Independent signaling pathways regulate cellular turgor during hyperosmotic stress and appressorium-mediated plant infection by Magnaporthe grisea
Independent signaling pathways regulate cellular turgor during hyperosmotic stress and appressorium-mediated plant infection by Magnaporthe grisea
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DOI：
10.1105/tpc.11.10.2045
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发表时间：
1999-10-01
期刊：
影响因子：
11.6
通讯作者：
Talbot, NJ
中科院分区：
文献类型：
--
作者：
Dixon, KP;Xu, JR;Talbot, NJ
稻瘟病菌（Magnaporthe grisea）有一种专门的感染细胞，称为附着胞，它可以机械地破坏植物的角质层。为了产生机械力，附着胞通过积累摩尔浓度的甘油产生巨大的静水压力。为了研究细胞膨压的遗传控制，我们分析了M。稻瘟病菌对高渗胁迫的反应。在急性和慢性高渗应激适应过程中，M.除了少量的甘油之外，稻瘟菌还积累阿拉伯糖醇作为其主要的相容溶质。从M.在稻瘟病菌中发现了一个编码高渗甘油1（HOG 1）功能同源物的基因，HOG 1编码一种调节酵母细胞膨压的促分裂原活化蛋白激酶。在M.通过靶向基因置换，将稻瘟病菌转化为稻瘟病菌，得到的突变体对渗透胁迫敏感，在高渗条件下生长时表现出形态缺陷。M. grisea Delta osm1突变体在菌丝体中积累阿拉伯糖醇的能力显著降低。令人惊讶的是，甘油积累和膨压产生附着胞未改变的Delta osm1无效突变，突变体是完全致病的。这一结果表明，在高渗胁迫和附着胞介导的植物感染过程中，独立的信号转导途径调节细胞膨压。与此相一致，M.稻瘟病菌附着胞对外部高渗胁迫诱导的OSM1依赖的阿拉伯糖醇的产生。
The phytopathogenic fungus Magnaporthe grisea elaborates a specialized infection cell called an appressorium with which it mechanically ruptures the plant cuticle. To generate mechanical force, appressoria produce enormous hydrostatic turgor by accumulating molar concentrations of glycerol. To investigate the genetic control of cellular turgor, we analyzed the response of M. grisea to hyperosmotic stress. During acute and chronic hyperosmotic stress adaptation, M. grisea accumulates arabitol as its major compatible solute in addition to smaller quantities of glycerol. A mitogen-activated protein kinase-encoding gene OSM1 was isolated from M. grisea and shown to encode a functional homolog of HIGH-OSMOLARITY GLYCEROL1 (HOG1), which encodes a mitogen-activated protein kinase that regulates cellular turgor in yeast. A null mutation of OSM1 was generated in M. grisea by targeted gene replacement, and the resulting mutants were sensitive to osmotic stress and showed morphological defects when grown under hyperosmotic conditions. M. grisea Delta osm1 mutants showed a dramatically reduced ability to accumulate arabitol in the mycelium. Surprisingly, glycerol accumulation and turgor generation in appressoria were unaltered by the Delta osm1 null mutation, and the mutants were fully pathogenic. This result indicates that independent signal transduction pathways regulate cellular turgor during hyperosmotic stress and appressorium-mediated plant infection. Consistent with this, exposure of M. grisea appressoria to external hyperosmotic stress induced OSM1-dependent production of arabitol.