Then why not say that and cite the source material so we can actually have an open conversation. The statistic is that 83% of the protein coding genes show divergence at an amino acid sequence level. The average is just a couple of codons but there are highly conserved genes showing dramatic divergence..
Exactly, the average is just a couple of codons. How does this make the average deceptive?
Unless you are talking about a gene 118 base pairs long with 18 substitutions. They like to average it across the whole genome because the sequence identity averages to managable levels. When you start looking at the particular genes it's a very different story.
But an average does not deny that much of the divergence may be concentrated in a few genes. In the example above, the divergence in this pair of genes is 15%. But if only 83% of genes show any divergence at all, then 17% show no difference at all. The average divergence of one of these genes with a gene that shows 15% divergence is 7.5% divergence. What is deceptive about that?
Most genes, you admit, show only a couple of codons different (and in many cases, only one base pair in the codon has changed--this is important when we are looking at divergence at the level of nucleotide sequence) Let us hypothesize a gene composed of 120 base pairs in which three bp have changed. The divergence in this pair of genes is now 3%. Add this comparison to the previous two and the average divergence over the three genes is 6%
Let's take it a little further. Since in most cases there are only a few changes, and the instances of a 15% divergence is rare, let us suppose that a 3% divergence is 10 times as common as a 15% divergence. Then let us take a 1000 genes divided proportionately into those that diverge by 0%, 3% and 15%. This gives us 170 genes diverging by 0%, 750 genes diverging by 3%, and 83 genes diverging by 15%. Average divergence over these 1000 genes works out to 3.5%
This is not deception. This is basic arithmetic.
Absolutly not!!! That is the height of deception to say that it is 98% the same when they know for a fact it is at least twice that.
What is at least twice what? Similarity cannot be greater than 100% and that is not twice 98%. A 98% similarity translates into a 2% divergence. So are you saying that it should be 4% divergence? I believe that when you include the whole genome, not just the genes, that is about right.
So what height of deception are you referring to?
When they are strong enough for natural selection to have an influence it is most often eliminated. The vast majority of the balance are deleterious and you are well aware of this empirically demonstrated fact.
Yes, I am. Are you aware that you are now focusing on a small subset of mutations? How does that change the overall average divergence?
Yet, dispite this glaring fact of genetics you would have to have dozens of mutations fixed per year for millions of years and then stop.
How did you calculate this rate?
You can have nucleotide changes that do not result in amino acid changes but not amino acid changes that don't involve nucleotide changes. When we are talking about the nucleotide sequence the reason we lump mutation rates in genes and noncoding sequences is because they are evenly dispersed.
I believe the figure of 98% similarity refers only to genes, but does include the non-coding segments of genes. These are not to be confused with non-coding DNA extraneous to genes altogether--a far larger part of the genome.
You never told me how the divergence is 30%-60% higher in introns then in noncoding regions.
I would be only speculating. I would prefer to wait and hear what hypothesis biologists come up with.
You do not have to assume anything, the amont of divergence tells you how many mutations.
No it doesn't. It tells us how many mutations were established permanently in the genome. It says nothing about how many other mutations there were that were not established in the genome.
Fixed means you will find them throughout the human lineage, that's all.
Yes, and by this definition, most of the mutations which cause serious genetic disorders are far from being fixed, appearing in many cases in fewer than 5% of the population.
What we find is that the differences in the human gemome are the result of deletions.
Irrelevant. This is still divergence.
My basic argument is that the vast majority of the effects are deleterious, when they actually have an effect. At least 3/4 of mutations that have an effect are eliminated for that very reason. The ones that remain are credited with a list of disease, disorder and death as long as your arm.
No one is quarreling with that. But you are treating this sub-set of mutations as if it involved most mutations. Most mutations by far have been determined to be neutral. So what sort of sub-set are we dealing with here? Maybe 10% of all mutations which come under the impact of natural selection? 3/4 of 10% is 7.5%. That leaves 2.5% that are not eliminated.
The rare beneficial effect are marginal advantages that do not overhaul the genes effecting highly conserved organs like the brain.
The difference is that those which cause disease and disorders (at least if they affect reproduction rates) do not become fixed. Check out your favorite genetic disorders, like microencephaly. What is the rate of occurence? Very small. But the beneficial effects are those that become fixed and accumulate and define the species. Some neutral changes can also become fixed through genetic drift.
77% of mutations that are strong enough to have an effect are sufficiently deleterious to be eliminated by natural selection.Around 25% reach readily detectable levels and signifigantly contribute to the genetics load. About 5% of the protein coding genes show inframe indels and around 4.5% show signs of adaptive evolution (assuming of course they are the result of evolution).
Again, remember that this 77% applies to a small subset of mutations. Also that "readily detectable levels" is not the same as fixation. A mutation that appears in 3% of the population is dectectable, but until it appears in over 95% of the population it is not considered fixed. In how many of the cases where mutations cause disease or other complications, do you find them in over 95% of the population?
When we are looking at the divergence between chimps and humans, we are looking at mutations that have become fixed, not at those that appear rarely and are exceptions to the species norm.
The list goes on, the rate of change simply does not happen in nature.
What is the rate of change and how do you know it does not happen in nature? Is there a standard rate of change? Does the rate of change not depend on the intensity of selective pressure?
Are you talking about homologous as opposed to othologous because I have yet to see what the point of that distinction is.
I had to check the meaning of "othologous" (do you mean "orthologous") because I had not heard it before. It appears to be a sub-set of homologous genes. By homologous genes, I mean approximately the same as homologous morphological traits i.e. genes which are similar in structure just as the skeletal structure of the vertebrate forelimb is similar across different vertebrate species and appear to be derived from a common ancestor.
Apparently the opposite of "orthologous" is "paralogous" and the difference between them is approximately the same as the difference between species that have emerged phyletically and those that have emerged cladistically. Both are sub-classifications of homologous genes.
An environmental factor will trigger a genetic mechanism that will result in an adaptation. Mutations are not nessacary for most of them, that is the dirty little secret.
The so-called "genetic mechanism" is natural selection. But I don't consider that really genetic. No, mutation does not need to occur simultaneously with natural selection. That is not a dirty little secret. It is the reason mutations are called random. They occur without reference to need. But should a variant trait originally introduced by a mutation some generations earlier become advantageous under new environmental pressures, then it will trigger selection for that trait.
It has also been found that in some species at least, strong environmental pressures speed up the rate of mutation, thus enhancing the possibility that an advantageous trait will appear.
It is the genes, prions, regulatory genes, recombinations and the predisposition of the functional part of the genome that is the arbiter of fitness. What the environment deals them is not the ultimate cause of the adaptation.
Neither the genes nor the environment is the ultimate cause of adaptation, but it is the environment which is the arbiter of fitness, determining which set of genes, prions, regulatory genes,recombinations, etc. will be passed on to future generations and in what proportions. This environmental screening of what will be inherited by the next generation is essential to adaptation, and is commonly called natural selection.
However, as creationists are fond of pointing out, selection implies something to be selected. Natural selection cannot lead to adaptation if there is no variant already in the population that is more adaptive than others. So, it is not the ultimate cause of adaptation, but neither are genes, etc, on their own.
