ArticleMolecular cell2009
Brh2 promotes a template-switching reaction enabling recombinational bypass of lesions during DNA synthesis.
Article in Molecular cell, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- ALTernative Telomere Maintenance and Cancer.Trends in cancer · 2015Article
- Dual DNA-binding domains shape the interaction of Brh2 with DNA.DNA repair · 2014Article
- Unraveling the mechanism of BRCA2 in homologous recombination.Nature structural & molecular biology · 2011Review
- Article
- Cooperation of RAD51 and RAD54 in regression of a model replication fork.Nucleic acids research · 2011Article
- Microtubule-dependent mRNA transport in fungi.Eukaryotic cell · 2010Review
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2 authors at 1 institution in 1 country.
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Abstract
Accumulating evidence for Rad51-catalyzed DNA strand invasion during double-strand break repair features a 3' single-stranded tail as the preferred substrate for reaction, but paradoxically, the preferred substrate in model reactions in vitro is the 5' end. Here, we examined the Rad51-promoted 5' end invasion reaction in the presence of Brh2, the BRCA2 family protein in Ustilago maydis. Using plasmid DNA and a homologous duplex oligonucleotide with 5' protruding single-stranded tail as substrates, we found that Brh2 can stimulate Rad51 to promote the formation of a four-stranded complement-stabilized D loop. In this structure, the incoming recessed complementary strand of the oligonucleotide has switched partners and can now prime DNA synthesis using the recipient plasmid DNA as template, circumventing a lesion that blocks elongation when the 5' protruding tail serves as template for fill-in synthesis. We propose that template switching promoted by Brh2 provides a mechanism for recombination-mediated bypass of lesions blocking synthesis during DNA replication.
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