53bp1 mutation enhances brca1 and bard1 embryonic lethality in C. elegans

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.