Conversion of midbodies into germ cell intercellular bridges

Dev Biol. 2007 May 15;305(2):389-96. doi: 10.1016/j.ydbio.2007.02.025. Epub 2007 Feb 24.

Abstract

Whereas somatic cell cytokinesis resolves with abscission of the midbody, resulting in independent daughter cells, germ cell cytokinesis concludes with the formation of a stable intercellular bridge interconnecting daughter cells in a syncytium. While many proteins essential for abscission have been discovered, until recently, no proteins essential for mammalian germ cell intercellular bridge formation have been identified. Using TEX14 as a marker for the germ cell intercellular bridge, we show that TEX14 co-localizes with the centralspindlin complex, mitotic kinesin-like protein 1 (MKLP1) and male germ cell Rac GTPase-activating protein (MgcRacGAP) and converts these midbody matrix proteins into stable intercellular bridge components. In contrast, septins (SEPT) 2, 7 and 9 are transitional proteins in the newly forming bridge. In cultured somatic cells, TEX14 can localize to the midbody in the absence of other germ cell-specific factors, suggesting that TEX14 serves to bridge the somatic cytokinesis machinery to other germ cell proteins to form a stable intercellular bridge essential for male reproduction.

Publication types

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

MeSH terms

  • Animals
  • CHO Cells
  • Cricetinae
  • Cricetulus
  • Cytokinesis / physiology
  • Extracellular Space / enzymology
  • Extracellular Space / physiology*
  • HeLa Cells
  • Humans
  • Intercellular Junctions / enzymology
  • Intercellular Junctions / physiology*
  • Male
  • Mice
  • Organelles / enzymology
  • Organelles / physiology*
  • Protein Serine-Threonine Kinases / physiology
  • Spermatozoa / cytology*
  • Spermatozoa / enzymology
  • Spermatozoa / metabolism
  • Subcellular Fractions / enzymology
  • Subcellular Fractions / physiology
  • Transcription Factors / physiology

Substances

  • TEX14 protein, mouse
  • Transcription Factors
  • Protein Serine-Threonine Kinases