New roles for RAD52 in DNA repair
Transcriptionally active genetic loci can be subject to the formation of DNA double strand breaks (DSBs) that arise due to the formation of R-loops.In a recent study published in Cell,Yasuhara and colleagues have revealed a remarkable new mechanism that allows cells to channel DSBs within active genes through a new repair pathway called transcriptionassociated homologous recombination repair.Double strand breaks (DSBs) are one of the most dangerous forms of DNA damage because they can cause the gross chromosomal rearrangements that are hallmarks of human cancers.Transcription is a leading source of DSBs.1 During transcription,the nascent RNA can hybridize with the DNA to form R-loops (Fig.1).Recent studies have revealed intriguing relationships betwee7n R-loops and homologous recombination (HR).2-4 For instance,Ohle et al.demonstrated that efficient HR in $.pombe actually requires the formation of R-loops.2 Moreover,Rad52 was found to promote DSB repair in 5.cerevisiae by allowing the cells to use the RNA as a template to guide DNA repair.3 Finally,Pomerantz and colleagues have defined two modes of RNA-directed DNA repair,both of which require RAD52.4 One mechanism involves RNA bridging to coordinate synapsis and ligation of DNA breaks,and the second mechanism uses RNA as a template for reverse transcription-dependent replacement of damaged DNA.4
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2019-01-12（万方平台首次上网日期，不代表论文的发表时间）
共2页
1127-1128
