises (or an existing mutation becomes strongly beneficial) and its frequency in the population rises rapidly because of selection. This causes the loss of genetic variation at that locus, and at linked loci, because variants linked to the beneficial mutation also spread (see genetic hitchhiking below). The hardness of a sweep is the result of the strength of selection; hard sweeps occur when selection is very strongly in favour of the allele.
Genetic Hitchhiking / Genetic Draft
This occurs when the frequency of an allele is affected by selection in other loci. This effect is very apparent in Y chromosomes where most of the chromosome does not recombine with the X. Effectively selection then acts on this single non-recombining unit, such that if a deleterious mutation arises on a Y with many good alleles then it will fare better than a similar mutation that arises on a Y with fewer good alleles. This is one reason that the Y chromosome is low in genetic variation; good variants cannot get away from bad variants at other loci, recombination allows mutations to be reshuffled and therefore raises the likelihood of making very good combinations of alleles.

"Under the classical view, recombination allows deleterious mutations to be eliminated more efficiently, and increases the rate at which favourable alleles can be brought together, despite their association with deleterious alleles." - Barton

The effect (signature) under a selective sweep is to see a decline in genetic/molecular variation around a given point (the point being the variant that was directly under selection), with variation being negatively correlated with the linkage (molecular variation increases with genetic distance from the locus that swept). Hard sweeps then have an obvious signature, but soft sweeps are more difficult to spot; soft sweeps can occur when selection on a novel mutation is relatively weak, or when selection suddenly favoured an existing neutral mutation (which therefore had time to become associated with multiple variants by recombination).
Background Selection
Similarly, if a variant is associated with deleterious alleles then it will come under background selection. In this case, neutral alleles can be removed from a population by the action of selection on deleterious variants at other loci. Again, the strength of selection and degree of linkage disequilibrium will affect the rate at which genetic variation is lost at a given locus.

"Under background selection, neutral alleles that are linked to detrimental alleles are driven to extinction, with more drastic effects when recombination rates are low." - Cutter and Payseur

Hill-Robertson effect
The benefit of recombination should be apparent to you from the above descriptions, linkage disequilibrium will slow the rate of adaptation, and the formal name for this is the Hill-Robertson effect (or Hill-Robertson interference), named after the scientists that described it. If there is no recombination in a species with two genes, each with two alleles then the most fit combination of alleles can only occur if the beneficial mutations occur in the same genetic background; recombination allows beneficial mutations to occur in separate lineages and come together later on. Specifically, if locus 1 has two alleles A and a where A is beneficial, and locus 2 has alleles B and b where B is beneficial, the most fit individuals would have A and B, but without recombination these individuals can only come about if the mutation from b->B (or a->A) occurs in an Ab (aB) individual; recombination allows the AB type to come about even if the A and B have distinct origins.
The phenomenon you describe (deleterious mutation spreads by linkage to beneficial mutation) is a form of interference. Adaptation, which would occur by i) spreading the beneficial allele at one locus and ii) purging the deleterious allele at the other locus, is being impeded because the two are under linkage disequilibrium. The net selection effect for this "complex" is closer to neutral than one (or both) selection effect for either locus. One could describe the phenomenon with something like:

"The deleterious allele spreads, despite its very deleterious effect, by Hill-Robertson interference caused by tight linkage to a highly beneficial allele."

Note (and credit to @DermotHarnett): Haplotype is the proper word for what you called a "complex".

+1. I guess the more usual term for a 'complex' of mutations like that would be "haplotype".

Thanks @DermotHarnett - seems haplotype would be a suitable word... I used "complex" because a) haplotype didn't occur to me, b) the op used complex so I stuck to the same language

I used complex because I wanted to be more general and not specific to biology (operating on the assumption that biology is not the only Darwinian system and that linkage could take forms other than due to chromosome recombination). I of course welcome your answer.


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Geographic/ethnic distribution of Neanderthal DNA in modern humans
There is a really good chance that various human populations have different levels of Neanderthal DNA in their genes.
And yet, the only thing I was able to find is the percentage of Neanderthal DNA in Europe, Asia and Africa.
Are there any studies with a finer resolution, such as regions, countries etc.?

Welcome to Biology.SE! Are you looking for a more fine grained (country-level say) frequency of Neanderthal DNA? Can you please to link to what you found so far? If you can't find country-level frequency of Neanderthal, it is probably because there is too little population structure at this small scale to be able to see any difference. Note, however, that I expect northern Africa to be much more Neanderthal than in Central Africa.

http://www.genetics.org/content/early/2013/02/04/genetics.112.148213
Region-level (Northern/Southern Europe, Middle East, India) data will be sufficient. Country-level data might produce some interesting insights.

Here is a link to the full text of the final published article.


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Extending a small fragment of DNA
Is there a way to extend a small fragment of DNA, say 150 bp, by making copies of itself and attaching each copy of that small fragment to the end of that 150 bp sequence?
For example, I want a 1 kbp+ DNA fragment made up of copies of that exact 150 bp sequence.
I am performing optical tests on DNA strands, but the issue is that the DNA fragments that I am targeting are too small.
However, if the DNA fragment is just a repeated sequence of the DNA fragment I am testing, the tests will yield the same results. For that reason, I am trying to create a long strand of DNA from just one DNA fragment copied over and over.
Is there a procedure that I can follow to accomplish this?

well you can use PCR in conjunction with some ligation technique...

What exactly are you trying to do? If you give a clearer explanation of your experimental setup and goals, we might be able to help you further. As it is, this question is rather vague.

@MattDMo Hi, basically I am performing optical tests on DNA strands but the issue is that the DNA fragments that I am targeting are too small. However, if the DNA fragment is just a repeated sequence of the DNA fragment I am testing, the tests will yield the same results. For that reason, That I am trying to create a long strand of DNA from just one DNA fragment copied over and over.

If the both ends satisfy the condition under which ligase works, you just treat with ligase. But you get various length of ligation products. You can cut from agarose after electrophoresis if you think the yield is enough.

Could you provide some more details? Does your fragment have blunt ends? Is the entire fragment important or could you cut in a little bit if need be?

If what you trying to get is 1kbp of repetitive 150bp sequences, then synthesis as a large chunk might be better idea. It costs ~150-300$ but will potentially save tons of time. (see gBlock from IDT in US)
PCR and ligation with repetitive sequences is pain the butt. It might be true that you save money, but time and frustration could be more expensive.

IDT doesn't like highly repetitive sequences, they become hard to do quality control on. It depends on your exact sequence though, so put your sequence in their form and see if it comes back with a problem. If not, this is probably a good cheap way to do it. Be sure to get PCR primers for your sequence too, so you can make more.

I suggest you to try Recursive Directional Ligation. It is meant to do exactly what you are aiming for, i.e. to "polymerize" short DNAs into a longer one.
You can find the protocol here http://pubs.acs.org/doi/abs/10.1021/bm015630n

Given the cost or DNA synthesis you could probably order the two single strands and anneal them together. Engineer two complementary restriction enzyme overhanging ends onto the sequence. For example, at one end engineer a partial Bam HI site and on the other end engineer a Bgl II site.  Those sticky ends will anneal but the resulting ligation product cannot be cut by either enzyme.
By alternating cycles of ligation, digestion, and ligation, you can build up concatemers of your starting fragment. Then you can gel purify the longer pieces and sub-clone them into a suitably prepared vector.

Instead put adaptors? (if orientation is not an issue)

If orientation is not an issue you can use a blunting enzyme or a blunt-end-polymerase during the PCR (like Phusion polymerase) and then go for a blunt-end ligation. N.B. primers need to be phosphorylated!