東京家政大学研究者情報データベース

オオニシ　ジュンジ onishi junji
大西　淳之

所属東京家政大学栄養学部管理栄養学科
東京家政大学大学院人間生活学総合研究科健康栄養学専攻
東京家政大学大学院人間生活学総合研究科人間生活学専攻
東京家政大学短期大学部短期大学部栄養科
職種教授

論文種別	原著
言語種別	英語
査読の有無	査読あり
表題	Nemo-like kinase-myocyte enhancer factor 2A signaling regulates anterior formation in Xenopus development.
掲載誌名	正式名：Molecular and Cellular Biology 略　称：Mol Cell Biol ISSNコード：02707306/10985549
掲載区分	国外
巻・号・頁	27(21),pp.7623-7630
著者・共著者	◎Satoh K, Ohnishi J, Sato A, Takeyama M, Iemura S, Natsume T, Shibuya H.
担当区分	2nd著者
発行年月	2007/11
概要	The development of anterior neural structure in Xenopus laevis requires the inhibition of bone morphogenic protein 4 and Wnt signaling. We previously reported that Nemo-like kinase (NLK) negatively regulates Wnt signaling via the phosphorylation of T-cell factor/lymphoid enhancer factor. However, the molecular events occurring downstream of NLK pathways in early neural development remain unclear. In the present study, we identified the transcription factor myocyte enhancer factor 2A (MEF2A) as a novel substrate for NLK. NLK regulates the function of Xenopus MEF2A (xMEF2A) via phosphorylation, and this modification can be inhibited by the depletion of endogenous NLK. In Xenopus embryos, the depletion of either NLK or MEF2A results in a severe defect in anterior development. The endogenous expression of anterior markers was blocked by the depletion of endogenous Xenopus NLK (xNLK) or xMEF2A but, notably, not by the depletion of other xMEF2 family proteins, xMEF2C and xMEF2D. Defects in head formation or the expression of the anterior marker genes caused by the depletion of endogenous xMEF2A could be eliminated by the expression of wild-type xMEF2A, but not xMEF2A containing mutated xNLK phosphorylation sites. Furthermore, the expression of xNLK-induced anterior markers was efficiently blocked by the depletion of endogenous xMEF2A in animal pole explants. These results show that NLK specifically regulates the MEF2A activity required for anterior formation in Xenopus development.
DOI	doi: 10.1128/MCB.01481-07