Beta-Microseminoprotein-related molecules may participate in formation of the mesoderm in the chick embryo.

Abstract

It has previously been shown that human beta-microseminoprotein enhances development of mesodermal structures in the chick embryo. The present study was carried out to elucidate the mechanism of action of human beta-microseminoprotein in the chick embryo. beta-Microseminoprotein brought about significant modulation of expression of Brachyury in gastrulating embryos. In approximately 50% of the treated embryos, Brachyury expression was enhanced around the Hensen's node. These cells not only expressed higher levels of Brachyury, but also appeared to switch off Brachyury expression prematurely, postinvagination. The spatial modulation of Brachyury is not clearly reflected in the northern blots, indicating that beta-microseminoprotein treatment results in redistribution of available transcripts or that the upregulation is compensated for by early switching off of Brachyury postinvagination. Because higher levels of Brachyury during gastrulation are believed to result in early exit of cells from the primitive streak, beta-microseminoprotein treatment appeared to have stimulated morphogenetic movements by upregulating Brachyury around the Hensen's node. This deduction was confirmed by scanning electron microscopic analysis that showed that altered morphogenetic movements accompany modulation of Brachyury. The specific responses elicited by beta-microseminoprotein indicate presence of a structurally related molecule in the chick. By western blotting, similar molecules were indeed detected in the chicken seminal plasma and in chick embryos. These data strongly suggest that beta-microseminoprotein-related molecule(s) participates in mesoderm formation in the chick embryo.