The slow wound-response of γVPE is regulated by endogenous salicylic acid in Arabidopsis
The slow wound-response of γVPE is regulated by endogenous salicylic acid in Arabidopsis
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DOI：
10.1007/s00425-003-1131-3
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发表时间：
2004-02-01
期刊：
影响因子：
4.3
通讯作者：
Hara-Nishimura, I
中科院分区：
文献类型：
--
作者：
Yamada, K;Nishimura, M;Hara-Nishimura, I
液泡加工酶（VPE）是一种半胱氨酸蛋白酶，在高等植物中负责各种液泡蛋白的成熟。拟南芥（Arabidopsis thaliana（L.）嘿γ VPE基因编码VPE同源物，在局部和系统叶片中响应于创伤而缓慢上调。为了阐明gammaVPE的激活机制，我们研究了激素处理后或受伤后的野生型和各种突变体植物的拟南芥中gammaVPE mRNA的积累。乙烯和茉莉酸（JA）都被认为是激活伤口反应基因的信号分子。然而，外源JA处理对γ-VPE反应的影响很小，尽管JA激活了典型的创伤反应基因--营养贮藏蛋白（VSP）基因。甚至在两种乙烯不敏感的植物（etr 1 -1和ein 2 -1）中，创伤激活了γ VPE。因此，创伤诱导的γ VPE表达是独立的乙烯和JA。我们发现，在两个SA缺陷的植物（pad 4 -1和NahG）的创伤诱导的表达γ VPE减少，而在这些突变体的创伤诱导的VSP的表达增加。受伤后，在局部或系统叶片中均未观察到SA的可观积累。这些结果表明，内源性SA增强创伤诱导的γ VPE的表达和减弱创伤诱导的VSP的表达，尽管SA不是直接激活这些基因的创伤信号。
Vacuolar processing enzyme (VPE) is a cysteine protease responsible for the maturation of various vacuolar proteins in higher plants. The Arabidopsis thaliana (L.) Heynh. gammaVPE gene, encoding a VPE homologue, is slowly up-regulated in both local and systemic leaves in response to wounding. To clarify the activation mechanism of gammaVPE, we examined the accumulation of gammaVPE mRNA after hormone treatments or after wounding in wild-type and various mutant plants of Arabidopsis. Both ethylene and jasmonic acid (JA) are known as signal molecules that activate the wound-responsive genes. However, treatment with exogenous JA had little effect on the gammaVPE response, although JA activated the vegetative storage protein (VSP) gene, a typical wound-responsive gene. Wounding activated gammaVPE even in two ethylene-insensitive plants (etr1-1 and ein2-1). Thus, the wound-induced expression of gammaVPE was independent of ethylene and JA. We found that the wound-induced expression of gammaVPE was reduced in two SA-deficient plants (pad4-1 and NahG), while the wound-induced expression of VSP increased in these mutants. Appreciable accumulation of SA was not observed in either the local or systemic leaves after wounding. These results suggest that endogenous SA enhances the wound-induced expression of gammaVPE and attenuates the wound-induced expression of VSP, although SA is not a wound-signal that directly activates these genes.