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rooters

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  1. In reference to the apparant "randomness" of ERV Insertions, what impact if any result in this example that ERV's are not that random afterall?

     

    http://www.sciencedaily.com/releases/2005/11/051128010951.htm

     

    A human DNA-associated protein called LEDGF is the first such molecule found to control the location of HIV integration in human cells, according to a new study from researchers at the University of Pennsylvania School of Medicine. This study, published in this week's early online edition of Nature Medicine, describes the first clear target for modulating where viruses insert into the human genome, which has implications for better design of gene-therapy delivery. Retroviral vectors are often used to introduce therapeutic genetic sequences into human chromosomes, such as in the delivery of Factor VIII for hemophilia patients
  2. I have an issue on Natural Selection:

     

    http://www.pnas.org/cgi/reprint/0508653103v1

     

    The new study – published online in the Proceedings of the National Academy of Sciences – provides empirical support for the proposition that natural selection is a general force behind the formation of new species by analyzing the relationship between natural selection and the ability to interbreed in hundreds of different organisms – ranging from plants through insects, fish, frogs and birds – and finding that the overall link between them is positive.

     

     

    The question is this (bolded in red). Comments much appreciated.

     

    Look I explained you this a thousand times. Ask any biologist he'll agree. Natural selection hapens AFTER the apearance of a new specie. First you need to have an evolved specie, then it can overpopulate through natural selection. That makes natural selection a secundairy force in evolution, not a driving force. What they meant in this article is that natural selection does have an effect they had a lousy choice of words by saying it's a driving force. What they meant is that it can steer evolution to a certain direction. But natural selection does not cause new DNA. get your cause and effect right.

     

    It's a forum debate, and I am simply asking what he suggested the answer will be if I ask any biologist, how accurate is this that is quoted above.

     

    Many thanks

  3. Thanks for that Azure,

     

    The only thing I find confusing is that should warm blooded mammals "dwarf" as a result of island isolation, then what is the mechanism as a distiction has been made that it is either natural selection or genetic mutation.

     

    My problem here is that is natural selection or genetical mutation for the two are the same are they not in that Natural selection or genetic variation all require mutation?

     

    Surely then island dwarfing is mutation driven???

  4. sometimes with mutation, but mostly with genetic variation due to recombinant genes, etc.

     

    so what is the difference, genetic variation is mutation is it not as the below reference points out.

     

    Genetic variation refers to the variation in the genetic material of a population or species, and includes the nuclear, mitochodrial, ribosomal genomes as well as the genomes of other organelles. New genetic variation is caused by genetic mutation, which may take the form of recombination, migration and/or alterations in the karyotype (the number, shape, size and internal arrangement of the chromosomes). Genetic drift is a statistical measure of the rate of genetic variation in a population.

     

    Source:http://en.wikipedia.org/wiki/Genetic_variation

  5. 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.

     

    Thanks for this.

     

    can I now ask, if genetical factors actively work to reduce a species size over subsequent generations is this then a mutational change. else, how does the change occur?

     

    many thanks

  6. Can I ask for comments on the below qouted please:

     

    1. Einstein's relativity theory show us that time is a dimension. And suggests that eternalism (were both present, future and past are simultaniously existing) is the right aproach to time.

     

    2. This suggests our notion of time is the result of an illusion. Like the motion in a movie is an illusion created by displaying pictures fast after one another, so should our notion of "time", as wel as our notion of "present" be the result of a movement through the dimension of time.

     

    3. What we can logically estimate this force will be like:

    *The force is constant, our notion of time doesn't stop.

    *The force is individual.

    *The force is out of our control, we cannot fastforeward, pauze or rewind.

    *The force is not distorted by the presence of energy, be it in the form of weak force, strong force, EM or gravity (gravity effects the dimension itself which is material, not our notion of time) so the force is probably metaphysical (not made up by the same energy as everything else in our universe that we know is made up out of).

     

    4. This is suprising close to dualism. It doesn't "proof" any religion, since most religions have this notion embedded, but it does pose rather dificult questions to atheism, hence I tried to bring it up here.

