期刊
NUCLEIC ACIDS RESEARCH
卷 46, 期 9, 页码 4505-4514出版社
OXFORD UNIV PRESS
DOI: 10.1093/nar/gky160
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资金
- National Natural Science Foundation of China (NSFC) [31501004, 31570173]
- National Key Research and Development Program [2017YFC1002002]
- NIH [1R01DE023810, 1R01DE026186]
- NSFC
Pseudomonas aeruginosa is an opportunistic pathogen with a relatively large genome, and has been shown to routinely lose genomic fragments during environmental selection. However, the underlying molecular mechanisms that promote chromosomal deletion are still poorly understood. In a recent study, we showed that by deleting a large chromosomal fragment containing two closely situated genes, hmgA and galU, P. aeruginosa was able to form 'brown mutants', bacteriophage (phage) resistant mutants with a brown color phenotype. In this study, we show that the brown mutants occur at a frequency of 227 +/- 87 x 10(-8) and contain a deletion ranging from similar to 200 to similar to 620 kb. By screening P. aeruginosa transposon mutants, we identified mutL gene whose mutation constrained the emergence of phage-resistant brown mutants. Moreover, the P. aeruginosa MutL (PaMutL) nicking activity can result in DNA double strand break (DSB), which is then repaired by non-homologous end joining (NHEJ), leading to chromosomal deletions. Thus, we reported a noncanonical function of PaMutL that promotes chromosomal deletions through NHEJ to prevent phage predation.
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