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ERS1和ETR1跨膜结构域III中的显性功能获得性突变表明该结构域在调节拟南芥乙烯反应强度方面具有新作用。

Dominant gain-of-function mutations in transmembrane domain III of ERS1 and ETR1 suggest a novel role for this domain in regulating the magnitude of ethylene response in Arabidopsis.

作者信息

Deslauriers Stephen D, Alvarez Ashley A, Lacey Randy F, Binder Brad M, Larsen Paul B

机构信息

Department of Biochemistry, University of California, Riverside, CA, 92521, USA.

Department of Biochemistry, Cellular and Molecular Biology, University of Tennessee, Knoxville, TN, 37996, USA.

出版信息

New Phytol. 2015 Oct;208(2):442-55. doi: 10.1111/nph.13466. Epub 2015 May 19.

Abstract

Prior work resulted in identification of an Arabidopsis mutant, eer5-1, with extreme ethylene response in conjunction with failure to induce a subset of ethylene-responsive genes, including AtEBP. EER5, which is a TREX-2 homolog that is part of a nucleoporin complex, functions as part of a cryptic aspect of the ethylene signaling pathway that is required for regulating the magnitude of ethylene response. A suppressor mutagenesis screen was carried out to identify second site mutations that could restore the growth of ethylene-treated eer5-1 to wild-type levels. A dominant gain-of-function mutation in the ethylene receptor ETHYLENE RESPONSE SENSOR 1 (ERS1) was identified, with the ers1-4 mutation being located in transmembrane domain III at a point nearly equivalent to the previously described etr1-2 mutation in the other Arabidopsis subfamily I ethylene receptor, ETHYLENE RESPONSE 1 (ETR1). Although both ers1-4 and etr1-2 partially suppress the ethylene hypersensitivity of eer5-1 and are at least in part REVERSION TO ETHYLENE SENSITIVITY 1 (RTE1)-dependent, ers1-4 was additionally found to restore the expression of AtEBP in ers1-4;eer5-1 etiolated seedlings after ethylene treatment in an EIN3-dependent manner. Our work indicates that ERS1-regulated expression of a subset of ethylene-responsive genes is related to controlling the magnitude of ethylene response, with hyperinduction of these genes correlated with reduced ethylene-dependent growth inhibition.

摘要

先前的研究工作鉴定出了拟南芥突变体eer5-1,其具有极端的乙烯反应,同时无法诱导包括AtEBP在内的一部分乙烯反应基因。EER5是核孔蛋白复合体一部分的TREX-2同源物,作为乙烯信号通路中一个隐秘部分发挥作用,该部分对于调节乙烯反应的强度是必需的。进行了抑制子诱变筛选,以鉴定能够将乙烯处理的eer5-1的生长恢复到野生型水平的第二位点突变。在乙烯受体乙烯反应传感器1(ERS1)中鉴定出一个显性功能获得性突变,其中ers1-4突变位于跨膜结构域III中的一个点,该点几乎等同于另一个拟南芥亚家族I乙烯受体乙烯反应1(ETR1)中先前描述的etr1-2突变。尽管ers1-4和etr1-2都部分抑制了eer5-1的乙烯超敏性,并且至少部分依赖于乙烯敏感性恢复1(RTE1),但还发现ers1-4以EIN3依赖的方式恢复了乙烯处理后的ers1-4;eer5-1黄化幼苗中AtEBP的表达。我们的工作表明,ERS1调节的一部分乙烯反应基因的表达与控制乙烯反应的强度有关,这些基因的过度诱导与乙烯依赖性生长抑制的降低相关。

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