乙烯是一種調(diào)控植物發(fā)芽、結(jié)果和其他重要過(guò)程的主要荷爾蒙,。以前的研究工作識(shí)別出一個(gè)線性通道(在該通道中，5種乙烯受體匯聚在一個(gè)單一的負(fù)調(diào)控因子CTR1上)和兩個(gè)關(guān)鍵的下游成分EIN2和EIN3,。此前,，CTR1怎樣調(diào)控下游正調(diào)控因子的過(guò)程仍然是一個(gè)謎。現(xiàn)在,，一種以前未知的,、涉及MKK9的“絲裂原活化蛋白激酶”(MAPK)通道已在擬南芥中被識(shí)別出來(lái)，其作用是積極控制乙烯信號(hào)作用中由EIN3調(diào)控的轉(zhuǎn)錄,。CTR1和MKK9的拮抗作用可能通過(guò)對(duì)EIN3的穩(wěn)定性具有相反作用的兩個(gè)MAPK磷酸化點(diǎn)來(lái)共同決定乙烯信號(hào)作用特異性和定量反應(yīng),?？茖W(xué)時(shí)報(bào)
生物谷推薦英文原文：
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: [email protected]) or S.-D. Y. (Email: [email protected]).
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.
