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Conversion of ectoderm into a neural fate by ATH‐3 , a vertebrate basic helix–loop–helix gene homologous to Drosophila proneural gene atonal
Author(s) -
Takebayashi Koichi,
Takahashi Shuji,
Yokota Chika,
Tsuda Hiroshi,
Nakanishi Shigetada,
Asashima Makoto,
Kageyama Ryoichiro
Publication year - 1997
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1093/emboj/16.2.384
Subject(s) - biology , ectoderm , xenopus , neural development , neural plate , neural tube , microbiology and biotechnology , neuroectoderm , mesoderm , neural cell , nervous system , gene , genetics , embryonic stem cell , embryogenesis , embryo , neuroscience , cell
We have isolated a novel basic helix–loop–helix (bHLH) gene homologous to the Drosophila proneural gene atonal , termed ATH‐3 , from Xenopus and mouse. ATH‐3 is expressed in the developing nervous system, with high levels of expression in the brain, retina and cranial ganglions. Injection of ATH‐3 RNA into Xenopus embryos dramatically expands the neural tube and induces ectopic neural tissues in the epidermis but inhibits non‐neural development. This ATH‐3 ‐induced neural hyperplasia does not require cell division, indicating that surrounding cells which are normally non‐neural types adopt a neural fate. In a Xenopus animal cap assay, ATH‐3 is able to convert ectodermal cells into neurons expressing anterior markers without inducing mesoderm. Interestingly, a single amino acid change from Ser to Asp in the basic region, which mimics phosphorylation of Ser, severely impairs the anterior marker‐inducing ability without affecting general neurogenic activities. These results provide evidence that ATH‐3 can directly convert non‐neural or undetermined cells into a neural fate, and suggest that the Ser residue in the basic region may be critical for the regulation of ATH‐3 activity by phosphorylation.