Shugoshin protects centromere pairing and promotes segregation of nonexchange partner chromosomes in meiosis

Proc Natl Acad Sci U S A. 2019 May 7;116(19):9417-9422. doi: 10.1073/pnas.1902526116. Epub 2019 Apr 24.

Abstract

Faithful chromosome segregation during meiosis I depends upon the formation of connections between homologous chromosomes. Crossovers between homologs connect the partners, allowing them to attach to the meiotic spindle as a unit, such that they migrate away from one another at anaphase I. Homologous partners also become connected by pairing of their centromeres in meiotic prophase. This centromere pairing can promote proper segregation at anaphase I of partners that have failed to become joined by a crossover. Centromere pairing is mediated by synaptonemal complex (SC) proteins that persist at the centromere when the SC disassembles. Here, using mouse spermatocyte and yeast model systems, we tested the role of shugoshin in promoting meiotic centromere pairing by protecting centromeric synaptonemal components from disassembly. The results show that shugoshin protects the centromeric SC in meiotic prophase and, in anaphase, promotes the proper segregation of partner chromosomes that are not linked by a crossover.

Keywords: PP2A; centromere pairing; meiosis; nonexchange chromosome; shugoshin.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Anaphase / physiology*
  • Animals
  • Cell Cycle Proteins / genetics
  • Cell Cycle Proteins / metabolism*
  • Centromere / genetics
  • Centromere / metabolism*
  • Chromosome Segregation / physiology*
  • Male
  • Mice
  • Mice, Knockout
  • Prophase / physiology*
  • Saccharomyces cerevisiae / genetics
  • Saccharomyces cerevisiae / metabolism
  • Spermatocytes / cytology
  • Spermatocytes / metabolism*
  • Spindle Apparatus / genetics
  • Spindle Apparatus / metabolism
  • Synaptonemal Complex / genetics
  • Synaptonemal Complex / metabolism

Substances

  • Cell Cycle Proteins
  • shugoshin protein, mouse