质体参与植物激素代谢以及光合作用。然而,质体逆行信号和植物激素协同调节质体生物发生的机制仍然难以捉摸。这里,我们研究了产生生物质体信号的抑制剂和突变对植物激素的影响,反之亦然。通过去甲氟拉松(NF)处理抑制质体生物生成和质体蛋白import2(ppi2)突变导致水杨酸(SA)和茉莉酸(JA)减少。这种效应可部分归因于参与SA和JA的生物合成和代谢的基因表达的改变。然而,在NF处理的植物和ppi2突变体中,对病因发生-相关基因的SA依赖性诱导几乎不受影响。相反,通过外源施用SA,这些植物中的叶绿素水平得到了部分恢复。与这一观察一致,响应于SA处理,在ppi2和NF处理的植物中,某些光合作用相关蛋白的水平增加。真叶中的这种调节似乎发生在转录后水平,因为SA处理没有诱导光合作用相关基因的表达。在水杨酸诱导缺陷2和病变模拟抗病性1突变体中,内源性SA通过转录和转录后机制调节光合作用相关蛋白的积累。这些数据表明,SA通过促进拟南芥中光合作用相关蛋白的积累,拮抗质体生物发生的抑制,表明SA和生物质体信号之间可能存在联系。
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.