  7. I have a question about Island dwarfing:

     

    A species becomes isolated on an island with limited resources. Firstly, is it correct to say that the prediction would be that the species would reduce in size.

     

    Secondly, how much is genetic mutation actively involved in this process and what is the cause of the physical change in size other than by a gentic mutation.

     

    Thirdly, if this makes any sense. I thought dna mutations were born out of luck rarther than a response to specific change in the environment (in this case limited island resources). If mutational change that causes the species to dwarf is luck, how can it be predicted.

     

    Regards as always

  8. Genome size differs considerably between speices. I found this page that lists the number of chromosomes for a few different species:

     

    http://morgan.rutgers.edu/morganwebf.../ChromNum.html

     

    I thought chromosome size differs within same species too such as the common house mouse, this I think is why chromosone numbers are not really related to ancestory modelling. Is the chromosone not the package that contains the dna and all species roughly have 30,000 dna "strings"

     

    I'm not entirely sure what you mean by building a human from a mouse. Do you mean, actually make a living mouse change into a human?

     

    I am referring to how the development of a mouse uses the same approx quantity od DNA as human and the similarity is quite large in a percentage. The main difference is how when and what order genes are turned on?

  9. I am no scientist (I wish I was but did not become interested in the sciences until I was 35 and I still am 35)!

     

    anyway, my contribution is that we could not exactly match human DNA since my DNA will differ from yours (the reader). If I understand correctly that we (all living species) roughly have 30,000 dna strings then I cannot see in the future how we could not build a human from a mouse! since it is looking like the only difference between us is the timing and sequence that genes activate etc etc..........

     

    feel free to criticise, or support :)

  10. It might just be me, but the answers so far don't seem to be definitive enough, I went back to the link I provided and noted the caption below the picture

     

    (A) Changes in the foxes’ coat color were the first novel traits noted, appearing in the eighth to tenth selected generations. In a fox homozygous for the Star gene, large areas of depigmentation similar to those in some dog breeds are seen.

     

    Am I right to assume that the colour changed due to depigmentation caused by either a chemical change in the make-up of the off-spring or a direcr genetic change such as this "star gene"?

     

    Thanks all

  11. Coincidence, either the what-the-soviets-where-looking-for gene was the same as the look-like-a-border-

     

    From what I understand, selection was based soley on tameness and not selected by colour.

     

    collie gene and just had two manifestiations or those two genes happened to come with the same foxes in the first generation of breeding so it stayed that way.

     

    But the collie is descended from wolves and not the fox unless you are suggesting that the fox shares close ancestory with the wolf?

     

    Any more ideas, I don't like the sound of yours. No offence.

  12. This is an interesting thread, and I am currently engaged into a debate over it's findings. Lack of knowledge is a real issue so scuse me if this is a dumb question.

     

    Are the insertions not random, and by this I mean that both Chimp & Human share the insertions but the insertions are not random. Meaning that the same virus inserts it's junk at the same place with both species!

     

    The reply I am trying to deal with is:

     

    But I already replyed to that remember, so why did you repeat yourself? You assume here that the insertion is random, whereas I replyed to that these processes aren’t likely to be random, as reactions on this micro level usually follow a strict causality. 3-dimensional structures are very important wwhen looking at chemical reactions with molecules of this big a size

     

    Regards

     

    Root

  13. Radical Edward

     

    Firstly, I must say that I enjoyed your post. For me as a devout evolutionist I find it at times complex and above my understanding with certain aspects. I used your post as a source for a forum debate. And I would be interested in your opinion on comments made against it.

     

    I’d say you’r on the wright track comparing chromosones. On the wright track but not completely there. Our genetic information is stored in our DNA, these strings are then wound around cromosones. If you really want to compare human DNA to ape DNA, compare the DNA itself not the chromosones on wich they are wound. Comparing cromosones to proove relativness is just like comparing a human cell to an animal cell, they both show simularitys (both have a double membrane, a nucleidcore containing these cromosones and so on...) but that doesn’t mean their DNA shows simularitys. So what you did was not comparing DNA but comparing chromosones to show simularity’s in DNA. That would be like comparing two panoramic pictures of two diffrent houses to proove that the bricks underneath the paint are in fact the same.

