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Our research is focused on studies of mismatch repair, DNA replication homologous recombination and the interplay between these pathways. Mismatch repair corrects DNA polymerase errors that escape the proofreading activity of the replicative polymerases. Mismatch repair contributes to the overall fidelity of the replication pathway ~1000-fold. Nearly half of all hereditary nonpolyposis colorectal cancers (HNPCC) are linked to defects in mismatch repair. We study the universal mechanisms of mismatch repair in the experimentally tractable organism B. subtilis. Like most organisms B. subtilis contains the highly conserved MutS and MutL proteins. Unlike the typical bacterial model E. coli, B. subtilis lacks the methyl-directed repair pathway characterized by the presence of DNA adenine methylase (Dam) and the endonuclease MutH. We combine live cell imaging with genetics and biochemistry to understand the cellular mechanisms that control mismatch repair protein recruitment to mismatches in vivo.
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bioRxiv : the preprint server for biology (2024)
BIOPHYSICAL JOURNALno. 3 (2024): 78A-78A
Frances Caroline Lowder,Lyle A. Simmons
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#Papers: 100
#Citation: 2843
H-Index: 30
G-Index: 50
Sociability: 5
Diversity: 3
Activity: 43
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