MORC2B is essential for meiotic progression and fertility

PLoS Genet. 2018 Jan 12;14(1):e1007175. doi: 10.1371/journal.pgen.1007175. eCollection 2018 Jan.

Abstract

The microrchidia (MORC) family proteins are chromatin-remodelling factors and function in diverse biological processes such as DNA damage response and transposon silencing. Here, we report that mouse Morc2b encodes a functional germ cell-specific member of the MORC protein family. Morc2b arose specifically in the rodent lineage through retrotransposition of Morc2a during evolution. Inactivation of Morc2b leads to meiotic arrest and sterility in both sexes. Morc2b-deficient spermatocytes and oocytes exhibit failures in chromosomal synapsis, blockades in meiotic recombination, and increased apoptosis. Loss of MORC2B causes mis-regulated expression of meiosis-specific genes. Furthermore, we find that MORC2B interacts with MORC2A, its sequence paralogue. Our results demonstrate that Morc2b, a relatively recent gene, has evolved an essential role in meiosis and fertility.

Publication types

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

MeSH terms

  • Animals
  • Chromosome Pairing / genetics
  • Female
  • Fertility / genetics*
  • Male
  • Meiosis / genetics*
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Oocytes / metabolism
  • Sequence Homology
  • Spermatocytes / metabolism
  • Transcription Factors / genetics
  • Transcription Factors / physiology*

Substances

  • MORC2 protein, mouse
  • Transcription Factors