CharonY

There are, in fact several elements. The main factor in Dolly was, if I remember correctly the telomere length. Human DNA is essentially linear meaning that during repication the ends might shorten (as the replication does not precisely start at the outermost base). To circuvent this problem the chromosomes possess highly repetitive regions, the mentioned telomeres which serve as a buffer for information loss. However over time the telomeres also shorten and thus might contribute to aging.

Another mechanism is modification of DNA. The DNA is methylated age-dependently. This modification is usually involved in certain regulatory processes which also affect cell development.

3. We already use DNA to create our own species. Its a common occurance in the lab. Scientist are always introducing pieces of DNA that confer antibotic resistance to certain Bacteria (technically its a new species, it can survive where other's can't).

Sorry, no. Technically it is a new strain, but same species (DNA : DNA hybridization is clearly above the threshhold).

This may seem like nitpicking but this time no technology exist to curate the genome up to a point that allows creation of a new species.

Well, technically there is a way (for bacteria) but it would simply involve taking a genome with large accessory genetic elements and cure them all. But my point is that atm we can only manipulate existing cells (to quite some extent, though), but we lack the ability of creating something completly de novo (as I assumed this thread was about), nor will this be possible by purely concentrating on DNA.

Actually it doesn't look like she is not aging. She is only arrested in her development. One should not confuse aging on the cellular level with maturation. In another report I read that they did not find any obvious chromosomal defects/differences btw.

Ugh you made me trying to remember stuff from my student days.

In general ecological simplification means a reduction of function, complexity and structure of a system.

- Reduction of function is the case if certain ecological processes/flows are disrupted. Examples might be carbon or nitrogen cycles. The nitrogen cycle for instance can be disrupted if for instance there is a significant loss of ammonifier/denitrifiers or for instance nitrogen fixers. Or plants using immobilised nitrogen and so forth. This is often coupled with

-reduction of the complexity of the system, meaning the loss of elements (usually species) in an eco system. Every species plays a specific role in a given ecosystem and as such a loff of them reduces both, complexity and function of a system. Finally there is

-reduction of the structure of a system. A higher structural complexity is characterized by higher diversity and variations of habitats in a given system.

Possible but only the far far future. Getting sequences is comparatively easy now. The identification of genes from this sequences is still rather tricky (especially for eukaryotes). Assigning functions to these genes extremely complicated. Even in well known, very basic bacteria like E. coli the amount of genes coding proteins of unknown function is around 20-40% at least. Then we do have intergenic regions which apparently do have a function (e.g. in regulation) but is nigh impossible to detect them as we know very little about it. Then of course there is the problem that not everything is determined genetically. That is, you also have to consider at the very least the cellular environment and then it gets really complicated...

I fear you have started with slightly wrong definitions of evolution.

First, evolution can be defined as a change in allele frequency in a population. Or a bit simpler, a change of the gene pool over time. There is no direction in this change per se (or at least one cannot infer it). There only has to be a change which is then described as an evolutionary event.

Now, mutations are one of the mechanisms which can lead to evolution. So in theory every mutation changes the gene pool a bit. However, most are lost or at least do not spread and therefore do not contribute to any lasting effects on the gene pool. Mutations alone however are in general considered randomised and by their very nature cannot give evolution any direction (or as you put it, "start a new phase").

So if we got mutations as the only mechanism, the only way evolution might happen is by a rapid accumulation of mutations. Now another factor comes in: natural selection. You assumed that

Those mutations don't survive in nature (hence the "survival of the fittest). In fact, the fact that these don't survive allow the better characteristics in an entire race to advance and evolve..

However, as I pointed out above, a change in the gene pool is evolution already. The only thing that selection adds is a direction. By no means does it mean that the gene pool might get "better" somehow. It only means that it forces the gene pool to adapt to these selective pressures.

So in selective sweeps and also random events mutations will either get lost or persist in the gene pool (loss of already established alleles in a gene pool is evolution, too btw) and thus contribute to evolution.

The frequency (or likelihood) of a certain mutation (or allele in general) to get established in the gene pool is a function of its frequency (how often does this mutation occur in the population?) and its effect on the fitness of the individuum (increasing/dcreasing/being neutral to reproduction chances).

Now that being said do humans prevent mutations?

