That doesn’t change the fact that cytochrome c differs by 40% between humans and C. elegans, and it functions in both species. You are claiming that this shouldn’t be the case.
I am claiming that there may be different versions of cytochrome c with different requirements. This would require different sequences.
It functions as a part of the electron transfer chain in mitochondria in both humans and C. elegans. It serves the same function in all species that have the gene, and it can differ by 40% between them. You are claiming that even the slightest changes will make this function go away, and yet it remains.
I am saying only part of the sequence in humans is required for electron transport. Other parts of the sequence may play a role in embryo development.
It may? Any evidence for these claims? Here is the protein comparison, and the differences are found throughout the rather short protein:
Query 2 GDVEKGKKIFIMKCSQCHTVEKGGKHKTGPNLHGLFGRKTGQAPGYSYTAANKNKGIIWG 61 GD EKGKKIF +C QCH V + KTGP L+G+ GR++GQ G+ Y+AANKNKG++W Sbjct 17 GDNEKGKKIFKQRCEQCHVVN-SLQTKTGPTLNGVIGRQSGQVAGFDYSAANKNKGVVWD 75 Query 62 EDTLMEYLENPKKYIPGTKMIFVGIKKKEERADLIAYLK 100 TL +YL +PKKYIPGTKM+F G+KK +ERADLI +++ Sbjct 76 RQTLFDYLADPKKYIPGTKMVFAGLKKADERADLIKFIE 114
I chose to write a longer piece than could be accommodated here. The link is below.
Thanks for writing that, Ann. So the problem
you see with orphans just comes down to the rarity of functional folds? @Agauger
I’m also curious as to why you didn’t include any sources when you were going through alternative explanations and why they didn’t work? You also didn’t mention gene loss. And one of the papers you did link to seems to contradict your comments. These alternative mechanisms do take place and they take place at varying rates.
Edit: my mistake. You did mention gene loss briefly.
I have to echo what @T.j_Runyon said. It seems to boil down to the ID claim that functional proteins are hard to come by.
Given the rate of emergence of orphan genes it would seem that it is quite easy to get functional proteins from previously non-coding DNA with relatively few mutations. At what point does this falsify the ID claim that functional proteins are hard to come by?
Here is evidence of additional function. There is more.
Cytochrome c (Cyt c ) is essential in mitochondrial electron transport and intrinsic type II apoptosis. Mammalian Cyt c also scavenges reactive oxygen species (ROS) under healthy conditions, produces ROS with the co-factor p66Shc, and oxidizes cardiolipin during apoptosis. The recent finding that Cyt c is phosphorylated in vivo underpins a model for the pivotal role of Cyt c regulation in making life and death decisions. An apoptotic sequence of events is proposed involving changes in Cyt c phosphorylation, increased ROS via increased mitochondrial membrane potentials or the p66Shc pathway, the oxidation of cardiolipin by Cyt c , and its release from the mitochondria. Cyt c regulation in respiration and cell death is discussed in a human disease context including neurodegenerative and cardiovascular diseases, cancer, and sepsis.
I didn’t include many references for the list of mechanisms because I was dealing with certain other conversations plus other work. I wasn’t intending to be scholarly because I didn’t think that was what you had asked for.
You can interpret the data two ways. I know the papers acknowledge the methods of creation and say that some of the orphans can be explained that way. That’s always possible. But I think it needs experimental verification that new genes are easy to come by.
What is being questioned here is the mechanism.
When I said protein sequence could change by 10%, I was not talking about comparing homologs. I was talking about how much mutation could be tolerated before an enzyme loses function. It’s based on a paper by Dan Tawfik probably ten years ago. The protein sees gradual loss of function up to the point that about 10% percent of its sequence has been changed, whereupon it undergoes catastrophic destabilization.
I didn’t find Tawfik but I did find this:
One of the comments I would make is that you seem to confuse gene with DNA. For example, you state:
You may want to be a bit more specific as to what you mean by “sequence”. In the paper on ant orphan genes they initially detected orphan genes by comparing protein sequences, not DNA sequences. As protein annotation improved in ant species, the number of orphan genes did decrease by quite a bit:
As you mention in a previous post, they have found orthologous DNA for the vast majority of ant orphan genes.
So that is 36+43.5=79.5% have their origins in DNA shared through common ancestry, and those are just the ones they were able to detect with the methods they used.
So what exactly needs to be verified? Which of these mutations or mechanisms of mutation are you saying could not occur?
Are they being questioned or simply ignored? It would be nice to see the mechanisms actually addressed. For example, why isn’t a frame shift mutation resulting in a new ORF a viable mechanism? How can you say that this can’t result in a viable protein when there examples in the ant genome of exactly this occurring?
Don’t forget antisense coding and overprinting.
It would seem that comparing homologs is a really good way of testing that idea. I would also think that different proteins will tolerate mutations very differently.
It is also interesting that many in the ID community keep arguing for function in large swaths of the human genome, even though those regions are accumulating mutations at a rate consistent with neutral drift. This seems to be in direct contradiction to the idea that the vast majority of mutations are not well tolerated.
No one is saying it cant. What we can infer is that it is the unlikely cause of what we are observing.
The mechanisms listed in the Wissler et al. (2013) paper are gene duplication, nondeleterious frame-shift mutations, overlap with mobile elements, horizontal gene transfer, overlapping genes, and transcription of intergenic DNA. For those who are interested in the origin of orphan genes it is well worth a read.