The BLM protein has helicase activity that unwinds forked DNA duplexes, a synthetic X-structure that models a Holliday junction, and G-quadruplex DNA. In addition, BLM dissolves double Holliday junctions with topoisomerase III alpha and can regress a stalled or collapsed replication fork. In addition, him-6 mutants are predominantly male and have reduced meiotic recombination. These genetic observations suggest that the HIM-6 protein may play a role in DNA repair and/or recombination. However, it is not yet known how the activity of HIM-6 is related to these phenotypes, and the biochemical activities of HIM-6 have not been investigated. We purified recombinant HIM-6 proteins lacking the Nterminal 20 amino acids that do not contain any conserved sequences or motifs. As expected for a RecQ homolog, our data indicated that HIM-6 has DNA-dependent ATPase and DNA helicase activities that can unwind D-loop and HJ structures. These results strongly support a role for HIM-6 in processing Evofosfamide CYP17 inhibitor recombination intermediates in vivo. BLM homologs function in HR in mitotic and meiotic cells. A D-loop is a strand invasion intermediate of HRmediated DSB repair, which is generated with a 39-ssDNA overhang and homologous DNA duplex, and is catalyzed by the Rad51 protein. The invaded DNA is synthesized using the 39end as a primer. D-loops can be processed in different ways, with different recombination product outcomes. For example, if the extended nascent strand is displaced from the D-loop and annealed with its original complementary strand, non-crossover recombination products are generated by synthesisdependent strand-annealing mechanisms in mitotic cells. In vivo and in vitro studies have shown that the yeast helicase Sgs1 displaces D-loops and promotes NCO formation by SDSA. In addition, the BLM helicase is able to dissociate D-loops made by the human Rad51 protein. These activities suggest that BLM might suppress crossover recombination products by dismantling D-loops. Thus, the ability of human BLM to unwind a D-loop may be relevant to the hyperrecombination phenotype exhibited by cells from Bloom syndrome patients. Although detailed HR defects have not been studied in C. elegans him-6 mutants, previous studies showed that him-6 mutants have enhanced irradiation sensitivity and mitotic chromosomal abnormalities. Our data showing that HIM-6 unwinds D-loops indicates that HIM-6 may disrupt recombination intermediates to promote the mitotic SDSA pathway of HR. Consistent with this model, it has been reported that DmBLM is required for SDSA. D-loops can also be processed to produce dHJs. When a D-loop is stabilized, a dHJ can be formed by capturing the other DSB end. A dHJ can then be processed further to produce a CO or an NCO product. BLM and DmBLM proteins were shown to form complexes with topoisomerase III alpha and disrupt dHJs through branch migration, which is also called dissolution, leading to the separation of the two joined molecules and ultimately the formation of an NCO.