NO of course not. Mutations are a mechanisms that happen all the time, we have no way of preventing it. So the human gene pool is and will continue to be subjected to mutation events.

However some mtuations that are detrimental can now be diagnosed. Now if we assume that all foeti with this detrimental alleles are aborted, do we stop evolution? Of course not. We simply add a selective pressure on the certain alleles.

Everything we do just changes selective pressures, but we do not and can not eliminate them completely. There are always some individuals with a higher fitness (higher reproductive chances) that are based on genetic elements. Sexual selection for instance will always work. A change in life condition can also dramatically change selective pressure. For instance let's assume that a thousand years ago being atheletic was a prerequisite to reproduce. Nowadays assume that it is less so. Therefore alleles contributing to an atheletic build will have less impact on fitness and the frequency of it could in theory decline. This too is evolution.

In contrast nowadays literacy is very important. So if we assume that there are alleles that prevent literacy (assuming there is such an extreme form of dyslexia that has a genetic basis), they might have been abundand thousands of years ago (few selection against it) but nowadays it is likely that the frequency is lower, due to the higher selective pressure.

And lastly I want to point out that humans are adapted to the given environement (and yes also the ability to change the environment is and adaptation) otherwise we will have died out already.

So what I wanted to say with this long post (for which I now have no time to check for spelling errors atm, my apologies) is that while human societies do change selective pressures, there is no way that evolution per se can be stopped.

During (aerobic) respiration reactive oxygen species (ROS) are formed (e.g. by the Fenton reaction). Of these hydroxyl radicals are probably the most reactive ones. The more agressive species directly act on e.g. proteins, DNA and lipids causing aggregation (cross-linking), fragmentations, deletions etc.

In fact it is a kind of corrosion, as in most cases corrosions are simple oxidation reactions, too.

Antioxidants however, either prevent the formation of these ROS or directly detoxify them. As such it is believed that antioxidants should help preventing cell damage (and thus aging), but I am not sure how large the impact of the intake of antioxidants really is. The body of course produces a number of enzymes involved in detoxification (e.g. catalases, peroxidases and superoxide dismutases..).

Nope. In order to preserve specimen all flesh is boiled away leaving only the fur and bones (otherwise they would rot away). Alternatively they are preserved in formalaldehyde or other alcohols.

This harsh treatment will effectively destroy DNA.

Technically this is not possible. As pointed out in a number of other similar threads the limiting factor is the quality of DNA. The specimens in museums are other stuffed or fossilized, bot of which will not yield any DNA. One needs an extremely well conserved (i.e. frozen), not to old sample to get DNA of sufficient quality.

PhD also means that you could be kinda dumb.

I think you can safely scrap that "could". In addition the lack of money you have to add that after getting phd it is even harder to keep your job. In quite a lot of countries there is a time limit in which you can be employed in universities unless you get tenure or something equivalent. So even if you wanted to (and who would?), you cannot stay postdoc forever. And finally especially in most biological areas there are far more scientists than positions. So for your career's sake you have to work even harder after your phd (if you want to stay in academia) to get a good publication record. PhD students routinely work at least 60 hs a week, (more during the "crunch time"). Depending on your position as postdoc more often than not you have to do some administrativa, teaching and training of students in addition to reasearch. So expect 70 hours or more, depending on your field and lab.

The only weird thing is that for my live I cannot imagine doing someething else. I suppose the solvents you use eventually degrade your brain...

ehm. Sequencing? I hope it is not the whole scope, is it? I mean the usual work in this field is the creation of libraries (either BAC or shotgun, depending on strategy). If you are really unlucky you'll gonna have to do the sequencing, too (hopefully with a capillary sequencer, or maybe a pyrosequencer system?).

After that it is only computer work (until you get to the polishing phase, depending on what you sequence).

Of course it is something different if you do postgenomics, that is, you already have the sequence and start working from there. In that case you can utilize genome information to do targeted genetic manipulations.

Actually human babies are not more vulnerable than compared to a large number of other animals. Take puppies or honey bee larvae for example. Human development is a bit slower than that of many other animals though, as is its lifespan.

If you want to learn techniques you should obviously look for groups that employ. Of course developing new techniques can be interesting, too, but such projects have several pitfalls. A) the technique might not work at all. B) budget confinements might hamper your progress.

