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The Xylanase Inhibitor TAXI-I Increases Plant Resistance to Botrytis cinerea by Inhibiting the BcXyn11a Xylanase Necrotizing Activity

机译:通过抑制BCXyn11a木聚糖酶坏死活性,木聚糖酶抑制剂的出租车 - 我增加了植物抵抗植物抵抗植物抵抗力

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摘要

During host plant infection, pathogens produce a wide array of cell wall degrading enzymes (CWDEs) to break the plant cell wall. Among CWDEs, xylanases are key enzymes in the degradation of xylan, the main component of hemicellulose. Targeted deletion experiments support the direct involvement of the xylanase BcXyn11a in the pathogenesis of Botrytis cinerea. Since the Triticum aestivum xylanase inhibitor-I (TAXI-I) has been shown to inhibit BcXyn11a, we verified if TAXI-I could be exploited to counteract B. cinerea infections. With this aim, we first produced Nicotiana tabacum plants transiently expressing TAXI-I, observing increased resistance to B. cinerea. Subsequently, we transformed Arabidopsis thaliana to express TAXI-I constitutively, and we obtained three transgenic lines exhibiting a variable amount of TAXI-I. The line with the higher level of TAXI-I showed increased resistance to B. cinerea and the absence of necrotic lesions when infiltrated with BcXyn11a. Finally, in a droplet application experiment on wild-type Arabidopsis leaves, TAXI-I prevented the necrotizing activity of BcXyn11a. These results would confirm that the contribution of BcXyn11a to virulence is due to its necrotizing rather than enzymatic activity. In conclusion, our experiments highlight the ability of the TAXI-I xylanase inhibitor to counteract B. cinerea infection presumably by preventing the necrotizing activity of BcXyn11a.
机译:在宿主植物感染期间,病原体产生各种细胞壁降解酶(CWDE)以破坏植物细胞壁。在CWDE中,木聚糖酶是Xylan降解的关键酶,半纤维素的主要成分。靶向缺失实验支持木聚糖酶BCxyn11a在Botrytis Cinerea的发病机制中的直接参与。由于Triticum Aestivum木聚糖酶抑制剂-i(出租车-I)已被证明抑制BCXyn11a,我们验证了出租车 - 我是否可以被利用以抵消B. cinerea感染。通过这种目标,我们首先生产尼古利亚纳塔巴蟾植物瞬间表达出租车 - 我,观察到B. cinerea的抗性增加。随后,我们转变拟南芥拟南芥来表达出租车 - 我组成型,我们获得了三种转基因系,表现出可变数量的出租车。具有较高水平的出租车-I表现出对B. cinerea的抗性增加,并且在用BCxyn11a渗透时没有坏死病变。最后,在野生型拟南芥叶上的液滴应用实验中,出租车 - 我阻止了Bcxyn11a的坏死性。这些结果将确认BCXyn11a对毒力的贡献是由于其坏死而不是酶活性。总之,我们的实验突出了出租车-I木聚糖酶抑制剂通过防止BCXyn11a的坏死活性来抵消B. ineerea感染的能力。

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