期刊
DEVELOPMENTAL BIOLOGY
卷 313, 期 1, 页码 246-255出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ydbio.2007.10.013
关键词
spermiogenesis; elongated spermatid; progressive and hyperactivated motility; sperm flagellar defects; sperm membrane protein
资金
- NATIONAL CENTER FOR RESEARCH RESOURCES [P20RR015588] Funding Source: NIH RePORTER
- NCRR NIH HHS [5P20RR015588-07, P20 RR015588-07, P20 RR015588] Funding Source: Medline
- NHLBI NIH HHS [R01 HL119374] Funding Source: Medline
Junctional adhesion molecules (JAMs) that are expressed in endothelial and epithelial cells and function in tight junction assembly, also perform important roles in testis where the closely-related JAM-A, JAM-B, and JAM-C are found. Disruption of murine Jam-B and Jam-C has varying effects on sperm development and function; however, deletion of Jam-A has not yet been studied. Here we show for the first time that in addition to expression in the Sertoli-Sertoli tight junctions in the seminiferous tubules, the similar to 32 kDa murine JAM-A is present in elongated spermatids and in the plasma membrane of the head and flagellum of sperm. Deletion of dam-A, using the gene trap technology, results in flagellar defects at the ultrastructural level. In Jam-A-deficient mice, which have reduced litter size, both progressive and hyperactived motility are significantly affected (P<0.0001) before and, more severely, after capacitation. The findings show that JAM-A is involved in sperm tail formation and is essential for normal motility, which may occur via its signal transduction and protein phosphorylation properties. Detection of JAM-A in human sperm proteins indicates that its role may be conserved in sperm motility and that JAM-A may be a candidate gene for the analysis of idiopathic sperm motility defects resulting in male subfertility in the human population. (c) 2007 Elsevier Inc. All rights reserved.
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