The Xenopus POU class V transcription factor XOct-25 inhibits ectodermal competence to respond to bone morphogenetic protein-mediated embryonic induction

Abstract

Bone morphogenetic proteins (BMPs) have been shown to play a key role in controlling ectodermal cell fates by inducing epidermis at the expense of neural tissue during gastrulation. Here, we present evidence that the Xenopus POU class V transcription factor XOct-25 regulates ectodermal cell fate decisions by inhibiting the competence of ectodermal cells to respond to BMP during Xenopus embryogenesis. When overexpressed in the ectoderm after the blastula stage, XOct-25 suppressed early BMP responses of ectodermal cells downstream of BMP receptor activation and promoted neural induction while suppressing epidermal differentiation. In contrast, inhibition of XOct-25 function in the prospective neuroectoderm resulted in expansion of epidermal ectoderm at the expense of neuroectoderm. The reduction of neural tissue by inhibition of XOct-25 function could be rescued by decreasing endogenous BMP signaling, suggesting that XOct-25 plays a role in the formation of neural tissue at least in part by inhibiting BMP-mediated epidermal induction (neural inhibition). This hypothesis is supported by the observation that ectodermal cells from XOct-25 morphants were more sensitive to BMP signaling than cells from controls in inducing both immediate early BMP target genes and epidermis at the expense of neural tissue, while cells overexpressing XOct-25 are less competent to respond to BMP-mediated induction. These results document an essential role for XOct-25 in commitment to neural or epidermal cell fates in the ectoderm and highlight the importance of a regulatory mechanism that limits competence to respond to BMP-mediated embryonic induction.

Pou2, a class V POU-type transcription factor in zebrafish, regulates dorsoventral patterning and convergent extension movement at different blastula stages

“…We noted some discrepancies even among different reports on Xenopus genes. Overexpression of Xenopus class V POU genes promoted neural induction (Cao et al, 2006;Snir et al, 2006;Takebayashi-Suzuki et al, 2007), which is apparently contradictory to the hypothesis that these contribute to the undifferentiated state of embryonic cells, whereas one report, however, showed that Oct25 suppressed neural development as revealed by defective neural structures and downregulation of N-CAM (Cao et al, 2004). One possible reason for this confusing situation may be attributable to gene duplication.…”

Xenopus Sox3 activates sox2 and geminin and indirectly represses Xvent2 expression to induce neural progenitor formation at the expense of non-neural ectodermal derivatives

“…With reduced Sox3, inhibition of BMP by Noggin does not effectively block epidermogenesis or induce neural tissue. One possibility is that neural induction by Noggin was only partially blocked in these experiments because maternal Sox3 protein or other factors such as XOct-25 that facilitate neural induction were present (Takebayashi-Suzuki et al, 2007). The relationship between such factors and Sox3 is unknown and they may work in conjunction or be redundant with Sox3.…”

Geminin cooperates with Polycomb to restrain multi-lineage commitment in the early embryo

“…Like their mouse counterparts, they control pluripotency maintenance in embryos, suppressing BMP-mediated ventral fate acquisition, inhibiting Activin-and FGF-induced mesodermal commitment, and promoting neural tissue formation. This activity contributes to maintaining proper tissue boundaries and preventing expansion of mesodermal and endodermal territories into pluripotent ectoderm (Cao et al, 2006;Henig et al, 1998;Morrison and Brickman, 2006;Snir et al, 2006;Takebayashi-Suzuki et al, 2007).…”