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Related Experiment Video

Updated: May 22, 2026

Medium-throughput Screening Assays for Assessment of Effects on Ca2+-Signaling and Acrosome Reaction in Human Sperm

Medium-throughput Screening Assays for Assessment of Effects on Ca²⁺-Signaling and Acrosome Reaction in Human Sperm

Published on: March 1, 2019

KLC3 is involved in sperm tail midpiece formation and sperm function.

Ying Zhang¹, Young Ou, Min Cheng

¹Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada T2N 4N1.

Developmental Biology

|May 8, 2012

Summary

Kinesin light chain 3 (KLC3) is crucial for male fertility. This study reveals KLC3

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Flow Cytometric Analysis of Biomarkers for Detecting Human Sperm Functional Defects

Flow Cytometric Analysis of Biomarkers for Detecting Human Sperm Functional Defects

Published on: April 21, 2022

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Last Updated: May 22, 2026

Medium-throughput Screening Assays for Assessment of Effects on Ca2+-Signaling and Acrosome Reaction in Human Sperm

Medium-throughput Screening Assays for Assessment of Effects on Ca²⁺-Signaling and Acrosome Reaction in Human Sperm

Published on: March 1, 2019

Flow Cytometric Analysis of Biomarkers for Detecting Human Sperm Functional Defects

Flow Cytometric Analysis of Biomarkers for Detecting Human Sperm Functional Defects

Published on: April 21, 2022

Area of Science:

Reproductive biology
Cell biology
Molecular genetics

Background:

Kinesin light chain 3 (KLC3) is exclusively expressed in post-meiotic male germ cells.
KLC3 associates with sperm structures, including mitochondria, during spermatogenesis.
Its precise role in midpiece formation and male fertility remains unclear.

Purpose of the Study:

To elucidate the molecular mechanisms of KLC3-mediated mitochondrial aggregation.
To investigate the function of KLC3 in spermatid development and sperm tail midpiece formation.
To determine the impact of KLC3 dysfunction on male reproductive efficiency.

Main Methods:

Utilized an inducible expression system to study KLC3-induced mitochondrial aggregation.
Identified KLC3 binding partners using biochemical approaches.
Developed a transgenic mouse model expressing a dominant-negative KLC3 mutant in spermatids.

Main Results:

KLC3 expression induces microtubule-dependent mitochondrial aggregation.
VDAC2 was identified as a KLC3 binding partner on the mitochondrial outer membrane.
Transgenic mice with KLC3 dysfunction exhibited reduced sperm count, impaired motility, and decreased litter size.

Conclusions:

KLC3 is essential for proper mitochondrial sheath development during spermiogenesis.
KLC3 plays a critical role in male reproductive efficiency and sperm function.
Dysregulation of KLC3 impacts sperm morphology and fertility.