Journal
JOURNAL OF NEUROSCIENCE
Volume 35, Issue 22, Pages 8493-8506Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.0377-15.2015
Keywords
bptf; neural posteriorization; nucleosome remodeling; smad2; wnt8a
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Funding
- National Natural Science Foundation of China [31322035, 31271532]
- Major Science Programs of China [2011CB943904, 2011CBA01101]
- Strategic Priority Research Program of the Chinese Academy of Sciences Grant [XDA01010104]
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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. Here, we report a requirement of the chromatin remodeling protein Bptf for neuroectodermal posteriorization in zebrafish embryos. 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-beta signaling, to promote the expression of wnt8a, a critical gene for neural posteriorization. Bptf and Smad2 directly bind to and activate the wnt8a promoter through recruiting NURF remodeling complex. When bptf function or TGF-beta signal transduction is inhibited, the nucleosome density on the wnt8a promoter is increased. We propose that Bptf and TGF-beta/Smad2 mediate nucleosome remodeling to regulate wnt8a expression and hence neural posteriorization.
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