1. Vascular Development Laboratory, Cancer Research UK London Research Institute, London WC2A 3PX, UK
2. Institute of Cell Biology, ZMBE, University Hospital Muenster, D-48149 Muenster, Germany
3. University of Geneva, CMU, Department of Pathology, CH-1211 Geneva, Switzerland

Correspondence to: Ralf H. Adams¹ Email: ralf.adams@cancer.org.uk

Abstract

During spermatogenesis in the mammalian testis, stem cells (spermatogonia) differentiate into spermatocytes, which subsequently undergo two consecutive meiotic divisions to give rise to haploid spermatids. These cells are initially round but progressively elongate, condense their nuclei, acquire flagellar and acrosomal structures, and shed a significant amount of their cytoplasm to form spermatozoa (the sperm cells) in a developmental cascade termed spermiogenesis^{1, 2}. Defects in these processes will lead to a lack of mature sperm cells (azoospermia), which is a major cause of male infertility in the human population³. Here we report that a cell-surface protein of the immunoglobulin superfamily, junctional adhesion molecule-C (JAM-C), is critically required for the differentiation of round spermatids into spermatozoa in mice. We found that Jam-C is essential for the polarization of round spermatids, a function that we attribute to its role in the assembly of a cell polarity complex.

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