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Article

REV1-Polζ maintains the viability of homologous recombination-deficient cancer cells through mutagenic repair of PRIMPOL-dependent ssDNA gaps.

Molecular cell - 7 Oct 2021

Taglialatela Angelo, Leuzzi Giuseppe, Sannino Vincenzo, Cuella-Martin Raquel, Huang Jen-Wei, Wu-Baer Foon, Baer Richard, Costanzo Vincenzo, Ciccia Alberto

Abstract excerpt

BRCA1/2 mutant tumor cells display an elevated mutation burden, the etiology of which remains unclear. Here, we report that these cells accumulate ssDNA gaps and spontaneous mutations during unperturbed DNA replication due to repriming by the DNA primase-polymerase PRIMPOL. Gap accumulation requires the DNA glycosylase SMUG1 and is exacerbated by depletion of the translesion synthesis (TLS) factor RAD18 or...

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Identifiers

PMID: 34508659
DOI: 10.1016/j.molcel.2021.08.016
PMCID: PMC8500949

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REV1-Polζ maintains the viability of homologous recombination-deficient cancer cells through mutagenic repair of PRIMPOL-dependent ssDNA gaps.PMID 34508659Read ↗

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