53bp1 mutation enhances brca1 and bard1 embryonic lethality in C. elegans
- PMID: 37581122
- PMCID: PMC10423319
- DOI: 10.17912/micropub.biology.000934
53bp1 mutation enhances brca1 and bard1 embryonic lethality in C. elegans
Abstract
In mice, mutation of brca1 results in embryonic lethality, which is partially suppressed by 53bp1 mutation. In contrast, mutation of the C. elegans BRCA1 ortholog, brc-1 , or its binding partner, brd-1 , lead to only mild embryonic lethality. We show that in C. elegans , brc-1 and brd-1 embryonic lethality is enhanced when 53bp1 ortholog, hsr-9 , is also mutated. This is not a consequence of activating polq-1 -dependent microhomology-mediated end joining, as polq-1 mutation does not suppress embryonic lethality of hsr-9 ; brc-1 mutants. Together, these results suggest that BRC-1 - BRD-1 and HSR-9 function in parallel pathways and do not act antagonistically as in mammals.
Copyright: © 2023 by the authors.
Conflict of interest statement
The authors declare that there are no conflicts of interest present.
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References
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- Cao L, Xu X, Bunting SF, Liu J, Wang RH, Cao LL, Wu JJ, Peng TN, Chen J, Nussenzweig A, Deng CX, Finkel T. A selective requirement for 53BP1 in the biological response to genomic instability induced by Brca1 deficiency. Mol Cell. 2009 Aug 28;35(4):534–541. doi: 10.1016/j.molcel.2009.06.037. - DOI - PMC - PubMed
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