"Mutation" is defined as a change in the sequence of amino acid molecules in DNA.
We get some DNA from our mother and some from our father. Any DNA we have that is different from both our mother and father is a mutation. That's by definition.
We can and do compare DNA sequences and detect mutations.
The differences between someone's DNA and both their parents, which we label as mutat, did not exist anywhere before. Not in the mother's DNA, not in the father's DNA, not anywhere. No amount of redefinition or argument can change that fact. It does not depend on assumptions or worldview.
Mother's DNA + father's DNA + mutations = your DNA. There's no other physically possible source of your DNA.
Well, but aren't you just talking about observed differences, and how do you know those differences are the result of mutations rather than the result of sexual recombination producing/selecting a new set of alleles?
Easier than pie.
All recombinations are identical to the corresponding sequence in one parent (or both). So we can comp the three genomes and detect the recombinations.
Some relatively small amount of the offspring's DNA will not appear in either parent. Those we label as mutations. The particular mutations do not exist anywh else. (It is poss it may exist somewhere else but that wouldn't be a copy of the offspring's DNA; it would have to arise independently.)
The main thing seems to be that you all see mutations where I see normal built in variation and this has never been satisfactorily sorted out
Only because you refuse to understand the many simple explanations.
Let's take eye color as an example. The father has BB, the mother has Bb. The child could have BB or Bb but not bb, because only one parent has one b.
But if there is a mutation in the b gene the mother has, the child gets BB or BÎ¶. Î¶ is a new gene that is probably very similar to b, but is not the same as b. It was created by the mutation. It did not pre-exist. it's very unlikely it exists anywhere else, and if it does it's because it arose independently.
There are only two types of genes in the inherited genome; those that are the same as the mother's or the father's, and those that are different. The latter is the definition of mutation; a change that makes something that is not the same as the mother or father but is brand new, created at some point during the process.
You denying they're facts doesn't affect reality. You saying they're assertions and ignoring the evidence we post also doesn't affect reality.
There are only four possibilities for the source of a human's gene alleles.
One copied from the mother and one copied from the father
Both copied from the mother
Both copied from the father
One of the above three except one or more changes in one (or both alleles, but unlikely) that create a brand-new allele (or alleles, but very rare) that never existed before
Those are facts. Note that there's no "rearrangement of existing alleles" other than the recombination.
Your vague hand-waving descriptions are worthless. To convince anyone who hasn't already drunk your Kool-aid you need rigorous operational definitions of all your terms, detailed descriptions of the steps in the process to establish plausibility, and experimental data to demonstrate that it happens.
A million Faiths couldn't do that in a million years.
quote:Extensive mapping has pinned it down to a 400-kilobase region containing 13 genes, none of which had any obvious role in wing coloration. Undeterred, scientists went on to isolate the gene responsible, and they describe their search in this weekâ€™s issue. It is called cortex, orthologous to a gene of the same name in Drosophila. The researchers have even gone further, and shown that the specific cause of the mutation is the insertion of a transposable element (popularly, a â€˜jumping geneâ€™) into the first intron of the cortex gene.
The insertion leads to increased transcription of the gene during a phase of development when the wing discs are forming. The cortex gene, then, is involved in wing development, but there is still no obvious association with coloration. In Drosophila, cortex is involved in cell-cycle regulation, in particular, marking proteins that are redundant in the cell cycle as being ready for disposal. What is going on?
Work from a different group of Lepidoptera might offer a solution. In a study also in this issue, another group of researchers shows that cortex is a key player in the coloration of the wings of butterflies in the genus Heliconius, long a favourite for the study of mimicry. They show that cortex is a member of a fast-evolving scion of an otherwise conservative group of cell-cycle regulator genes known as the fizzy family, a name redolent of activity, growth and fervour, and possibly involved in the regulation of wing-scale development. This is important, because it is the size, density and surface properties of the wing scales that determine colour in butterflies and moths. Flies, such as Drosophila, lack these structures, perhaps explaining why it was initially hard to associate the cortex gene with wing development.
There is a further, satisfying twist to the tale. Although it is possible that melanic mutants existed undetected at a very low level in the peppered-moth population for centuries, the specific mutation behind their coloration is relatively recent, appearing around 1819 â€” in plenty of time for it to be noted down in Manchester a couple of decades later.