sciborg

Thanks. I assume all the folds are ironed out in skin cell cloning? Is it thought the folding involves long stretches of DNA? Therefore the physical position of a gene on a chromosome is critical to whether it gets expressed? Genes in the same locus area would tend to be expressed or suppressed together?

I have read that that at least two things cause differentiation of cells: first, the "signal" environment changes in reference to protein signals that then cause gene expression to change. Second, genes are progressively "tagged" by methylization which inactivates some genes causing differences in expression depending on where we are in a cell division scenario. Presumably fewer genes are tagged in "stem" cells (near the beginning of a division tree) and therefore more genes can potentially be activated (or deactivated) by the signal environment. If you chop tissue out of an organism and put it in a petri dish the signal environment changes as signals are washed away. This presumably partly explains why cells in vitro don't behave as they do in vivo. If this is right, is mutation, that is permanent alteration of the cell genetic data required to explain differences in gene expression? Apparently, animals can be cloned from skin cells. Skin cells would appear to be (but not necessarily) pretty far down a cell division tree. So apparently, somehow, the tagging does not cause a problem for the cloned animal. Why not?

Yes. Aging and death have a number of plausible benefits for the species, society, culture, tribe, etc. The difficulty has been in developing a sequence of events that could explain how an individually adverse characteristic could propagate regardless of its greater benefit. Wouldn't the individuals that live longer have more descendents? Wouldn't aging select out according to Darwin's theory. Therefore, the currently most accepted theories of aging all postulate that aging and death are not desirable traits and did not evolve.

Darwin's theory says that traits that cause organisms to live longer and therefore to breed more, or just to breed more are the traits that are "selected". Mutational changes that cause an organism to die earlier or breed less are "selected out". Therefore there cannot be an evolved trait that causes an organism to live less long and/or breed less. Aging and some other observed traits conflict with this view resulting in 145 years of argument among biologists. Aging theories have had to work around this difficulty. Darwin's view was that all organisms (not just bacteria) are driven to survive and breed to absolutely the greatest extent possible and all the limitations such as starvation, predators and disease were externally imposed. Any internal restraint such as you describe is incompatible with the preceeding paragraph. This leads to the idea that Darwinian evolution requires "individual" benefit and cannot support the evolution of traits that provide "genetic betterment" or other future benefit at the expense of a breeding or life span disadvantage to current organisms. See http://www.azinet.com/evolution/ for a brief overview of this issue. I think that you are right and Darwin was wrong. Evolution is more complicated than just survival of the fittest.

Tormod: Some species (Pacific Rockfish, Sturgeon, some turtles) apparently do not age according to some researchers. Generic degradation theories ("machinery fails") do not explain why some species have drastically different life spans than other similar species (e.g. different varieties of salmon, different birds, etc.). There are other problems with generic degradation theories. Biochemist: Yes. But the $64 billion question is are the cell division limitations a fundamental limitation (unlikely for reasons stated above) or part of a "programmed death" biological suicide mechanism. Cell division is thought to stop because telomeres shorten each division. However, an enzyme, telomerase, can repair the telomeres. Possibly the suicide mechanism controls the availability of telomerase? As you point out there does not appear to be any fundamental limitation on cell division since cancer cells can divide indefinately. Normal cells need to be regulated in their division. Boerseun: Yes. That is essentially the Weismann theory of 1882. Unfortunately, it is incompatible with Darwinian evolution theory. This has caused 145 years of argument!

Did we evolve aging as part of our design because it performs some needed function? This site (http://www.azinet.com/aging/) provides numerous arguments that aging is necessary to the process of evolution, especially to the evolution of certain traits such as intelligence. What do you think? If we are designed to age would that have implications for medical research?

Female humans do have slightly more DNA than males (a few percent). Also the DNA in mitochondria comes only from females. Finally, the original copy of the machinery that reads the message in DNA comes from the female. See http://www.azinet.com/aging/Genetics.html