ERCC2, Mutation, and Evolution?

[pctopgs]

hey guys, sorry for coming here with these potentially stupid topics, but tbo, this is the closest thing I have to biologists or biology enthusiasts on the subject.

My question came from creationist who does not accept evolution...He says that evolution is false because mutations are repaired by the ERCC2 gene. He says he found out about it when he spoke to his doctor about mutations and the doctor laughed and said it isn't possible because the ERCC2 gene repairs the DNA to the original... Does this discredit evolution in the least?

 

[Vagn]

hey guys, sorry for coming here with these potentially stupid topics, but tbo, this is the closest thing I have to biologists or biology enthusiasts on the subject.

My question came from creationist who does not accept evolution...He says that evolution is false because mutations are repaired by the ERCC2 gene. He says he found out about it when he spoke to his doctor about mutations and the doctor laughed and said it isn't possible because the ERCC2 gene repairs the DNA to the original... Does this discredit evolution in the least?

Cancer can be caused by the mutation of genes controlling cell division, so no it doesn't discredit evolution in the slightest. Also what does he suggest would happen if the gene mentioned underwent a mutation?

 

[pctopgs]

Cancer can be caused by the mutation of genes controlling cell division, so no it doesn't discredit evolution in the slightest. Also what does he suggest would happen if the gene mentioned underwent a mutation?

According the the wiki, the gene is essential to the cell (at least in mammals/vertebrates)...I was thinking that the repairing gene can only detect and repair certain types of mutations...Sorry but I have a limited capacity on the subject.

 

[Vagn]

According the the wiki, the gene is essential to the cell (at least in mammals/vertebrates)...I was thinking that the repairing gene can only detect and repair certain types of mutations...Sorry but I have a limited capacity on the subject.

Background: ERCCl and ERCC2 are human DNA repair genes that are associated with in vitro resistance to selected DNA-damaging agents.

http://jnci.oxfordjournals.org/content/84/19/1512.full.pdf+html

This seems to agree that the gene is limited in scope as you suggest.

 

[bobze]

There are lots, and lots of genes involved in the repair and monitoring of DNA. They aren't perfect though. Certainly they reduce the number of mutations that happen, but mutations still slip through.

Ask your friend if he is so confident in his body's ability to repair any mutations why he doesn't bath in carcinogens.

You should reason, that if this were true--People wouldn't get cancers. They do however, life goes on. People get mutations, we actually all have them. Hundreds of them. In coding regions even. Most of us get along just fine with them though.

Most mutations are essential neutral as far as evolution is concerned. Being neutral can be by numerous ways as well. It could be the mutation is in a region that doesn't control or affect control of a gene. It could be that the mutation didn't change the amino acid sequence at all. It could be that the mutation did change amino acid, but its biochemical properties are close enough it doesn't make much a difference. Etc.

Note: By neutral, I mean invisible to selection.

 

[Evo]

This has nothing to do with evolution, it has to do with creationist misinformation. We're not going to play that game here.

And tell your friend to get another doctor, that one is a quack.

 

[Ken Natton]

If I might presume to make a contribution here that perhaps others can confirm or even expand upon. I’m pretty sure that what I am remembering comes from Sean Carroll’s Endless Forms Most Beautiful. In that book he makes the point that it is vital to understand the difference between damaged DNA and a mutated DNA sequence. I might be conflating different books here, I think it might be Dawkins who makes the point that actually, what is remarkable about the DNA copy process is how accurate it is, how few the errors are relative to the size of the data set as it were. But there are mechanisms to repair any damaged DNA. At the first level, it is the simple business of the double helix. Because each of the bases can only pair with one other, if the damage is only to one strand, the sequence is preserved in the other strand, and it is not at all surprising that the repair is perfect. But there are mechanisms to repair damage even when the damage is to both strands. But a mutation is not damage. It is a change in the sequence of codons, but the change is as valid as the original so the repair mechanisms are not triggered.

