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Nuclear mislocalization of enzymatically active RanGAP causes segregation distortion in Drosophila

A Kusano1, C Staber, B Ganetzky

  • 1Laboratory of Genetics, University of Wisconsin-Madison, 53706, USA.

Developmental Cell
|November 13, 2001
PubMed

Insights

Segregation Distorter (SD) causes preferential chromosome transmission in Drosophila by mislocalizing a truncated RanGAP protein to nuclei. This disrupts nuclear transport and leads to sperm dysfunction.

Area of Science:

  • Genetics
  • Molecular Biology
  • Developmental Biology

Background:

  • Segregation Distorter (SD) is a genetic system in Drosophila inducing biased inheritance.
  • SD functions by causing the dysfunction of sperm carrying the wild-type chromosome.
  • The Sd locus encodes a truncated Ran GTPase activating protein (RanGAP).

Purpose of the Study:

  • To investigate the molecular mechanism of meiotic drive by Segregation Distorter.
  • To determine the role of the truncated Sd-RanGAP protein in the distortion process.
  • To elucidate how Sd-RanGAP affects nuclear transport and sperm function.

Main Methods:

  • Analyzing the enzymatic activity and subcellular localization of Sd-RanGAP.
  • Perturbing Sd-RanGAP's enzymatic activity and nuclear localization.
  • Overexpressing Ran and RanGEF in the male germline.
  • Assessing nuclear transport using a GFP reporter in salivary glands.

Main Results:

  • Sd-RanGAP retains enzymatic activity but is mislocalized to nuclei.
  • Disruption of Sd-RanGAP's activity or nuclear localization abolishes distortion.
  • Overexpression of Ran or RanGEF suppresses distortion.
  • SD impairs nuclear transport of a GFP reporter.

Conclusions:

  • Mislocalization of Sd-RanGAP disrupts the nuclear Ran signaling pathway by reducing nuclear RanGTP.
  • This disruption leads to sperm dysfunction and meiotic drive.
  • SD imposes a defect in nuclear transport, potentially explaining sperm dysfunction.

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