Salicylic Acid Acts Antagonistically to Plastid Retrograde Signaling by Promoting the Accumulation of Photosynthesis-associated Proteins in Arabidopsis
Salicylic Acid Acts Antagonistically to Plastid Retrograde Signaling by Promoting the Accumulation of Photosynthesis-associated Proteins in Arabidopsis
复制标题
DOI：
10.1093/pcp/pcab128
复制
发表时间：
2021-09-15
影响因子：
4.9
通讯作者：
Inaba, Takehito
中科院分区：
文献类型：
--
作者：
Hirosawa, Yoshihiro;Tada, Akari;Inaba, Takehito
质体参与植物激素代谢和光合作用。然而，质体逆行信号和植物激素协同调控质体生物发生的机制仍然是难以捉摸的。在这里，我们研究了抑制剂和突变，产生生物质体信号对植物激素的影响，反之亦然。抑制质体生物合成的氟草酮（NF）处理和质体蛋白导入2（ppi 2）突变引起水杨酸（SA）和茉莉酸（JA）的减少。这种效应可以部分归因于参与SA和JA的生物合成和代谢的基因的表达改变。然而，SA-依赖诱导的致病性-pathogenesis-associated ATED 1基因几乎不受NF-处理的植物和ppi 2突变体。相反，在这些植物中的叶绿素水平部分恢复了外源性SA的应用。与此观察结果一致，一些光合作用相关蛋白的水平增加PPI 2和NF处理的植物响应SA处理。在真叶中的这种调节似乎发生在转录后水平，因为SA处理没有诱导光合相关基因的表达。在水杨酸诱导缺陷2和模拟病害抗性1突变体中，内源SA通过转录和转录后机制调节光合相关蛋白的积累。这些数据表明，SA通过促进拟南芥中光合相关蛋白的积累来拮抗质体生物发生的抑制，这表明SA和生物质体信号传导之间可能存在联系。
Plastids are involved in phytohormone metabolism as well as photosynthesis. However, the mechanism by which plastid retrograde signals and phytohormones cooperatively regulate plastid biogenesis remains elusive. Here, we investigated the effects of an inhibitor and a mutation that generate biogenic plastid signals on phytohormones and vice versa. Inhibition of plastid biogenesis by norflurazon (NF) treatment and the plastid protein import2 (ppi2) mutation caused a decrease in salicylic acid (SA) and jasmonic acid (JA). This effect can be attributed in part to the altered expression of genes involved in the biosynthesis and the metabolism of SA and JA. However, SA-dependent induction of the PATHOGENESIS-RELATED1 gene was virtually unaffected in NF-treated plants and the ppi2 mutant. Instead, the level of chlorophyll in these plants was partially restored by the exogenous application of SA. Consistent with this observation, the levels of some photosynthesis-associated proteins increased in the ppi2 and NF-treated plants in response to SA treatment. This regulation in true leaves seems to occur at the posttranscriptional level since SA treatment did not induce the expression of photosynthesis-associated genes. In salicylic acid induction deficient 2 and lesions simulating disease resistance 1 mutants, endogenous SA regulates the accumulation of photosynthesis-associated proteins through transcriptional and posttranscriptional mechanisms. These data indicate that SA acts antagonistically to the inhibition of plastid biogenesis by promoting the accumulation of photosynthesis-associated proteins in Arabidopsis, suggesting a possible link between SA and biogenic plastid signaling.