Abstract:
:The DNA polymerase beta (Pol beta) null background renders mouse embryonic fibroblast (MEF) cells base excision repair deficient and hyper-mutagenic upon treatment with the monofunctional alkylating agent, methyl methanesulfonate (MMS). This effect involves an increase in all types of base substitutions, with a modest predominance of G to A transitions. In the present study, we examined the hypothesis that the MMS-induced mutagenesis in the Pol beta null MEF system is due to a lesion bypass mechanism. We studied the effect of RNAi mediated down-regulation of the lesion bypass factor REV1. The steady-state level of REV1 protein was reduced by more than 95% using stable expression of a siRNA construct in a Pol beta null cell line. We found that REV1 expression is required for the MMS-induced mutagenesis phenotype of Pol beta null MEF cells. In contrast, cell survival after MMS treatment is not reduced in the absence of REV1.
journal_name
DNA Repair (Amst)journal_title
DNA repairauthors
Poltoratsky V,Horton JK,Prasad R,Wilson SHdoi
10.1016/j.dnarep.2005.05.002keywords:
subject
Has Abstractpub_date
2005-09-28 00:00:00pages
1182-8issue
10eissn
1568-7864issn
1568-7856pii
S1568-7864(05)00113-8journal_volume
4pub_type
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