Would you also agree that the genetic differences responsible for phenotypic differences between species follow a noisy tree-like structure?
This is a good question. We need to filter the signal from the noise here so the mutations that are creating phenotypic change can become visible.
That’s the tough part. Linking genetic differences to phenotypic differences is very difficult. The human genome is the most studied genome in the world, and scientists have barely started to scratch the surface.
The main point I would leave you with is that genetic differences in functional DNA follow a noisy tree-like structure, the one we would expect from evolutionary mechanisms. We know the genetic differences that are responsible for phenotypic differences are somewhere in that functional DNA. This is why scientists have concluded that evolution is responsible for these differences, because the differences follow the pattern we would expect from evolutionary mechanisms.
What could be done is to eliminate known random mutation like mis match mutations. Does the signature pattern still hold? What does this new pattern look like?
How do you determine if a difference is due to a “mis match mutation”?
Not sure we currently can. We need to see that matched pair in the DNA. If the pair is AC or GT or other the AT CG we know it is due to a mutation that the repair mechanism did not catch.
We would only see that in the initial cell where the mutation takes place. Subsequent copying of each strand will produce the proper complementary base. So if there is an AC mismatch that the DNA repair mechanisms don’t catch the strands will be separated during replication and then copied. You will end up with one pair of DNA strands with a GC and another pair of DNA strands with an AT at the same position.
Indeed. Cheap fast DNA sequencing has provided a mountain of raw data. Maybe there needs to be more emphasis on interpreting the data we already have.
This becomes more complicated when we consider that the same genome can give rise to different phenotypes based on environmental stimuli/ developmental cycles. For example the difference between the worker bees and queen bees, the difference between caterpillars and butterflies etc.
Its not just the content of the genome, but also the regulation.
The current trend in biomedical research is towards “big data” experiments. For example, you might have a biofilm model where you measure the species diversity within a biofilm and the gene expression patterns of all the microorganisms within that biofilm using technology such as RNAseq. Once you have that massive amount of data, what does it all mean? That’s the tough part. All of these new technologies are absolutely amazing, but it is beginning to outpace our ability to make sense of it all. I am sure that @swamidass and @glipsnort are much more aware of the progress being made on the theory/analysis side than I am.
Except common descent is the ultimate redundant assumption. We are still using the basic Linnaean taxonomy complete with his hierarchy because it worked in 1758 as well as today. Yet we all know he had no need – as we don’t – for the “common descent” hypothesis that came 100 years later anyway. Furthermore, taxonomy is based on observable ‘shared characteristics’, not on the imagined but never observed “common descent”.
This brings back Carl Sagan’s funny definition of life: “a system capable of evolution by natural selection”:
Astronaut: “Houston, we found something that looks like life”
Houston: “Well, is it capable of evolution by natural selection”
Astronaut: “How would I check that? Let me ask it.”
Modern scientists use cladistics, not Linnaean taxonomy. You are absolutely wrong on this point.
Just as forensics is based on evidence found at the crime scene, not on direct observation of the crime. Common ancestry is the hypothesis, and the pattern of shared morphology and genetics is what we use to test that hypothesis.
We test common ancestry through phylogenetics, as has been exhaustively explained.