Introduction to Genetics

30 to 50 mutations total in germ line cells for each child born. For a human population of 6 billion, this guarantees that every possible non-lethal substitution mutation is present in the current population. I am explaining how reality differs from your fantasy world. The same way that the HapMap project is doing it. Sequence the genomes. The only artificiality is dividing DNA into DNA you care about and DNA you don't care about.Edited by Taq, : No reason given.

While I agree that this thread is not an introduction to genetics, I also have great doubts that such a thread is going to change my orientation in the first post as snapdragon thinks. Because I HAVE read basic descriptions of DNA and how it works, have watched animations showing the replication processes and so on. I don't see how a review of all this is going to redirect my questions. I'm sure it would include lots of information I'm not up on, but it isn't going to change my understanding of the basic framework of how DNA works.

That's scary.But the question does remain: what do those non-lethal mutations actually DO and if they don't do anything of benefit at all what is the point of even counting them as an increase in genetic variability?Edited by Faith, : No reason given.

These mutations will improve fitness, reduce fitness, or not change fitness at all, just as they always have.What is the point of talking about genetic variability if you ignore genetic variability?

Well I'd put it "DNA that actually affects the organism for good versus not so good or doesn't do anything at all."

But that too sounds like an article of faith that it does what alleles do, and "fitness" is way past where I am in this discussion anyway. I'm trying to talk about the formation of new observable phenotypes from new gene/allele frequencies in a new daughter population, that mostly just change the "look" of the population, without "fitness" entering into it. And again, where's your EVIDENCE that your mutations affect fitness (ABE: For the better I mean of course /ABE)or anything else? All this just sounds like the Evo Creed over and over: the ToE SAYS it affects fitness, therefore it affects fitness. . Right, IF mutations WERE functioning genetic alternatives you'd have a point. AND if you could SHOW that they DO anything in my daughter population.Edited by Faith, : No reason given.

Junk DNA makes up 80 to 90% of the genome. Junk DNA accumulates mutations at a rate consistent with neutral selection. That is how it is identified. This can be done by comparing genetic variability among humans, or comparing the human genome to the genome of other species.Open reading frames (ORF's) are much easier to identify since they will be intact and not interrupted by frameshift mutations. You will also be able to find transcription factors and other intact promoters upstream of the open reading frames. However, RNA genes and other non-coding functional DNA can not be identified by looking for ORF's, but they can be identified by finding sequence that is under selection. The classic examples is the lac operon found in E. coli, and it is still the example that students become familiar with in introductory classes in genetics. The operon has the B-galactosidase and other genes which which are responsible for breaking down lactose for energy. Upstream of the B-gal gene are two DNA binding sites. First, you have the cAMP protein binding site. As glucose gets low the levels of cAMP increase in the bacterium causing the protein to bind and increase production of the lac operon genes. Next is the lac repressor site. This is there the lac repressor protein binds and blocks RNA transcriptase from binding to the DNA. When lactose metabolites are present it binds to the repressor and releases the repressor from the DNA. This allows RNA polymerase to bind and transcribe the genes. If the cAMP protein is also bound to the upstream DNA binding site, it increases RNA polymerase binding and also increases transcription.

It's not, as I have shown in previous posts. Compare the fitness of humans and chimps in an arboreal or savanna environment. The mutations that have given humans their species specific morphology is beneficial in an open savanna. The mutations that chimps have give them increased fitness in an forest setting. That is the evidence, the observed and beneficial differences in the two genomes caused by mutations.

It would be really nice to get this sorted out if possible. The reason I started this thread is that I DON'T know much about how the genome functions. I know the basics about DNA but all the stuff that goes into the daily work that's done on the genome I know nothing, like what they are actually looking at and everything else. I'm completely in the dark. I have a rudimentary understanding of how DNA functions, replicates and all that, and from this thread I've learned that "junk DNA" is scattered throughout the genome. It's valuable to me to learn anything about these things.But I"M A CREATIONIST, and the reason I come here is that I'm trying out various creationist ideas and they are of course NOT the same ideas that geneticists work under. I don't suspect any "underlying agenda," but when you are working within a particular scientific paradigm you simply always interpret the facts in accord with that paradigm.And that's all I'm doing too. Mutations are not to a creationist what they are to an evolutionist. And when I say it looks like this or that is simply assumed, I think it's clear that it is simply assumed. Functioning mutations are ASSUMED. All alleles in the genome are assumed to have been originally mutations. That's an assumption based on the ToE, it hasn't been proved and it can't be proved, and what is actually known about mutations, that gets described here, doesn't offer any evidence to back that assumption. So I answer with my creationist point of view that it IS just an assumption, and they are simply CALLING functioning alleles mutations because that's what the theory requires. You don't need an "underlying agenda," you just need to believe in your paradigm. What you call "distortion" really ought to be understood as my different paradigm. I'm always talking from my different model. It's different from the ToE model. Most of the time all I can do is describe it. That can sound like being a know it all, but I'm simply spelling out the creationist system in answer to the ToE system. I want to keep it on the table. I have some ideas about how to prove aspects of it, but I'm not in any position to do the necessary tests. Meanwhile I can at least counter the ToE with the YEC view. OF COURSE it changes things. Sometimes I just repeat it so that it will become familiar and not just get buried in the usual ToE assumptions. If I describe a whole different way of looking at these questions than the ToE does I keep getting called a liar, but all I'm doing is spelling out my different model. Only your commitment to YOUR model makes mine a lie, but rightly you should see what I'm trying to do as presenting a different interpretation of some of the facts I am up on. It has nothing to do with lying, it has to do with a different theory. I have no doubt they know how DNA works, ABE: that's why I'm asking questions, I do expect to get true answers to my questions /ABE but that doesn't guarantee that the support you find in the DNA for the ToE is not skewed by your commitment to your paradigm. Whenever interpretation of data is involved you can be wrong and not see your error. This has nothing to do with lying or having an agenda.All you are really saying is that I don't have a right to think differently about the facts.Edited by Faith, : No reason given.Edited by Faith, : No reason given.Edited by Faith, : No reason given.

You don't even seem to know all you are doing is reciting your theory. You're assuming that mutations are alleles as I've said. If the actual mutations do not actually contribute anything to the fitness of the chimpanzee you wouldn't know that because you are assuming that all functioning alleles are mutations. You have no proof of this, it is simply an article of faith in the ToE although you are specifically denying this.

Yes, theories backed by evidence. What is wrong with that? No such assumption is being made. The evidence demonstrates that these are mutations that have occurred in each lineage since sharing common ancestry. This is a conclusion drawn from evidence, not an assumption. I have 150 years of gathered scientific evidence, from transitional fossils to genetic evidence.

You've never presented any evidence that supports your claim that all the alleles were originally mutations.

It is found throughout the other threads and throughout the scientific literature. As a start, you can check out this paper on ERV's shared by humans and chimps as smoking gun evidence of common ancestry and the evolution of sequence through mutation and selection.Just a moment...However, I have this haunting suspicion that you don't give a lick about the facts, so why bother showing you evidence that you will ignore?

That is still an artificial separation of DNA sequences.

It isn't artificial if it's true.But it IS an artificial position to take to pronounce it all normal alleles if it isn't -- again, an assumption, an article of faith.