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Sperm from mice carrying one or two t haplotypes are deficient in investment and oocyte penetration

L R Johnson1, S H Pilder, J L Bailey

  • 1Department of Anatomy and Cell Biology, Temple University School of Medicine, Philadelphia, Pennsylvania 19140.

Developmental Biology
|March 1, 1995
PubMed

Insights

Mouse t haplotypes cause defective sperm function, impacting fertilization. These genetic factors in t-complex mutations affect sperm motility and binding, potentially explaining sterility and transmission ratio distortion.

Area of Science:

  • Reproductive Biology
  • Genetics
  • Developmental Biology

Background:

  • Mouse t haplotypes, located on chromosome 17, are known to influence male fertility.
  • Males with two t haplotypes (tx/ty) are sterile with severely impaired sperm motility and egg penetration.
  • Even in fertile males with one t haplotype (t/+), sperm carrying the normal chromosome 17 (+t) exhibit fertilization defects.

Purpose of the Study:

  • To investigate the specific defects in sperm function caused by t haplotypes during fertilization.
  • To compare the fertilization defects in sperm from t/+ males with those from tx/ty males.
  • To identify the roles of t haplotypes in sperm-egg interactions.

Main Methods:

  • Development of a unique low sperm:egg ratio in vitro fertilization (IVF) assay.
  • Assessment of sperm ability to penetrate the zona pellucida and zona-free oocytes.
  • Evaluation of sperm binding to the zona and oolemma.

Main Results:

  • Sperm from tw5/+ mice showed reduced ability to penetrate the zona and zona-free oocytes compared to controls.
  • Sperm from tw5/tw32 mice exhibited defects in zona penetration, oocyte penetration, zona binding, and oolemma binding.
  • These deficits in sperm function mirror those seen in tx/ty males, suggesting a common genetic basis.

Conclusions:

  • t haplotypes significantly impair multiple sperm functions essential for fertilization, including motility, zona penetration, and binding.
  • The identified sperm function deficits are linked to both transmission ratio distortion and male sterility.
  • The t complex represents a valuable resource for discovering genes critical for successful sperm-egg interaction.

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