Abstract

Junctional Adhesion Molecule-A (JAM-A), an immunoglobulin superfamily (IgSF) member has been shown to be a multifunctional protein playing important role in the process of cell adhesion, leukocyte transmigration, angiogenesis, platelet activation and is a receptor for respiratory enteric orphan virus (reovirus). Interestingly, Jam-A null mice survive, indicating possible compensation by some other member related to JAM-A. Junctional adhesion molecule-C (JAM-C), a member of JAM family share most of the functions carried by JAM-A, exhibit about 32% similarity at the amino acid level with it thus appearing to be an ideal candidate compensating for the absence of JAM-A. Western blot, immunostaining and in situ hybridization techniques were used to detect any change in expression pattern of JAM-C both at the protein as well as transcript level in various organs including brain, heart, kidney, testis, lung, liver and spleen isolated from Jam-A null adult mouse and were compared to those from the wild type (WT). In order to check if compensation was occurring early during embryo development, timed pregnancy was carried out to isolate both WT and Jam-A null embryos at different stages of development and using the above mentioned techniques, expression pattern of JAM-C was studied and compared between WT and Jam-A null embryos.

Although, upregulation or downregulation of JAM-C was not detected in the Jam-A null tissues compared to the WT both in adult and in embryo, some very interesting findings regarding the expression pattern of JAM-C in various tissues were noted. In tissues isolated from adult mice, JAM-C expression was detected in both the endothelial and epithelial component, the expression in either epithelial or endothelial or in both being organ specific e.g. JAM-C was detected only in the lung epithelium while both the endothelium and epithelium expressed JAM-C in the testis. Some important findings with regards to the temporal and spatial parameters of JAM-C expression during embryonic development have been documented here as well. JAM-C was expressed in the neuroepithelium (NE) as early as 7.5 days post coitum (dpc, E7.5)) and continued as the telencephalic vesicle, optic vesicle, mesencephalic vesicle and hindbrain started to develop by 10.5 dpc. JAM-C expression was also prominent in the NE of cerebellar primordium, choroid plexus and fourth ventricle as these structures developed from 13.5 dpc to 17.5 dpc. Interestingly, JAM-C unlike JAM-A, was never expressed in the embryonic endothelial component identified by platelet endothelial cell adhesion molecule-1 (PECAM-1). JAM-C was also detected in adult mouse brain in the ventricles, choroid plexus and in the cerebellum. Besides brain, JAM-C expression was detected in the optic vesicle, otic sac, olfactory epithelium, developing lung and gut. This is the first report documenting expression pattern of JAM-C during embryonic development. NE is a vital tissue giving rise to progenitor cells that ultimately gives rise to neurones and glial cells. Based on the presence of JAM-C in NE, it is tempting to speculate that JAM-C might be playing some role in the process of neurogenesis although more work needs to be done before reaching a conclusion about the functional role of JAM-C in the NE.