Ipl1/Aurora B kinase coordinates synaptonemal complex disassembly with cell cycle progression and crossover formation in budding yeast meiosis

Philip Jordan, Alice Copsey, Louise Newnham, Elizabeth Kolar, Michael Lichten, Eva Hoffmann

Research output: Contribution to journalArticlepeer-review

Abstract

Several protein kinases collaborate to orchestrate and integrate cellular and chromosomal events at the G2/M transition in both mitotic and meiotic cells. During the G2/M transition in meiosis, this includes the completion of crossover recombination, spindle formation, and synaptonemal complex (SC) breakdown. We identified Ipl1/Aurora B kinase as the main regulator of SC disassembly. Mutants lacking Ipl1 or its kinase activity assemble SCs with normal timing, but fail to dissociate the central element component Zip1, as well as its binding partner, Smt3/SUMO, from chromosomes in a timely fashion. Moreover, lack of Ipl1 activity causes delayed SC disassembly in a cdc5 as well as a CDC5-inducible ndt80 mutant. Crossover levels in the ipl1 mutant are similar to those observed in wild type, indicating that full SC disassembly is not a prerequisite for joint molecule resolution and subsequent crossover formation. Moreover, expression of meiosis I and meiosis II-specific B-type cyclins occur normally in ipl1 mutants, despite delayed formation of anaphase I spindles. These observations suggest that Ipl1 coordinates changes to meiotic chromosome structure with resolution of crossovers and cell cycle progression at the end of meiotic prophase.

Original languageEnglish (US)
Pages (from-to)2237-2251
Number of pages15
JournalGenes and Development
Volume23
Issue number18
DOIs
StatePublished - Sep 15 2009
Externally publishedYes

Keywords

  • Cdc5/polo-like kinase
  • Chromosome structure
  • Ipl1/Aurora B kinase
  • Meiosis
  • Synaptonemal complex

ASJC Scopus subject areas

  • Genetics
  • Developmental Biology

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