| 175499 | B6VQ60 | BRCA1_CAEEL | Breast cancer type 1 susceptibility protein homolog (EC 2.3.2.27) (RING-type E3 ubiquitin transferase BRCA1) | DISRUPTION PHENOTYPE | Animals are viable (PubMed:18219312, PubMed:19646877). However, there is defective double strand break repair (PubMed:18219312, PubMed:19646877, PubMed:26903030). During the early stages of meiosis, this is characterized by impaired homologous recombination in germ cells with increased apoptosis and increased numbers of rad-51-positive foci (PubMed:18219312, PubMed:19646877). Increased sensitivity to UV and IR irradiation and topoisomerase inhibitor camptothecin compared to wild-type (PubMed:24424777, PubMed:26903030). Following either IR irradiation or camptothecin treatment, there is reduced egg hatching (PubMed:26903030). Furthermore, there are also DNA damage repair defects following ionizing radiation and UV irradiation characterized by reduced ubiquitination at DNA damage sites and reduced rad-51-positive foci, respectively (PubMed:16628214, PubMed:24424777, PubMed:26903030). High levels of embryonic lethality and abolished brd-1 expression following DNA damage induced by ionising radiation (PubMed:30383754). Double knockout with brd-1 impairs rad-51 localization to DNA damage sites following DNA damage induced by ionising radiation (PubMed:30383754). RNAi-mediated knockdown results in high X chromosome non-disjunction leading to a high incidence of males (him) phenotype (PubMed:14711411). RNAi-mediated knockdown in addition to gamma-irradiation at the L4 stage of larval development, results in reduced progeny, increased cep-1/p53-dependent germ cell death, chromosome fragmentation and DNA repair defects (PubMed:14711411). {ECO:0000269|PubMed:14711411, ECO:0000269|PubMed:16628214, ECO:0000269|PubMed:18219312, ECO:0000269|PubMed:19646877, ECO:0000269|PubMed:24424777, ECO:0000269|PubMed:26903030, ECO:0000269|PubMed:30383754}. |