Semaphorin 7A promotes axon outgrowth through integrins and MAPKs

Striking parallels exist between immune and nervous system cellular signalling mechanisms. Molecules originally shown to be critical for immune responses also serve neuronal functions, and similarly neural guidance cues can modulate immune function. We show here that semaphorin 7A (Sema7A), a membrane-anchored member of the semaphorin family of guidance proteins previously known for its immunomodulatory effects, can also mediate neuronal functions. Unlike many other semaphorins, which act as repulsive guidance cues, Sema7A enhances central and peripheral axon growth and is required for proper axon tract formation during embryonic development. Unexpectedly, Sema7A enhancement of axon outgrowth requires integrin receptors and activation of MAPK signalling pathways. These findings define a previously unknown biological function for semaphorins, identify an unexpected role for integrins and integrin-dependent intracellular signalling in mediating semaphorin responses, and provide a framework for understanding and interfering with Sema7A function in both immune and nervous systems.     

Genetically haploid spermatids are phenotypically diploid

Because chromosomal homologues segregate from one another during meiosis, spermatids are genetically different. Post-meiotic gene expression could lead to gametic differences, some of which might lead to preferential transmission of certain alleles over others. In both insects and mammals, however, all the cells derived from a single spermatogonial cell develop within a common syncytium formed as a result of incomplete cytokinesis at each of the mitotic and meiotic cell divisions. It has been proposed that the intercellular bridges connecting the cells, which are about 1 micron in diameter, permit the sharing of cytoplasmic constituents, thus ensuring the synchronous development of a clone of cells and gametic equivalence between haploid spermatids. By analysing the product of a transgene which is expressed exclusively in post-meiotic germ cells in hemizygous transgenic mice, we have shown that genetically distinct spermatids share the product of the transgene and hence can be phenotypically equivalent.