Alonso Jose M, Stepanova Anna N, Solano Roberto, Wisman Ellen, Ferrari Simone, Ausubel Frederick M, Ecker Joseph R
Plant Biology Laboratory, The Salk Institute for Biological Studies, La Jolla, CA, 92037, USA.
Proc Natl Acad Sci U S A. 2003 Mar 4;100(5):2992-7. doi: 10.1073/pnas.0438070100. Epub 2003 Feb 26.
Five ethylene-insensitive loci (wei1-wei5) were identified by using a low-dose screen for "weak" ethylene-insensitive mutants. wei1, wei2, and wei3 seedlings showed hormone insensitivity only in roots, whereas wei4 and wei5 displayed insensitivity in both roots and hypocotyls. The genes corresponding to wei1, wei4, and wei5 were isolated using a positional cloning approach. The wei1 mutant harbored a recessive mutation in TIR1, which encodes a component of the SCF protein ubiquitin ligase involved in the auxin response. wei4, a dominant mutant, resulted from a mutation in the ethylene receptor ERS, whereas wei5, a semidominant mutant, was caused by a mutation in the EIN3-related transcription factor gene EIL1. The simultaneous loss of functional WEI5EIL1 and EIN3 nearly completely abolished the ethylene response in etiolated seedlings, and adult plants were highly susceptible to infection by the necrotrophic fungal pathogen Botrytis cinerea. Moreover, wei5eil1 ein3 double mutants were able to fully suppress constitutive signaling caused by ctr1, suggesting a synergistic interaction among these gene products. Unlike previously known root ethylene-insensitive mutants, wei2 and wei3 were not affected in their response to auxin and showed a normal response to gravity. Genetic mapping studies indicate that wei2 and wei3 correspond to previously unidentified ethylene pathway genes that may control cell-elongation processes functioning at the intersection of the ethylene and auxin response pathways.
通过对“弱”乙烯不敏感突变体进行低剂量筛选,鉴定出了五个乙烯不敏感位点(wei1-wei5)。wei1、wei2和wei3幼苗仅在根中表现出激素不敏感性,而wei4和wei5在根和下胚轴中均表现出不敏感性。使用定位克隆方法分离出了与wei1、wei4和wei5相对应的基因。wei1突变体在TIR1中存在隐性突变,TIR1编码参与生长素反应的SCF蛋白泛素连接酶的一个组分。wei4是一个显性突变体,由乙烯受体ERS中的突变导致,而wei5是一个半显性突变体,由EIN3相关转录因子基因EIL1中的突变引起。功能性WEI5EIL1和EIN3的同时缺失几乎完全消除了黄化幼苗中的乙烯反应,并且成年植株对坏死性真菌病原体灰葡萄孢高度敏感。此外,wei5eil1 ein3双突变体能够完全抑制由ctr1引起的组成型信号传导,表明这些基因产物之间存在协同相互作用。与先前已知的根乙烯不敏感突变体不同,wei2和wei3对生长素的反应不受影响,并且对重力表现出正常反应。遗传图谱研究表明,wei2和wei3对应于先前未鉴定的乙烯途径基因,这些基因可能控制在乙烯和生长素反应途径交叉点起作用的细胞伸长过程。