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Molecular evidence for the involvement of a polygalacturonase-inhibiting protein, GhPGIP1, in enhanced resistance to Verticillium and Fusarium wilts in cotton

机译:抑制聚乳糖醛酸酶抑制蛋白,GHPGIP1的分子证据,在棉花中增强对牙菌和镰刀菌菌株的抗性

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Polygalacturonase-inhibiting protein (PGIP), belonging to a group of plant defence proteins, specifically inhibits endopolygalacturonases secreted by pathogens. Herein, we showed that purified GhPGIP1 is a functional inhibitor of Verticillium dahliae and Fusarium oxysporum f. sp. vasinfectum, the two fungal pathogens causing cotton wilt. Transcription of GhPGIP1 was increased in cotton upon infection, wounding, and treatment with defence hormone and H2O2. Resistance by GhPGIP1 was examined by its virus-induced gene silencing in cotton and overexpression in Arabidopsis. GhPGIP1-silenced cotton was highly susceptible to the infections. GhPGIP1 overexpression in transgenic Arabidopsis conferred resistance to the infection, accompanied by enhanced expression of pathogenesis-related proteins (PRs), isochorismate synthase 1 (ICS1), enhanced disease susceptibility 1 (EDS1), and phytoalexin-deficient 4 (PAD4) genes. Transmission electron microscopy revealed cell wall alteration and cell disintegration in plants inoculated with polygalacturonase (PGs), implying its role in damaging the cell wall. Docking studies showed that GhPGIP1 interacted strongly with C-terminal of V. dahliae PG1 (VdPG1) beyond the active site but weakly interacted with C-terminal of F. oxysporum f. sp. vasinfectum (FovPG1). These findings will contribute towards the understanding of the roles of PGIPs and in screening potential combat proteins with novel recognition specificities against evolving pathogenic factors for countering pathogen invasion.
机译:抑制蛋白质(PGIP),属于一组植物防御蛋白质,具体抑制病原体分泌的内核酶酶。在此,我们表明纯化的GHPGIP1是患有黄石菊酯的官能抑制剂和镰刀菌。 sp。血染蛋白,两种真菌病原体导致棉花枯萎病。通过防御激素和H 2 O 2对棉花进行GHPGIP1的转录增加。通过拟南芥中的棉花和过表达的病毒诱导的基因检查GHPGIP1的抵抗力。 GHPGIP1沉默的棉花极易患感染。转基因拟南芥的GHPGIP1过表达赋予感染的抵抗力,伴随着增强的发病机制相关蛋白(PRS),同化性合酶1(ICS1),增强疾病易感性1(EDS1)和植物缺乏4(PAD4)基因的表达。透射电子显微镜显示植物中接种的植物中的细胞壁改变和细胞崩解,暗示其在损害细胞壁中的作用。对接研究表明,GHPGIP1与V. Dahliae PG1(VDPG1)的C末端相互作用,超出活性位点,但与F. oxysporum f的C末端弱相互作用。 sp。 vasinfectum(fovpg1)。这些发现将有助于了解PGIPS的作用以及筛选具有新颖识别特异性的潜在作战蛋白,免受用于抵抗病原体侵袭的不断致病因子。

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