Genetics as it applies to evolution, molecular biology, and medical aspects.
5 posts • Page 1 of 1
I need help in understanding some article.Article is about transcription induced mutations.It is basically about cytosine deamination to thymine during transcription and this mutation(deamination) happens in the coding strand(non trancribing strand).The article says that it doesn't get repaired by nucleotide excision repair system because the repair system is biased.I need help in understanding the whole paragraph.Please help.Here is the paragraph.
''If separation of DNA strands increases the risk of hydrolytic
deamination, cellular processes such as transcription, replication,
conjugation, and recombination have the potential of
promoting C to T mutations. For example, in a simple model
for transcription elongation, the nontranscribed strand should
be transiently in single-strand form when the transcription
bubble passes through. Such potential deamination risk for
cytosines in the nontranscribed strand during transcription has
been noted before (17–20), but has not been investigated in
depth. A possible reason for this inattention is the existence of
strand bias in nucleotide excision repair. In E. coli (21) and in
mammalian cells (22), transcription-blocking lesions are repaired
preferentially when present in the transcribed strand.
Transcription-coupled nucleotide excision repair has helped
explain the observed bias in mutations caused by mutagens
such as UV light in favor of the nontranscribed strand (23–25),
and has raised the possibility that all observations of strand
bias in mutations may be explained by strand bias in DNA
repair. In fact, Skandalis et al. (19) have argued that there is
a strand bias in 5meC to T mutations in the human hprt gene
and have suggested that this is the result of strand bias in a base
excision repair process that repairs T:G mismatches.''
a strand bias in this case just means that one strand, here the transcribed one, is preferantially repaired by a certain DNA repair mechanism over the other one. Therefore mutations seem to be preferentially occuring at only one of the strands. I actually don't know what is the reason of the repair bias regarding NER, but for example direct reversion of UV photoproducts by photolyases is slowed down by the presence of chromatin/nucleosomes, which causes a bias in repair between the transcribed and the non-transcribed strand.
at the non-transcribed strand, because here repair is slow/absent --> mutations
5 posts • Page 1 of 1
Who is online
Users browsing this forum: No registered users and 1 guest