Mouse mismatch repair gene Msh2 is not essential for transcription-coupled repair of UV-induced cyclobutane pyrimidine dimers.
The human mutS homolog gene MSH2 is essential for DNA mismatch repair (MMR) and defects in this gene can result in increased mutagenesis, genomic instability and hereditary nonpolyposis colorectal cancer (HNPCC). Besides correcting mismatch errors arising from DNA replication, it was shown that deficiencies in bacterial and human MMR genes including MSH2 resulted in defective transcription-coupled repair (TCR) of UV-induced photolesions. Here we show that MMR-deficient fibroblasts derived from two independent isogenic mouse strains with defined Msh2 deficiencies are as proficient in TCR of UV-induced cyclobutane pyrimidine dimers (CPD) as wildtype fibroblasts. Our results indicate that in mouse cells Msh2 is not essential for TCR of UV-induced CPD in contrast to bacteria and human cells and suggest that the biological effects of UV in mouse Msh2(-/-) cells and mice are not due to defective TCR.
Sonneveld
E
E
Department of Cell Biology and Genetics-MGC, Erasmus University Rotterdam, P.O. Box 1738, 3000 DR Rotterdam, The Netherlands.
Vrieling
H
H
Mullenders
L H
LH
van Hoffen
A
A
D000818:Animals; D020137:Base Pair Mismatch; D004260:DNA Repair; D004268:DNA-Binding Proteins; D051379:Mice; D051718:MutS Homolog 2 Protein; D011518:Proto-Oncogene Proteins / Q000378:metabolism*; D011740:Pyrimidine Dimers / Q000378:metabolism*; D014158:Transcription, Genetic; D014466:Ultraviolet Rays / Q000009:adverse effects*
D004268:DNA-Binding Proteins; D011518:Proto-Oncogene Proteins; D011740:Pyrimidine Dimers; C497173:Msh2 protein, mouse; D051718:MutS Homolog 2 Protein