downregulation of chloroplast rps1 negatively modulates nuclear heat-responsive expression of hsfa2 and its target genes in arabidopsisdownregulation叶绿体rps1负调节核热敏hsfa2表达式及其目标基因在拟南芥.pdfVIP
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downregulation of chloroplast rps1 negatively modulates nuclear heat-responsive expression of hsfa2 and its target genes in arabidopsisdownregulation叶绿体rps1负调节核热敏hsfa2表达式及其目标基因在拟南芥
Downregulation of Chloroplast RPS1 Negatively
Modulates Nuclear Heat-Responsive Expression of HsfA2
and Its Target Genes in Arabidopsis
Hai-Dong Yu, Xiao-Fei Yang, Si-Ting Chen, Yu-Ting Wang, Ji-Kai Li, Qi Shen, Xun-Liang Liu, Fang-
Qing Guo*
The National Key Laboratory of Plant Molecular Genetics and National Center for Plant Gene Research (Shanghai), Institute of Plant Physiology and Ecology, Shanghai
Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China
Abstract
Heat stress commonly leads to inhibition of photosynthesis in higher plants. The transcriptional induction of heat stress-
responsive genes represents the first line of inducible defense against imbalances in cellular homeostasis. Although heat
stress transcription factor HsfA2 and its downstream target genes are well studied, the regulatory mechanisms by which
HsfA2 is activated in response to heat stress remain elusive. Here, we show that chloroplast ribosomal protein S1 (RPS1) is a
heat-responsive protein and functions in protein biosynthesis in chloroplast. Knockdown of RPS1 expression in the rps1
mutant nearly eliminates the heat stress-activated expression of HsfA2 and its target genes, leading to a considerable loss of
heat tolerance. We further confirm the relationship existed between the downregulation of RPS1 expression and the loss of
heat tolerance by generating RNA interference-transgenic lines of RPS1. Consistent with the notion that the inhibited
activation of HsfA2 in response to heat stress in the rps1 mutant causes heat-susceptibility, we further demonstrate that
overexpression of HsfA2 with a viral promoter leads to constitutive expressions of its target genes in the rps1 mutant, which
is sufficient to reestablish lost heat tolerance and recovers heat-susceptible thylakoid stability to wild-type levels. Our
findings reveal a heat-r
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