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拟南芥ROF1(FKBP62)通过与HSP90.1相互作用并影响HsfA2调控的小分子热激蛋白(sHSPs)的积累来调节耐热性。

Arabidopsis ROF1 (FKBP62) modulates thermotolerance by interacting with HSP90.1 and affecting the accumulation of HsfA2-regulated sHSPs.

作者信息

Meiri David, Breiman Adina

机构信息

Department of Plant Sciences, Tel Aviv University, Tel Aviv, Israel.

出版信息

Plant J. 2009 Aug;59(3):387-99. doi: 10.1111/j.1365-313X.2009.03878.x. Epub 2009 Apr 2.

Abstract

Arabidopsis ROF1 (AtFKBP62) is a peptidyl prolyl cis/trans isomerase and a member of the FKBP (FK506 binding protein) family. ROF1 expression is induced by heat stress and developmentally regulated. In this study, we show that ROF1 binds heat shock proteins HSP90.1 via its tetratricopeptide repeat domain, and localizes in the cytoplasm under normal conditions. Exposure to heat stress induces nuclear localization of the ROF1-HSP90.1 complex, which is dependent upon the presence of the transcription factor HsfA2, which interacts with HSP90.1 but not with ROF1. Nuclear localization of ROF1 was not detected in Arabidopsis HSP90.1 and HsfA2 knockout mutants. The rof1 knockout plants exhibited collapse when 24-48 h passed between acclimation at 37 degrees C and exposure to 45 degrees C. Transgenic ROF1 over-expressors showed better survival in response to exposure to 45 degrees C than wild-type plants did. In rof1 knockout mutants, the level of expression of small HSPs regulated by HsfA2 was dramatically reduced after exposure to 37 degrees C and recovery for 24-48 h, and correlates well with the mutant phenotype. We suggest a role for ROF1 in prolongation of thermotolerance by sustaining the levels of small HSPs that are essential for survival at high temperatures.

摘要

拟南芥ROF1(AtFKBP62)是一种肽基脯氨酰顺/反异构酶,属于FKBP(FK506结合蛋白)家族成员。ROF1的表达受热胁迫诱导且受发育调控。在本研究中,我们发现ROF1通过其四肽重复结构域与热休克蛋白HSP90.1结合,并且在正常条件下定位于细胞质中。热胁迫处理会诱导ROF1 - HSP90.1复合物的核定位,这依赖于转录因子HsfA2的存在,HsfA2与HSP90.1相互作用但不与ROF1相互作用。在拟南芥HSP90.1和HsfA2基因敲除突变体中未检测到ROF1的核定位。当在37℃驯化和暴露于45℃之间间隔24 - 48小时时,rof1基因敲除植株出现萎蔫。转基因ROF1过表达植株在暴露于45℃时比野生型植株表现出更好的存活率。在rof1基因敲除突变体中,经37℃处理并恢复24 - 48小时后,受HsfA2调控的小分子热休克蛋白的表达水平显著降低,且与突变体表型密切相关。我们认为ROF1通过维持高温下生存所必需的小分子热休克蛋白水平,在延长耐热性方面发挥作用。

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