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Using DDX41 knockout (KO) cells, we found that these cells were sensitive to bleomycin, camptothecin, and UV. DDX41 deficiency led to increased genomic instability, indicated by elevated DNA double-strand breaks (DSBs) and comet tails. We found that R-loop formation increased in DDX41\u2013KO cells. DDX41 wild-type (WT) protein resolved DNA:RNA hybrid of R-loops\u00a0in vitro, but the mutant R525H failed. DDX41\u2013R525H expressing cells were sensitive to DNA damage agents and had significantly more R-loops than DDX41\u2013WT expressing cells. Interestingly, DDX41 colocalized with DSB marker \u03b3H2AX and R-loop marker S9.6, and knockdown of DDX41 in the U2OS GFP reporter cells resulted in reduced homologous recombination (HR) repair. Moreover, increased and prolonged RPA and reduced RAD51 foci were found in DDX41 KO and DDX41\u2013R525H expressing cells, indicating a defect in the transition from end resection to RAD51 filament assembly. Overall, our results suggest that DDX41 utilizes its unwinding activity to resolve R-loops, which may play a key role in HR-based repair, and dysregulation of this pathway may lead to MDS\/AML.<\/jats:p>","DOI":"10.1093\/nar\/gkag219","type":"journal-article","created":{"date-parts":[[2026,2,28]],"date-time":"2026-02-28T12:53:43Z","timestamp":1772283223000},"source":"Crossref","is-referenced-by-count":0,"title":["MDS\/AML-associated DDX41 helicase facilitates homologous recombination repair by potentially resolving R-loops"],"prefix":"10.1093","volume":"54","author":[{"given":"Aanchal","family":"Aggarwal","sequence":"first","affiliation":[{"name":"Department of Biochemistry, Microbiology and Immunology, University of Saskatchewan , Health Sciences Building, 107 Wiggins Road, Saskatoon, Saskatchewan S7N 5E5 ,","place":["Canada"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shizhuo","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of 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