Take a look at a phylogenetic tree of those species that show branch lengths for the actual answer to all those questions.
2 Likes
What would you expect if you mutated cytochrome c in a mouse to the human sequence?
Mice were not ancestral to humans.
Even I am surprised that you donât know this.
Why is alpha actin identical in both species?
This might help. But maybe not.
2 Likes
Specifically why? I canât answer that. But in general: It presents no problems for evolutionary theory that some sequences will be highly conserved between humans and mice, and others less so
1 Like
There hasnât been enough time for non-synonymous neutral and/or beneficial mutations to accumulate between mice and rats compared to humans and mice.
Still waiting for an answer to this question:
Looking at cycs protein sequences, I get the following two comparisons:
Human-mouse: 90.5% similar
Human-chicken: 81.6% similar
According to intelligent design, what would you expect to see with the percentage similarity between mouse and chicken, and why?
1 Like
Why does the DNA sequence of the coding regions differ by 8% between humans and mice for the beta-actin gene? How does ID explain this?
2 Likes
Redundancy in the DNA code explains this.
That doesnât explain where the differences came from, or why we see them. How does ID explain this? Why are there fewer differences between mouse and rat at the DNA level than between mouse and human?
2 Likes
The problem is that sequences are being highly conserved between species with different sequences. What is the origin of these sequences that cannot mutate yet they are different in different species. In your diagram humans and mice share a common ancestor sometime in the distant past and that explains the similarity of alpha actin however why did cytochrome c diverge so much?
Why did it get stuck in Rats and Mice and stuck in humans and chimps with 2 different sequences? Rats and mice have 100 generations to every human or chimp generation.
The sequence differences are not following the tree. Mice and dogs are closer than horses and dogs.
So what?
Also, please try to use accurate language. The term scientists use is â38% identicalâ or â38% similar,â the latter only for protein sequences.
1 Like
Excellent question. However, weâre discussing the cardiac sarcomere in the other thread in a similar way. We are testing the hypothesis that
How many different human MYH7 sequences will perform the specific function, Bill?
Please reply in the other thread.
Here, we are discussing Gilâs testable ID hypothesis:
I donât think thatâs the problem. I think that you are ignoring most of the data.
1 Like
Self-contradictory statement. At the same time theyâre âhighly conservedâ(which implies there is little to no difference between different speces), yet also in different species they have âdifferent sequencesâ.
Another self-contradictory statement. They can mutate, otherwise they wouldnât be different. And the differences we see match up well with the phylogeny. Generally speaking, the further back the species have ancestry, the more differences do we see between species.
Go to http://timetree.org/ to find estimations of the time since two species shared common ancestry.
Rats and mice share ancestry about 20 million years ago. Over those 20 million years, we see no amino acid level differences having fixed in the population(fixed is not to be confused with no mutations having happened, or that no variation exists in each of those populations). We do see DNA sequence differences completely consistent with transition bias, hence we infer the differences at the DNA level are due to mutation.
Humans and mice share a common ancestor roughly 90 million years ago. Over these 90 million years, about 10% of the amino acid protein sequence appears to have changed.
Humans and horse share an ancestor about 96 million years ago, but horse has longer generation times, so there have been fewer mutations having occurred over that time period compared to mice.
Another factor that affects the rate of change in sequence in a population is effective population size. In population genetics, the strength of selection positively correlates with effective population size. The bigger the effective population size, the less an effect will random sampling (genetic drift) have. That means any putative weakly deleterious mutants are more likely to be removed because theyâre still visible to selection in large effective populations. That explains why in the 20 million years since the rat-mouse common ancestor, no nonsynonymous mutations have been allowed to fix.
Chicken is even more distantly related, so even more time has passed since the common ancestor there, hence more changes have had time to accumulate.
Etc. etc.
1 Like
They can mutate. Conservation occurred after the divergence of humans from mice/rats.
One was more conserved than the other. Evolutionary theory does not predict that every sequence will be subjected to the same degree of selection in all lineages. Why on earth would you think that it does?
Conservation occurring the those lineages after those divergences.
This is all consistent with evolutionary predictions. They are not consistent with ID Creationist predictions, because (not being a theory or even a hypothesis with a model or putative mechanism) ID Creationism makes no predictions.
2 Likes
How well does Corinneâs babyâs DNA match Father Timâs? How does Billy Tate stay sane? These questions and many others will be answered on tomorrowâs episode of SOPE.
5 Likes
Thatâs not what I saw for alpha-actin at the DNA level:
mou hor dog
1: mouse 100.00 91.89 91.01
2: horse 91.89 100.00 95.68
3: dog 91.01 95.68 100.00Mouse-dog = 91.0% similar
Horse-Dog = 95.7% similar
Care to explain?
2 Likes
Why? Rats and mice have 100 times the generation rates vs humans and chimps therefore 100x neutral mutations should get fixed in the population given the same divergence time. Was the mouse/rat sequence the original sequence? You are claiming that it mutated then somehow became unable to mutate.
An alternative is that separate sequences were designed for Rats/Mice and Humans/Chimps that were optimized for electron transport, apoptosis control and embryo development.
An interesting paper that foreign mitochondria from mammal to mammal is lethal.
https://www.nature.com/articles/srep14512#citeas
Can we please see your math?
That doesnât explain the phylogenetic signal.
1 Like