Nature：植物乙烯信号作用的调控机制
乙烯是一种调控植物发芽、结果和其他重要过程的主要荷尔蒙。以前的研究工作识别出一个线性通道(在该通道中，5种乙烯受体汇聚在一个单一的负调控因子CTR1上)和两个关键的下游成分EIN2和EIN3。此前，CTR1怎样调控下游正调控因子的过程仍然是一个谜。现在，一种以前未知的、涉及MKK9的“丝裂原活化蛋白激酶”(MAPK)通道已在拟南芥中被识别出来，其作用是积极控制乙烯信号作用中由EIN3调控的转录。CTR1和MKK9的拮抗作用可能通过对EIN3的稳定性具有相反作用的两个MAPK磷酸化点来共同决定乙烯信号作用特异性和定量反应。科学时报
生物谷推荐英文原文：
Nature 451, 789-795 (14 February 2008) | doi:10.1038/nature06543; Received 25 October 2007; Accepted 10 December 2007
Dual control of nuclear EIN3 by bifurcate MAPK cascades in C2H4 signalling
Sang-Dong Yoo1, Young-Hee Cho1, Guillaume Tena1, Yan Xiong1 & Jen Sheen1
- Department of Molecular Biology, Massachusetts General Hospital, Department of Genetics, Harvard Medical School, Boston, Massachusetts 02114, USA
Correspondence to: Sang-Dong Yoo1Jen Sheen1 Correspondence and requests for materials should be addressed to J. S. (Email: sheen@molbio.mgh.harvard.edu) or S.-D. Y. (Email: yoo@molbio.mgh.harvard.edu).
Abstract
A principal question in MAP kinase (MAPK/MPK) cascade signalling is how similar components dictate different specificity in the information-processing machineries from yeast to humans and plants. In Arabidopsis, how MPK3/6 modulates distinct outputs in diverse signal transduction pathways remains elusive. By combining systematic cellular and genetic screens, here we uncover a previously unexpected MKK9–MPK3/MPK6 cascade promoting ethylene-insensitive 3 (EIN3)-mediated transcription in ethylene signalling. The mkk9 mutant exhibits a broad spectrum of moderate ethylene-insensitive phenotypes, and translocated MKK9 governs nuclear signalling downstream of receptors. Breaking a linear model and conventional MAPK signalling, ethylene inactivates the negative regulator constitutive triple response 1 (CTR1, a Raf-like MAPK kinase kinase (MAPKKK)) to activate the positive MKK9–MPK3/6 cascade. The bifurcate and antagonistic CTR1 and MKK9 pathways are both critical in determining ethylene-signalling specificity through two MAPK phosphorylation sites with opposite effects on EIN3 stability. The results suggest a new paradigm for linking intertwined MAPK cascades to control quantitative responses and specificity in signalling networks.
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