KLP-7 acts through the Ndc80 complex to limit pole number inC. elegansoocyte meiotic spindle assembly
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ABSTRACT: During oocyte meiotic cell division in many animals, bipolar spindles assemble in the absence of centrosomes, but the mechanisms that restrict pole assembly to a bipolar state are unknown. We show that KLP-7, the single mitotic centromere–associated kinesin (MCAK)/kinesin-13 inCaenorhabditis elegans, is required for bipolar oocyte meiotic spindle assembly. Inklp-7(−)mutants, extra microtubules accumulated, extra functional spindle poles assembled, and chromosomes frequently segregated as three distinct masses during meiosis I anaphase. Moreover, reducing KLP-7 function in monopolarklp-18(−)mutants often restored spindle bipolarity and chromosome segregation. MCAKs act at kinetochores to correct improper kinetochore–microtubule (k–MT) attachments, and depletion of the Ndc-80 kinetochore complex, which binds microtubules to mediate kinetochore attachment, restored bipolarity inklp-7(−)mutant oocytes. We propose a model in which KLP-7/MCAK regulates k–MT attachment and spindle tension to promote the coalescence of early spindle pole foci that produces a bipolar structure during the acentrosomal process of oocyte meiotic spindle assembly.
SUBMITTER: Amy A. Connolly
PROVIDER: S-JCBD-201412010 | bioimages |
REPOSITORIES: bioimages
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