Already defined that in the opening post.
"In biology, a mutation is a permanent change of the nucleotide sequence of the genome of an organism, virus, or extrachromosomal DNA or other genetic elements. Mutations result from damage to DNA which is not repaired or to RNA genomes (typically caused by radiation or chemical mutagens), errors in the process of replication, or from the insertion or deletion of segments of DNA by mobile genetic elements.[1][2][3] Mutations may or may not produce discernible changes in the observable characteristics (phenotype) of an organism."
https://en.wikipedia.org/wiki/Mutation
We can get to that in the future. Right now we need to agree on something much simpler.
Are the differences between humans and chimps due to the differences in the DNA sequences of their genome? Yes or no?
Do you think those differences in protein coding genes are responsible for the physical differences between humans and chimps?
Why talk about mutations if you can't even agree that changes in DNA sequence will cause any differences?
Excellent, that should go a long way to avoid equivocating adaptations with changes in DNA sequences due to transcription errors.
That's not even a question, it's more like a given.
Yes of course, "~29% being identical and the typical orthologue differing by only two amino acids, one per lineage." (Nature 2005)
We must talk about mutations because it's the only way to explain the divergence aside from special and independent creation. I have long contended that the divergence exceeds any reasonable mutation rate when you include the indels and gross structural differences in the protein coding genes:
Taken together, gross structural changes affecting gene products are far more common than previously estimated (20.3% of the PTR22 proteins. (DNA sequence and comparative analysis of chimpanzee chromosome 22, Nature)
I've always thought of you as a true believer, the majority of the trollers haven't a clue and these scientific types know they are putting out shallow misdirections. You on the other hand seem convinced, which is commendable in some ways. The problem is that you spend too much time swimming on the surface. Try a little back ground reading LM, how do the protein coding genes of humans and chimps diverge? Last time I check it was some 40,000 amino acids. Then ask yourself the obvious question, what is the most likely result of an indel in a protein coding gene.
Errors in transcription don't change DNA sequences, so I don't see how that would be a problem to begin with.
Which means that 30% are 100% identical and the other 70% are about 98-99% identical. Why is this a problem?
"Here, we report the high-quality DNA sequence of 33.3 megabases of chimpanzee chromosome 22. By comparing the whole sequence with the human counterpart, chromosome 21, we found that 1.44% of the chromosome consists of single-base substitutions in addition to nearly 68,000 insertions or deletions."
1.44% of 33.3 MB is ~480,000 substitution mutations. They also report 68,000 indels. Again, substitution mutations are much more common than indels, and don't cause frame shifts.
"In contrast, 47 PTR22q genes show significant structural changes affecting at least one of their transcript isoforms. Fifteen genes have indels within their coding region yet retain frame consistency in all but one case (TCP10L) (Supplementary Table 4)."
So we only have one gene that has a frame shift mutation due to an indel, and 14 genes that have an indel but no frame shift mutation. Also, not all of the "structural changes" were indels.
The most likely result of an index in a protein coding gene is a frame shift mutation which would most likely be selected against and removed from the population. However, all indels that are multiples of 3 will not result in a frame shift mutation.
On the flip side, substitution mutations are 7 times more common than indels and they don't cause frame shift mutations. You always seem to forget that.
You might want to read your own links. Mutations are from errors in dna replication (dna copied to dna). Transcription is the process of voting dna to rna. Any errors here wouldn't end up in the genome since we aren't making any dna in transcription.It is amazing how many fundamental errors you make in a row. An error during transcription is the source of Genetic mutations:
DNA Transcription
In the living cell, DNA undergoes frequent chemical change, especially when it is being replicated (in S phase of the eukaryotic cell cycle). Most of these changes are quickly repaired. Those that are not result in a mutation. Thus, mutation is a failure of DNA repair.
Mutations
The deleterious effect of mutations on protein coding genes. Of course if you never bother to learn basic genetics that would not effect your understanding one bit and you obviously are not interested.
Here's the quote in context:
By comparing the whole sequence with the human counterpart, chromosome 21, we found that 1.44% of the chromosome consists of single-base substitutions in addition to nearly 68,000 insertions or deletions. These differences are sufficient to generate changes in most of the proteins. Indeed, 83% of the 231 coding sequences, including functionally important genes, show differences at the amino acid sequence level
That's 83% of the protein coding genes with 20% showing gross structural differences.
Estimates of nucleotide substitution rates of aligned sequences range from 1.23% by bacterial artificial chromosome (BAC) end sequencing to about 2% by molecular analysis, whereas the overall sequence difference was estimated to be approximately 5% by taking regions of insertions or deletions (indels) into account
In other words, it's between 1% and 2% when you count just single base substitutions (differences). If you count those of length, and some of them are millions of base pairs genome wide, it's 5% at least. Your just going to sit there and say so what?
You forget, the explanation for the difference is mutations. Ultimately they are just differences that assume indels as the cause. Of course there wouldn't be frame shifts if the lineages were independently created.
Which assumes two things, one that the three are an actual amino acid, there are only 22. It also assumes that the sequence will fold into a useful, functional protein.
No, the most likely result of a single base substitution isn't a frame shifts, it's more likely a
Missense mutation (Sickle Cell), Nonsense mutation (Cystic Fibrosis), Silent mutations (Don't effect product), Splice-site mutations (Loss of an intron). Your problem is that after all these years you still haven't leaned basic biology and genetics
It is amazing how many fundamental errors you make in a row. An error during transcription is the source of Genetic mutations:
DNA Transcription
In the living cell, DNA undergoes frequent chemical change, especially when it is being replicated (in S phase of the eukaryotic cell cycle). Most of these changes are quickly repaired. Those that are not result in a mutation. Thus, mutation is a failure of DNA repair.
The deleterious effect of mutations on protein coding genes. Of course if you never bother to learn basic genetics that would not effect your understanding one bit and you obviously are not interested.
In other words, it's between 1% and 2% when you count just single base substitutions (differences). If you count those of length, and some of them are millions of base pairs genome wide, it's 5% at least. Your just going to sit there and say so what?
You forget, the explanation for the difference is mutations. Ultimately they are just differences that assume indels as the cause. Of course there wouldn't be frame shifts if the lineages were independently created.
Which assumes two things, one that the three are an actual amino acid, there are only 22. It also assumes that the sequence will fold into a useful, functional protein.
No, the most likely result of a single base substitution isn't a frame shifts, it's more likely a
Missense mutation (Sickle Cell), Nonsense mutation (Cystic Fibrosis), Silent mutations (Don't effect product), Splice-site mutations (Loss of an intron). Your problem is that after all these years you still haven't leaned basic biology and genetics