     

    As a second argument against this “proof” one could say your reasoning is flawned, because even if the DNA has simularitys that doesn’t mean one origenated from another. If two houses are simular in desing, build out of the same material, in the same style and shape, that doesn’t mean that one house is the descendant of another. In fact it would seem more logical to assume that both are simply designed by the same architect rather then formulating a theory of how one house had mutaded offsprings. Tell me why do you assume that for creationism to work, a creator created all creatures in totaly difrent ways? If it’s not broken why fix it?

     

    First of all you have two agdmit that you made 2 assumptions. First of all you asume that the proces of proviral integration is random. It could very well be that this integration is only possible at a certain loci, either determined by the structure of the virus or by the structure of the DNA. Do not forget the importance of 3dimensional structures when studying processes at this level. Such an inhibition by a virus in DNA is not likely to be coincedental, but rather a result of it’s characteristics.

     

    Second of all you asume that even though genetic drift is random, it is possible for a whole population to carry the endogenous virus due to a single proviral integration. Not only is this very unlickely to have happened, it is also the only alternative to assuming multiple viri infiltrated the DNA with multiple hosts at the same loci.

     

    Lets take a look at those last phrases again. Basicly we have the factor of “luck” being faveroble for both sides. You could say it’s unlikely for multiple viri to inhibit the same loci, while I can say it’s very unlikely that a whole population inhereted this from a single source. The only diffrence between my unlikely theory and your unlikely theory is that I have arguments to take take the chance factor down (being the inability of the virus to integrate another loci). I think this shows how it’s very biased to dismiss the posibility that both apes and humans to have aquired this endogenous virus in simular ways rather then from heritage.

     

    Also take note that this is somewhat contrading. Evolution tells us that humans and apes did not evolve from one another but evolved from a thirth species. As difrent branches in a tree rather then a strict line, while the added illustration chart of ERV distributions suggest a straigh lineage.

     

    It’s not just a matter of where hot spots are situated as you commmented. When looking at chemical reactions with molecules of this magnitude a simple cis-trans isomere can make a world of diffrence. To claim that there’s an absent of ERV’s that don’t match the phylogenetic tree as an argument against hotspots is again assuming it’s coincedential nature. And also neglecting the fact that we have only mapped human DNA a couple years ago and still haven’t searched all primate DNA with a fine-thooth-comb.

     

    The second problem that it’s strange that some viruses have infected every single primate rather then skipping one is again biased on the 2 assumptions.

    1. That it’s likely for a whole population to carry this from a single source.

    2. That it’s unlickly to happen more then once on the same loci at different species

    If one would assume the opposite, by reasons I mentioned above, you would see that for this ERV to become present in a whole population it must by nature be a virus that was widely spread and that integrates the DNA sequence easily. So then it doesn’t seem far fetched for this virus to have spread interspecial and to have integrated all these species. Also, the absence of a retrovirus that is compatible with all those species at current time, does not mean it doesn’t exist. Our knowledge on ancient viri isn’t that big seeing our only source of information is those ERV, so that argument is completely backwards.

     

    To assume the crippledness of the virus is also a factor against multiple integrations is again overestimating the randomness of the proces. It’s very likely to have happened in a specific way due to specific reasons. These things don’t just happen out of the blue in total randomness, there’s fysical laws, and chemical characteristics to take in account. These so called changes that would have been made to the ERV later on way very well be due to the proces of integration.

     

    Now moving on to your thirth argument, Phylogenetic.

    I think I have a pretty good idea why your friend Radical Edward failed to give you much information to go along with this argument. Simply because there is none. As I said before, we haven’d mapped primate DNA, so a heritigal study cannot be made. Secondly this is, as you said unique for a single family rather then a whole population, so it’s merely impossible to study this, even if in fact man evolved from monkey, it would still be hard to find wich human family carries proof of wich ape familly

     

    I know it's long. But I am interested in your opinion and others here.

     

    Many thanks

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