Other than that you should look for a topic with a biological question (rather than technique) that interests you. You'll learn the techniques on the fly. So esentially you probably want to look for a group that goes in the direction of viral infections (probably primarily human pathogens). In that case you have to keep in mind that experiments with human pathogens require a certain lab security level, which is not available in many universities.

You probably do not want to drift too much in the direction of virology/microbiology, though.

Other examples may include certain aspects of immunology, medical research, for instance.

So basically check out the topics of interest and then look, if the groups are employing techniques you want to learn (either ask them or read their papers).

Actually it is a bit more complicated. The notion that nature is essentially in balance is an illusion. Biotic and abiotic elements in almost any give ecosystem is constantly shifting. Sometimes around some kind of equilibrium, but more often than not there are gradual (if slow) changes. A very intuitive way to see that is considering the fact that species within an ecosystem are evolving and thus open up new niches in a given system.

In general I'd say that ecological damage is probably given as a more or less sudden disruption of the given state of a system, resulting in an ecosystem that is distinctly different from the starting point (just pulling some ideas out of nowhere...).

If you could sequence enough DNA fragments, you could eventually reconstruct their entire genome inside of a computer via statistical analysis.

Uhm, no, sorry. Even with bacteria this isn't possible (would be a dream of whole genome shotgun projects, though).

However, ideally you should let them check all your calculations together. It can be very disruptive if you go and ask every few minutes.

Experiments (unless very simple ones) are ideally checked in groups.

That's not true. We had a postdoc from the MIT as a guest scientist. She was not able to make buffers. She told us that in her lab all buffers were made by the TAs. So probably asking TAs is a good start...

Let's say, 1l?

Regarding DNA preservations, under permafrost conditions it has been estimated that DNA might be preserved up to 1 mio years (Journal of Human Evolution

Volume 45, Issue 3 , September 2003, Pages 203-217.)

Regarding the mammoth DNA, a metagenome approach was made yielding around 28 megabases, of which around half was found to be mammoth DNA (by comparing to elephant sequences). Note that the whole genome cannot be reconstructed with this method.

Well, and if you work with solvents you will find % (v/v) a lot. Even in molecular biology labs

However, a good question to keep students occupied is to tell them to make 5 M HCl starting from a 32% HCl solution...

Well, if one decides to go into academia (especially basic research) and gets his PhD for it, one does not really except reasonable payment.

It's been asked before (a poll, even, so you can track results)

 

Ain't the search function a useful tool?

Pity that one can't see who voted what

Actually it is not wrong. You are only argueing on different levels. The proximate cause of sex determination is indeed testosterone. SRY is a transcriptionfactor that leads to the expression of genes which in turn lead to testis formation (and thus, testosterone production).

Sorry, just noticed that my post was quite meaningless. Posted in a hurry.

Basically it should not be population dependent since a longer pupation time correlates with a higher starting density,

Actually, upon reflecting I found one point a little bit unclear after all. Let me elaborate:

Assume that qx (or mortality rate) is 0.5. Furthermore the mortality rate is calculated in arbitrary steps (could be days, weeks, whatever).

Now assume a starting density of 10 and assume that one time step is needed till pupation for this density. This would result in 5 survivors and 5 deads (5/10=0.5). Or in other words, 5 larvae enter pupation.

Now double the density to 20.

Step 1: 10 survivors 10 dead. 10 survivors can enter step 2 (due to increased time it takes to enter pupation because of higher density)

Step 2: 5 survivors, 5 dead. So you end up again with 5 survivors.

And so on. But this would only apply if the start of the pupation phase is dependent on the current population size so that starting with a population size of 80 it does not take 8 steps but 4 (80 ->40 ->20 -> 10 -> 5-> pupation). At least that’s how I understood it.

Same applies to them. There was always a variation in size. Natural selection "provides" different fitnesses to them. As such especially your 3rd point iskinda weak to discuss.

But still:

2) A decrease in size can be the result from genetical factors but also e.g. by nutrient limitation. If they are taken out of the limiting situation and still remain small (or their progenies rather) then it is mostly genetically determined.

3) mutations are (mostly) random. as such you cannot expect a mutation for small size to happen.