In mice, mutation of <i>brca1</i> results in embryonic lethality, which is partially suppressed by <i>53bp1</i> mutation. In contrast, mutation of the <i>C. elegans</i> BRCA1 ortholog, <i>
brc-1 ,</i> or its binding partner, <i>
brd-1</i> , lead to only mild embryonic lethality. We show that in <i>C. elegans</i> , <i>
brc-1</i> and <i>
brd-1</i> embryonic lethality is enhanced when <i>53bp1</i> ortholog, <i>
hsr-9</i> , is also mutated. This is not a consequence of activating <i>
polq-1</i> -dependent microhomology-mediated end joining, as <i>
polq-1</i> mutation does not suppress embryonic lethality of <i>
hsr-9 ;
brc-1</i> 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.