作者: Erwan Watrin , Alexander Schleiffer , Koichi Tanaka , Frank Eisenhaber , Kim Nasmyth
DOI: 10.1016/J.CUB.2006.03.049
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摘要: Summary Background Sister-chromatid cohesion depends on the cohesin complex whose association with chromatin is mediated by Scc2 and Scc4 in budding yeast. Both have been conserved from yeast to humans, but no orthologs identified. Mutation of causes defects cohesion, transcription, development, resulting Cornelia de Lange syndrome humans. Results We identified a family tetratricopeptide repeat proteins that share weak sequence similarities Scc4. This includes MAU-2, which required for development nervous system Caenorhabditis elegans . show human member this associated Scc2, bound telophase until prophase, during interphase. Cells lacking lose sister-chromatid precociously arrest prometaphase. Mitotic chromosomes Scc4-depleted cells lack cohesin, even though cohesin-protecting Sgo1 Bub1 are normally enriched at centromeres separase does not seem be active. Conclusion Our data indicate chromatin, prerequisite establishment chromosome biorientation mitosis. The proteinaceous machinery loading onto therefore finding MAU-2 an ortholog further supports notion Scc2-Scc4 developmental processes metazoans.