Mammalian sperm are dependent on JAM‐A for normal motility: progressing from mice to humans

Abstract

Defective sperm motility (asthenozoospermia) is a primary cause of male infertility. Junctional Adhesion Molecule‐A (JAM‐A) has been recently shown to be essential for mouse sperm motility. However, to date it has not been studied in human sperm. The objective of this study is to determine if JAM‐A is present in human sperm and to characterize its expression. In silico analysis reveals 83% similarity in the amino acid sequence of JAM‐A in mice and humans, indicating that the proteins are conserved. This suggests that JAM‐A may also play a role in human sperm motility. Western analysis of human sperm proteins revealed the presence of JAM‐A with a MW of ~32kDa, identical to that of the mouse. Immunocytochemistry was used to localize the expression of JAM‐A in human sperm. Flow cytometry confirmed the Western blot data and revealed the presence of the protein on the sperm membrane in one of two individuals attending an infertility clinic. Once JAM‐A has been fully characterized in human sperm, the next step will be to determine its interacting protein partners by attempting to co‐immunoprecipitate it with candidate proteins. The localization and characterization of JAM‐A in human sperm is expected to increase our understanding of genetic factors leading to human male infertility and subfertility, laying the groundwork for diagnosis of a subset of couples with fertility issues. Funded by NIH‐COBRE grant #5P20RR015588‐07.