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在拟南芥中,光敏色素生色团缺乏会导致茉莉酸过量产生以及茉莉酸响应基因的表达升高。

Phytochrome chromophore deficiency leads to overproduction of jasmonic acid and elevated expression of jasmonate-responsive genes in Arabidopsis.

作者信息

Zhai Qingzhe, Li Chang-Bao, Zheng Wenguang, Wu Xiaoyan, Zhao Jiuhai, Zhou Guoxin, Jiang Hongling, Sun Jiaqiang, Lou Yonggen, Li Chuanyou

机构信息

State Key Laboratory of Plant Genomics and National Center for Plant Gene Research, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, PR China.

出版信息

Plant Cell Physiol. 2007 Jul;48(7):1061-71. doi: 10.1093/pcp/pcm076. Epub 2007 Jun 13.

Abstract

An Arabidopsis mutant line named hy1-101 was isolated because it shows stunted root growth on medium containing low concentrations of jasmonic acid (JA). Subsequent investigation indicated that even in the absence of JA, hy1-101 plants exhibit shorter roots and express higher levels of a group of JA-inducible defense genes. Here, we show that the hy1-101 mutant has increased production of JA and its jasmonate-related phenotype is suppressed by the coi1-1 mutation that interrupts JA signaling. Gene cloning and genetic complementation analyses revealed that the hy1-101 mutant contains a mutation in the HY1 gene, which encodes a heme oxygenase essential for phytochrome chromophore biosynthesis. These results support a hypothesis that phytochrome chromophore deficiency leads to overproduction of JA and activates COI1-dependent JA responses. Indeed, we show that, like hy1-101, independent alleles of the phytochrome chromophore-deficient mutants, including hy1-100 and hy2 (CS68), also show elevated JA levels and constant expression of JA-inducible defense genes. We further provide evidence showing that, on the other hand, JA inhibits the expression of a group of light-inducible and photosynthesis-related genes. Together, these data imply that the JA-signaled defense pathway and phytochrome chromophore-mediated light signaling might have antagonistic effects on each other.

摘要

一个名为hy1-101的拟南芥突变株系被分离出来,因为它在含有低浓度茉莉酸(JA)的培养基上表现出根系生长受阻。随后的研究表明,即使在没有JA的情况下,hy1-101植株也表现出较短的根,并表达一组JA诱导型防御基因的较高水平。在这里,我们表明hy1-101突变体中JA的产生增加,并且其茉莉酸相关表型被中断JA信号传导的coi1-1突变所抑制。基因克隆和遗传互补分析表明,hy1-101突变体在HY1基因中存在一个突变,该基因编码一种对光敏色素发色团生物合成至关重要的血红素加氧酶。这些结果支持了一个假设,即光敏色素发色团缺乏导致JA的过量产生,并激活依赖COI1的JA反应。事实上,我们表明,与hy1-101一样,包括hy1-100和hy2(CS68)在内的光敏色素发色团缺陷突变体的独立等位基因也显示出JA水平升高和JA诱导型防御基因的持续表达。另一方面,我们进一步提供证据表明,JA抑制一组光诱导和光合作用相关基因的表达。总之,这些数据表明JA信号传导的防御途径和光敏色素发色团介导的光信号传导可能相互拮抗。

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