During vertebrate embryogenesis, the neuroectoderm is induced from dorsal ectoderm and then partitioned into anterior and posterior neuroectodermal domains by posteriorizing signals, such as Wnt and fibroblast growth factor. However, little is known about epigenetic regulation of posteriorizing gene expression.

In a paper published online by Journal of Neuroscience on June 03, scientists from the Institute of Zoology, Chinese Academy of Sciences, discovered a requirement of the chromatin remodeling protein Bptf for neuroectodermal posteriorization in zebrafish embryos.

Bptf is the largest subunit of the nucleosome remodeling factor (NURF) complex, which was recognized to catalyze nucleosome sliding in an ATP-dependent manner to assist transcriptional activation. They found that Knockdown of bptf leads to an expansion of the anterior neuroectoderm at the expense of the posterior ectoderm. Bptf functionally and physically interacts with p-Smad2, which is activated by non-Nodal TGF-β signaling, to promote the expression of wnt8a, a critical gene for neural posteriorization.

Their data demonstrated that Bptf and Smad2 bind to adjacent binding motifs and recruit other NURF components, such as Smarca1, to decrease nucleosome density in the wnt8a promoter. Their data indicated that Bptf- and TGF-β/Smad2-regulated nucleosome remodeling events on cis-regulatory elements of the wnt8a promoter is indispensable for zebrafish neural posteriorization.

This work was supported by National Natural Science Foundation of China Grants, Major Science Programs of China Grants, and Strategic Priority Research Program of the Chinese Academy of Sciences Grant.

A Model for Transcriptional Activation of NURF/Bptf and TGF-β/Smad2 by Promoting Nucleosome Remodeling on wnt8a Promoter. (Image by Prof. WANG Qiang's research group)