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These alterations are mainly due to deficiencies in DNA repair mechanisms. The Fanconi anemia pathway is evolutionarily conserved, allowing functional studies in model organisms like\n                      <jats:italic>Caenorhabditis elegans<\/jats:italic>\n                      , where it promotes and executes error-free homologous-recombination over the mutagenic non-homologous-end-joining pathway;\n                      <jats:italic>fcd-2<\/jats:italic>\n                      (FANCD2 ortholog) plays a key role in this regulation to preserve genome stability. In this study, we report that the choice of DNA repair pathway for resolving double-strand breaks is influenced by absence of the RAD-51 long isoform, a key component of the Fanconi anemia pathway that plays a central role in homologous strand exchange during recombination.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      In\n                      <jats:italic>C. elegans<\/jats:italic>\n                      , which is predicted to encode three RAD-51 isoforms, we find that loss of RAD-51 isoform A enhances homologous recombination efficiency. Additionally, RAD-51 isoform A depletion decreases developmental and meiotic defects in\n                      <jats:italic>fcd-2<\/jats:italic>\n                      mutants as well as reduces chromosome aggregation in\n                      <jats:italic>fcd-2<\/jats:italic>\n                      -deficient germ cells.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      Together, these findings reveal a novel role for RAD-51\n                      <jats:italic>C. elegans<\/jats:italic>\n                      , suggesting that the pattern of RAD-51 isoform expression modulates the balance between homologous recombination and non-homologous-end-joining, thereby preserving genome stability.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/s12915-026-02652-1","type":"journal-article","created":{"date-parts":[[2026,6,23]],"date-time":"2026-06-23T01:26:56Z","timestamp":1782178016000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Loss of the RAD-51 isoform A redirects DNA repair and preserves genome stability in FANCD2-deficient Caenorhabditis elegans"],"prefix":"10.1186","volume":"24","author":[{"given":"Alessandra","family":"Masullo","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marcello","family":"Germoglio","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rosanna","family":"Mattossovich","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Claudia","family":"Esposito","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anna","family":"Valenti","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Adele","family":"Adamo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,6,23]]},"reference":[{"key":"2652_CR1","doi-asserted-by":"publisher","unstructured":"Sakai W, Sugasawa K. 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