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低谷胱甘肽调节拟南芥中的基因表达以及细胞核和细胞质的氧化还原电位。

Low glutathione regulates gene expression and the redox potentials of the nucleus and cytosol in Arabidopsis thaliana.

作者信息

Schnaubelt Daniel, Queval Guillaume, Dong Yingping, Diaz-Vivancos Pedro, Makgopa Matome Eugene, Howell Gareth, De Simone Ambra, Bai Juan, Hannah Matthew A, Foyer Christine H

机构信息

Centre for Plant Sciences, School of Biology, University of Leeds, Leeds, LS2 9JT, UK.

出版信息

Plant Cell Environ. 2015 Feb;38(2):266-79. doi: 10.1111/pce.12252. Epub 2014 Jan 13.

Abstract

Reduced glutathione (GSH) is considered to exert a strong influence on cellular redox homeostasis and to regulate gene expression, but these processes remain poorly characterized. Severe GSH depletion specifically inhibited root meristem development, while low root GSH levels decreased lateral root densities. The redox potential of the nucleus and cytosol of Arabidopsis thaliana roots determined using roGFP probes was between -300 and -320 mV. Growth in the presence of the GSH-synthesis inhibitor buthionine sulfoximine (BSO) increased the nuclear and cytosolic redox potentials to approximately -260 mV. GSH-responsive genes including transcription factors (SPATULA, MYB15, MYB75), proteins involved in cell division, redox regulation (glutaredoxinS17, thioredoxins, ACHT5 and TH8) and auxin signalling (HECATE), were identified in the GSH-deficient root meristemless 1-1 (rml1-1) mutant, and in other GSH-synthesis mutants (rax1-1, cad2-1, pad2-1) as well as in the wild type following the addition of BSO. Inhibition of auxin transport had no effect on organ GSH levels, but exogenous auxin decreased the root GSH pool. We conclude that GSH depletion significantly increases the redox potentials of the nucleus and cytosol, and causes arrest of the cell cycle in roots but not shoots, with accompanying transcript changes linked to altered hormone responses, but not oxidative stress.

摘要

还原型谷胱甘肽(GSH)被认为对细胞氧化还原稳态有强大影响并能调节基因表达,但这些过程仍未得到充分表征。严重的GSH耗竭特异性抑制根分生组织发育,而低水平的根GSH会降低侧根密度。使用roGFP探针测定的拟南芥根细胞核和细胞质的氧化还原电位在-300至-320 mV之间。在谷胱甘肽合成抑制剂丁硫氨酸亚砜胺(BSO)存在下生长会使细胞核和细胞质的氧化还原电位增加到约-260 mV。在GSH缺乏的无根分生组织1-1(rml1-1)突变体、其他GSH合成突变体(rax1-1、cad2-1、pad2-1)以及添加BSO后的野生型中,鉴定出了GSH响应基因,包括转录因子(SPATULA、MYB15、MYB75)、参与细胞分裂的蛋白质、氧化还原调节蛋白(谷氧还蛋白S17、硫氧还蛋白、ACHT5和TH8)以及生长素信号传导蛋白(HECATE)。生长素运输的抑制对器官GSH水平没有影响,但外源生长素会降低根中的GSH库。我们得出结论,GSH耗竭会显著增加细胞核和细胞质的氧化还原电位,并导致根而非地上部分的细胞周期停滞,同时伴随与激素反应改变相关的转录变化,但与氧化应激无关。

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