Male infertility-linked point mutation disrupts the Ca2+ oscillation-inducing and PIP(2) hydrolysis activity of sperm PLCζ

Biochem J. 2011 Mar 1;434(2):211-7. doi: 10.1042/BJ20101772.

Abstract

A male infertility-linked human PLCζ (phospholipase Cζ) mutation introduced into mouse PLCζ completely abolishes both in vitro PIP(2) (phosphatidylinositol 4,5-bisphosphate) hydrolysis activity and the ability to trigger in vivo Ca2+ oscillations in mouse eggs. Wild-type PLCζ initiated a normal pattern of Ca2+ oscillations in eggs in the presence of 10-fold higher mutant PLCζ, suggesting that infertility is not mediated by a dominant-negative mechanism.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Calcium / metabolism*
  • Calcium Signaling
  • Female
  • Humans
  • Hydrolysis
  • Infertility, Male / genetics*
  • Male
  • Mice
  • Oocytes / metabolism
  • Phosphatidylinositol 4,5-Diphosphate / metabolism*
  • Phosphoinositide Phospholipase C / genetics*
  • Phosphoinositide Phospholipase C / metabolism*
  • Point Mutation*
  • Spermatozoa / enzymology*
  • Spermatozoa / metabolism

Substances

  • Phosphatidylinositol 4,5-Diphosphate
  • PLCZ1 protein, human
  • Phosphoinositide Phospholipase C
  • Plcz1 protein, mouse
  • Calcium