Polygalacturonase inhibiting protein (PGIP)

  • 文章类型: Journal Article
    病原体分泌的多聚半乳糖醛酸酶(PGs)通过裂解同半乳糖醛酸(HG)中D-半乳糖醛酸残基之间的α-(1→4)连接来改变植物细胞壁结构,浸软细胞壁,促进感染。植物PG抑制蛋白(PGIP)脱离病原体PG,损害感染。大豆胞囊线虫,异dera甘氨酸,专性根寄生虫产生分泌物,产生一个叫做合胞体的多核护士细胞,200-250个根细胞合并细胞质的副产品,通过细胞壁浸渍发生。常见的细胞质池,被完整的质膜包围着,提供H.glycines从中获得营养的来源,但在易感反应期间不会杀死被寄生的细胞。合胞体也是发生在特定G.max基因型中的天然发生的防御反应的位点。从经历防御过程的合胞体中分离的RNA的转录组学分析已经确定了11G最大PGIP中的一个,GmPGIP11在防御过程中表达。功能性转基因分析显示,与核糖体蛋白21(GmRPS21)对照相比,经历GmPGIP11过表达(OE)的根的相对转录物丰度(RTA)增加,与过表达对照相比,导致H.glycines寄生虫减少。与GmRPS21对照相比,经历RNAi的GmPGIP11经历其RTA降低,其中与RNAi对照相比,转基因根经历H.glycines寄生增加。显示病原体相关分子模式(PAMP)触发的免疫(PTI)和效应子触发的免疫(ETI)成分会影响GmPGIP11的表达,而许多农作物显示具有同源物。
    Pathogen-secreted polygalacturonases (PGs) alter plant cell wall structure by cleaving the α-(1 → 4) linkages between D-galacturonic acid residues in homogalacturonan (HG), macerating the cell wall, facilitating infection. Plant PG inhibiting proteins (PGIPs) disengage pathogen PGs, impairing infection. The soybean cyst nematode, Heterodera glycines, obligate root parasite produces secretions, generating a multinucleate nurse cell called a syncytium, a byproduct of the merged cytoplasm of 200-250 root cells, occurring through cell wall maceration. The common cytoplasmic pool, surrounded by an intact plasma membrane, provides a source from which H. glycines derives nourishment but without killing the parasitized cell during a susceptible reaction. The syncytium is also the site of a naturally-occurring defense response that happens in specific G. max genotypes. Transcriptomic analyses of RNA isolated from the syncytium undergoing the process of defense have identified that one of the 11 G. max PGIPs, GmPGIP11, is expressed during defense. Functional transgenic analyses show roots undergoing GmPGIP11 overexpression (OE) experience an increase in its relative transcript abundance (RTA) as compared to the ribosomal protein 21 (GmRPS21) control, leading to a decrease in H. glycines parasitism as compared to the overexpression control. The GmPGIP11 undergoing RNAi experiences a decrease in its RTA as compared to the GmRPS21 control with transgenic roots experiencing an increase in H. glycines parasitism as compared to the RNAi control. Pathogen associated molecular pattern (PAMP) triggered immunity (PTI) and effector triggered immunity (ETI) components are shown to influence GmPGIP11 expression while numerous agricultural crops are shown to have homologs.
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  • 文章类型: Journal Article
    The plant cell wall structure can be altered by pathogen-secreted polygalacturonases (PGs) that cleave the α-(1→4) linkages occurring between D-galacturonic acid residues in homogalacturonan. The activity of the PGs leads to cell wall maceration, facilitating infection. Plant PG inhibiting proteins (PGIPs) impede pathogen PGs, impairing infection and leading to the ability of the plant to resist infection. Analyses show the Glycine max PGIP11 (GmPGIP11) is expressed within a root cell that is parasitized by the pathogenic nematode Heterodera glycines, the soybean cyst nematode (SCN), but while undergoing a defence response that leads to its demise. Transgenic experiments show GmPGIP11 overexpression leads to a successful defence response, while the overexpression of a related G. max PGIP, GmPGIP1 does not, indicating a level of specificity. The analyses presented here have identified PGIPs from 51 additional studied proteomes, many of agricultural importance. The analyses include the computational identification of signal peptides and their cleavage sites, O-, and N-glycosylation. Artificial intelligence analyses determine the location where the processed protein localize. The identified PGIPs are presented as a tool base from which functional transgenics can be performed to determine whether they may have a role in plant-pathogen interactions.
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