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Histone acetylation is a checkpoint in FGF‐stimulated mesoderm induction
Author(s) -
Xu RenHe,
Peng Ying,
Fan Jing,
Yan Donghong,
Yamagoe Satoshi,
Princler Gerald,
Sredni Dvora,
Ozato Keiko,
Kung HsiangFu
Publication year - 2000
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/1097-0177(2000)9999:9999<::aid-dvdy1024>3.0.co;2-h
Subject(s) - biology , mesoderm , trichostatin a , hdac4 , histone deacetylase , hdac11 , histone deacetylase 5 , microbiology and biotechnology , fgf and mesoderm formation , sap30 , histone h2a , histone h1 , histone methyltransferase , acetylation , cancer research , histone , genetics , embryonic stem cell , gene
We have previously demonstrated that the transcription factor, AP‐1 (c‐jun/c‐fos heterodimer), mediates fibroblast growth factor (FGF) signaling during mesoderm induction in Xenopus embryo. In the present studies, we show that histone acetylation is involved in FGF‐mediated signaling leading to mesoderm induction. Histone acetylation is a dynamic process regulated by the activities of two histone‐modifying enzymes, the histone acetyltransferase(s) and histone deacetylase(s) (HDACs). We found that basal and FGF‐regulated activator protein 1 (AP‐1) activity in Xenopus embryo is markedly reduced by treatment of trichostatin A (TSA), a specific inhibitor of HDAC. However, activity of another transcription factor, NFκB, is enhanced by TSA treatment. AP‐1‐mediated mesoderm induction in the animal caps is dramatically suppressed by TSA at a dose‐dependent manner. This suppression can be rescued by ectopic expression of HDAC3 at early stage. Finally, we found that histone acetylation in animal caps is inhibited by FGF whereas enhanced by TSA (as a control). Therefore, we propose that histone acetylation is a checkpoint for transduction of the FGF/AP‐1 signals to induce mesoderm. Published 2000 Wiley‐Liss, Inc.