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To investigate the role\n                      <jats:italic>san-1<\/jats:italic>\n                      , the MAD3 homologue, has in\n                      <jats:italic>Caenorhabditis elegans<\/jats:italic>\n                      embryos we used RNA interference (RNAi) to identify genes synthetic lethal with the viable\n                      <jats:italic>san-1(ok1580)<\/jats:italic>\n                      deletion mutant.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      The\n                      <jats:italic>san-1(ok1580)<\/jats:italic>\n                      animal has low penetrating phenotypes including an increased incidence of males, larvae arrest, slow growth, protruding vulva, and defects in vulva morphogenesis. We found that the viability of\n                      <jats:italic>san-1(ok1580)<\/jats:italic>\n                      embryos is significantly reduced when HCP-1 (CENP-F homologue), MDF-1 (MAD-1 homologue), MDF-2 (MAD-2 homologue) or BUB-3 (predicted BUB-3 homologue) are reduced by RNAi. Interestingly, the viability of\n                      <jats:italic>san-1(ok1580)<\/jats:italic>\n                      embryos is not significantly reduced when the paralog of HCP-1, HCP-2, is reduced. The phenotype of\n                      <jats:italic>san-1(ok1580);hcp-1(RNAi)<\/jats:italic>\n                      embryos includes embryonic and larval lethality, abnormal organ development, and an increase in abnormal chromosome segregation (aberrant mitotic nuclei, anaphase bridging). Several of the\n                      <jats:italic>san-1(ok1580);hcp-1(RNAi)<\/jats:italic>\n                      animals displayed abnormal kinetochore (detected by MPM-2) and microtubule structure. The survival of\n                      <jats:italic>mdf-2(RNAi);hcp-1(RNAi)<\/jats:italic>\n                      embryos but not\n                      <jats:italic>bub-3(RNAi);hcp-1(RNAi)<\/jats:italic>\n                      embryos was also compromised. Finally, we found that\n                      <jats:italic>san-1(ok1580)<\/jats:italic>\n                      and\n                      <jats:italic>bub-3(RNAi)<\/jats:italic>\n                      , but not\n                      <jats:italic>hcp-1(RNAi)<\/jats:italic>\n                      embryos, were sensitive to anoxia, suggesting that like SAN-1, BUB-3 has a functional role as a spindle checkpoint protein.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      Together, these data suggest that in the\n                      <jats:italic>C. elegans<\/jats:italic>\n                      embryo, HCP-1 interacts with a subset of the spindle checkpoint pathway. Furthermore, the fact that\n                      <jats:italic>san-1(ok1580);hcp-1(RNAi)<\/jats:italic>\n                      animals had a severe viability defect whereas in the\n                      <jats:italic>san-1(ok1580);hcp-2(RNAi)<\/jats:italic>\n                      and\n                      <jats:italic>san-1(ok1580);hcp-2(ok1757)<\/jats:italic>\n                      animals the viability defect was not as severe suggesting that\n                      <jats:italic>hcp-1<\/jats:italic>\n                      and\n                      <jats:italic>hcp-2<\/jats:italic>\n                      are not completely redundant.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/1747-1028-3-6","type":"journal-article","created":{"date-parts":[[2008,2,5]],"date-time":"2008-02-05T02:13:53Z","timestamp":1202177633000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":27,"title":["Genetic analysis of the spindle checkpoint genes san-1, mdf-2, bub-3 and the CENP-F homologues hcp-1 and hcp-2 in Caenorhabditis elegans"],"prefix":"10.1186","volume":"3","author":[{"given":"Vinita A","family":"Hajeri","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anil M","family":"Stewart","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Landon L","family":"Moore","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pamela A","family":"Padilla","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2008,2,4]]},"reference":[{"key":"67_CR1","volume-title":"J Cell Biochem","author":"YH Chi","year":"2007","unstructured":"Chi YH, Jeang KT: Aneuploidy and cancer. 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