The function of RAD52 N-terminal domain is essential for viability of BRCA-deficient cells

Kritika Hanamshet, Alexander V. Mazin

Research output: Contribution to journalArticlepeer-review

13 Scopus citations


RAD52 is a member of the homologous recombination pathway that is important for survival of BRCA-deficient cells. Inhibition of RAD52 leads to lethality in BRCA-deficient cells. However, the exact mechanism of how RAD52 contributes to viability of BRCA-deficient cells remains unknown. Two major activities of RAD52 were previously identified: DNA or RNA pairing, which includes DNA/RNA annealing and strand exchange, and mediator, which is to assist RAD51 loading on RPA-covered ssDNA. Here, we report that the N-terminal domain (NTD) of RAD52 devoid of the potential mediator function is essential for maintaining viability of BRCA-deficient cells owing to its ability to promote DNA/RNA pairing. We show that RAD52 NTD forms nuclear foci upon DNA damage in BRCA-deficient human cells and promotes DNA double-strand break repair through two pathways: homology-directed repair (HDR) and single-strand annealing (SSA). Furthermore, we show that mutations in the RAD52 NTD that disrupt these activities fail to maintain viability of BRCA-deficient cells.

Original languageEnglish (US)
Pages (from-to)12778-12791
Number of pages14
JournalNucleic acids research
Issue number22
StatePublished - Dec 16 2020
Externally publishedYes

ASJC Scopus subject areas

  • Genetics


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