And this tactic of creationists is an old and easily recognised one. There is something more consistent about just rejecting the scientific evidence all together. To be selective about which parts of the science you want to accept and which bits you want to reject because they are inconvenient to you is, in truth, just dishonest.

 

[Ryan_m_b]

Any protein involved in DNA repair is imperfect. I remember when I did a course on DNA repair mechanisms back in my undergrad we looked at how many errors would appear over time without any then added the different systems one by one to change the numbers. At the end it was still not perfect (unfortunately I can't remember the number.

No system is 100% efficient and some things slip through the gaps.

 

[pctopgs]

Thanks for the info guys.

Here's the link to the article he uses as evidence:

http://www.ncbi.nlm.nih.gov/pubmed/2591959

 

[Ryan_m_b]

Thanks for the info guys.

Here's the link to the article he uses as evidence:

http://www.ncbi.nlm.nih.gov/pubmed/2591959

Really? This is the paper he uses? If I were you I would ask him what exactly he thinks supports him in this paper.

Firstly this is a paper outlining an investigation into the location of a new repair gene found on human chromosome 19. The authors frequently mention that this is an evolutionary conserved gene that has homology with a similar gene found on hamster chromosome 9.

There is nothing in this paper claiming that ERCC2 prevents mutation, in fact Fig. 1 adequately shows that the cell cultures possessing ERCC2 show better but not perfect survival rates compared to cells without it. This invalidates your friends claim that ERCC2 can prevent mutation, it cannot completely repair DNA.

Here are the only mentions of evolution within this paper;

Cross-hybridization of the human cDNAs for the repair genes to Chinese hamster DNA on a hybrid clone panel informative for hamster chromosomes enabled us to determine the evolutionary conservation of the linkage group, chromosomal assignments of these loci in the Chinese hamster, and the genetic consequences of those assignments on the frequency of mutations at these loci in CHO cells

Chinese hamster genes homologous to ERCCI, ERCC2, and XRCCI are in an Evolutionarily conserved linkage group on Chinese hamster chromosome 9. This observation and its consequences with respect to mutagenesis in CHO cells are discussed below.

human chromosome 19 has been observed to be fairly phylogenetically extensive. At least 10 long-arm markers of the human 19 (GPI, PEPD, etc.) have been shown to be linked on the mouse 7 (Lalley et al., 1987). GPI and PEPD have also been shown to be on the
same chromosome, not only in numerous mammalian species but also in evolutionary diverse forms such as amphibians (D. A. Wright et al., 1983) and two different families of teleost fish (J. E. Wright et al., 1983; Morizot, 1986). The cDNA clones for the repair genes are now being studied in the fish system, where they have been found to hybridize and detect restriction fragment length polymorphisms (RFLPs) in crosses informative for linkage (Morizot, personal communication). As more genes are identified within this conserved linkage group and its boundaries are understood, this region may become attractive for studying the forces responsible for such conservation.

Lastly here are the authors closing remarks

The demonstrated bias for the apparent clustering of DNA repair genes on human chromosome 19 suggests that there may be many other DNA repair genes in the human genome. Since the mapping and cloning of the chromosome 19 repair genes were made possible by the ready isolation of rodent mutations in the homologous loci, the search for additional rodent lines that are hemizygous for other areas of the genome would seem important. Such lines might produce new spectra of mutants appropriate for identifying and cloning heretofore unknown human DNA repair genes.

Nothing about the efficacy of ERCC2, nothing about how it prevents mutation and nothing about discrediting evolution.

I would advise your friend to type in ERCC2 polymorphisms into pubmed and read some of the articles he gets. There's been a hell of a lot of study on people with mutated DNA repair genes and ERCC2 is amongst them. If this gene is meant to prevent mutation how could it be mutated...?

 

[pctopgs]

thanks for the replies

 

[Ryan_m_b]

thanks for the replies

I'd be interested to know, how did the discussion pan out in the end?