The non-host pathogen Botrytis cinerea enhances glucose transport in Pinus pinaster suspension-cultured cells
The non-host pathogen Botrytis cinerea enhances glucose transport in Pinus pinaster suspension-cultured cells
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DOI：
10.1093/pcp/pci248
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发表时间：
2006-02-01
影响因子：
4.9
通讯作者：
Tavares, RM
中科院分区：
文献类型：
--
作者：
Azevedo, H;Conde, C;Tavares, RM
灰葡萄孢（Botrytis cinerea）是海松灰霉病的病原菌，是海松的一种非寄主性坏死营养型病原菌。最近的证据表明，病原体挑战可以改变植物细胞的碳吸收;然而，人们对激发子衍生的信号通路如何控制糖转运活性知之甚少。Ppinaster悬浮细胞能够以高亲和力吸收D-[C-14]葡萄糖，具有H+依赖性转运系统（K-m，0.07 mM; V-max，1.5 nmol min（-1）mg（-1）DW），对D-葡萄糖、D-果糖、D-半乳糖和D-木糖具有特异性，并且经受葡萄糖阻遏。当被B引出时。在灰霉病孢子中，悬浮细胞表现出钙依赖性双相活性氧（ROS）产生，第二次爆发也依赖于NADPH氧化酶、促分裂原活化蛋白激酶（MAPK）以及从头转录和蛋白质合成。激发后24小时，在无糖培养基中孵育的挑战悬浮细胞导致葡萄糖转运能力比非激发培养物增加高达3倍，比用2%葡萄糖孵育的激发细胞增加14倍。葡萄糖摄取的增强依赖于NADPH氧化酶和钙内流，而不是MAPK。相反，糖饥饿诱导的葡萄糖转运活性的增加依赖于MAPK的激活，而不是NADPH氧化酶。这两种反应似乎都依赖于从头转录和蛋白质合成。
Botrytis cinerea is the causal agent of grey mould disease and a non-host necrotrophic pathogen of maritime pine (Pinus pinaster). Recent evidence suggests that pathogen challenge can alter carbon uptake in plant cells; however, little is known on how elicitor-derived signalling pathways control sugar transport activity. P pinaster suspended cells are able to absorb D-[C-14]glucose with high affinity, have an H+-dependent transport system (K-m, 0.07 mM; V-max, 1.5 nmol min(-1) mg(-1) DW), are specific for D-glucose, D-fructose, D-galactose and D-xylose, and are subject to glucose repression. When elicited by B. cinera spores, suspended cells exhibit calcium-dependent biphasic reactive oxygen species (ROS) production, the second burst also being dependent on NADPH oxidase, mitogen-activated protein kinase (MAPK), and de novo transcription and protein synthesis. Challenging suspended cells incubated in sugar-free medium resulted in an up to 3-fold increase in glucose transport capacity over non-elicited cultures 24 h after elicitation, and a 14-fold increase over elicited cells incubated with 2% glucose. Enhanced glucose uptake depended on NADPH oxidase and calcium influx, but not MAPK. In contrast, the increase of glucose transport activity induced by sugar starvation was dependent on the activation of MAPK but not NADPH oxidase. Both responses appeared to be dependent on de novo transcription and protein synthesis.