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拟南芥盐敏感突变体中脯氨酸积累及盐胁迫诱导的基因表达

Proline accumulation and salt-stress-induced gene expression in a salt-hypersensitive mutant of Arabidopsis.

作者信息

Liu J, Zhu J K

机构信息

Department of Plant Sciences, University of Arizona, Tucson 85721, USA.

出版信息

Plant Physiol. 1997 Jun;114(2):591-6. doi: 10.1104/pp.114.2.591.

DOI:10.1104/pp.114.2.591
PMID:9193091
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC158341/
Abstract

The sos1 mutant of Arabidopsis thaliana is more than 20 times more sensitive to NaCl stress than wild type Arabidopsis. Because proline (Pro) is generally thought to have an important role in plant salt tolerance, the sos1 mutant and the wild type were compared with respect to their capacity to accumulate Pro under NaCl stress, and sos1 mutant plants accumulated more Pro than wild-type. The P5CS gene, which catalyzes the rate-limiting step in Pro biosynthesis, is induced by salt stress to a higher level in sos1 than in the wild type. Although a defective high-affinity K uptake system in sos1 causes K deficiency and inhibits growth in NaCl-treated plants, this decrease is not a sufficient signal for Pro accumulation and P5CS gene expression. Not all salt-stress-induced genes have a higher level of expression in sos1. The expression levels of AtPLC and RD29A, which encode a phospholipase C homolog and a putative protective protein, respectively, are the same in sos1 as in the wild type. However, the expression of AtMYB, which encodes a putative transcriptional factor, is induced to a much higher level by salt stress in sos1. Thus, the SOS1 gene product serves as a negative regulator for the expression of P5CS and AtMYB, but has no effect on AtPLC and RD29A expression.

摘要

拟南芥的sos1突变体对NaCl胁迫的敏感性比野生型拟南芥高20多倍。由于脯氨酸(Pro)通常被认为在植物耐盐性中起重要作用,因此比较了sos1突变体和野生型在NaCl胁迫下积累Pro的能力,结果发现sos1突变体植株比野生型积累了更多的Pro。催化Pro生物合成限速步骤的P5CS基因,在盐胁迫下在sos1中的诱导水平高于野生型。尽管sos1中存在缺陷的高亲和力钾吸收系统会导致钾缺乏并抑制NaCl处理植株的生长,但这种减少并不是Pro积累和P5CS基因表达的充分信号。并非所有盐胁迫诱导基因在sos1中的表达水平都更高。分别编码磷脂酶C同源物和假定保护蛋白的AtPLC和RD29A的表达水平在sos1和野生型中相同。然而,编码假定转录因子的AtMYB的表达在盐胁迫下在sos1中被诱导到更高水平。因此,SOS1基因产物作为P5CS和AtMYB表达的负调节因子,但对AtPLC和RD29A的表达没有影响。

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