Mutation in Bmp7 exacerbates the phenotype of Bmp8a mutants in spermatogenesis and epididymis.

The specificity of bone morphogenetic proteins (BMPs) to their putative heteromeric receptor complexes in vivo is largely unclear. Closely related BMPs may use the same or different receptor complexes for signaling in a time- and space-dependent manner during development and differentiation. We have shown that Bmp7 expression in epididymal epithelium is developmentally regulated. Here, we further show that Bmp7 expression is also developmentally regulated in male germ cells. Bmp7 transcripts are detected in spermatogonia and early primary spermatocytes during early puberty and in stage-7 to -15 spermatids of the adult mice. Since Bmp7 homozygous mutants die perinatally and heterozygotes do not show obvious defects in the testis and the epididymis, the role of Bmp7 in spermatogenesis and epididymal function cannot be revealed by simply examining these mutants. Therefore, we have used a genetic approach by creating Bmp7/Bmp8a double mutants to investigate the role of Bmp7 in spermatogenesis and epididymal function. Here, we report that removal of one allele of Bmp7 exacerbates the phenotype of Bmp8a null mutants in spermatogenesis and epididymis of the adult. These indicate that, similar to Bmp8a, Bmp7 plays a role in both the maintenance of spermatogenesis and epididymal function and it further suggests that BMP8 and BMP7 signal through the same or similar receptors in these two systems.