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bacteria:t3e:xopc [2020/08/07 15:29] kalyanmondal [XopC] |
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- | ====== XopC ====== | ||
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- | Author: [[https:// | ||
- | Internal reviewer: [[https:// | ||
- | Expert reviewer: FIXME | ||
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- | Class: XopC\\ | ||
- | Family: XopC\\ | ||
- | Prototype: XCV2435 (// | ||
- | RefSeq ID: [[https:// | ||
- | 3D structure: Unknown | ||
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- | ===== Biological function ===== | ||
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- | === How discovered? === | ||
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- | XopC was discovered in //X. campestris// | ||
- | === (Experimental) evidence for being a T3E === | ||
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- | A chimeric protein consisting of XopC fused to a c-myc epitope (first 466 amino acids plus 5 kDa epitope) was secreted into culture supernatants of a strain with a constitutively active form of HrpG in a type III secretion-dependent manner (Noël //et al//., 2003). Another chimeric protein consisting of XopC fused to an N-terminally deleted derivative of the effector protein AvrBs3 (XopC< | ||
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- | Type III-dependent secretion was also confirmed using a calmodulin-dependent adenylate cyclase reporter assay, with a Δ//hrpF// mutant strain serving as negative control (Roden //et al//., 2004). | ||
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- | Translocation of the XopC:: | ||
- | === Regulation === | ||
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- | The //xopC// gene was shown to be expressed in a //hrpG//- and // | ||
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- | qRT-PCR revealed that transcript levels of 15 out of 18 tested non-TAL effector genes (as well as the regulatory genes //hrpG// and //hrpX//), including //xopC//, were significantly reduced in the // | ||
- | === Phenotypes === | ||
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- | * A deletion of // | ||
- | * Roden et al. did not find significant growth defects of a // | ||
- | * Later, 86 // | ||
- | * The absence of // | ||
- | * Virus-induced gene silencing (VIGS) of OAS-TL in planta abolished the acceleration of AvrBs1-mediated HR formation induced by the absence of // | ||
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- | === Localization === | ||
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- | XopC localises to the plant cell cytoplasm and the nucleus (Herzfeld, 2013). | ||
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- | === Enzymatic function === | ||
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- | XopC contains a predicted phosphoribosyl transferase domain and a putative haloacid dehalogenase (HAD)-like hydrolase domain in its C-terminal end. Phenotype of point mutation in catalytic domain have shown that HAD-like hydrolase activity is required for the XopC deleterious effect in yeast (Salomon //et al//., 2011). | ||
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- | === Interaction partners === | ||
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- | Yeast-2-hybrid studies revealed a XopC interactor, which also interacted with XopC in planta. The interactor localises to the plant cell cytoplasm and carries typical features of plant cytosolic O-acetylserine (thiol)lyases (OAS-TL). It shows OAS-TL activity in vivo and in vitro. The latter one is enhanced by adding XopC (Herzfeld, 2013). | ||
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- | ===== Conservation ===== | ||
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- | === In xanthomonads === | ||
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- | Close, full-length homologs (>90% sequence identity) of XopC1 have only been found in several strains of clade-2 xanthomonads, | ||
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- | The distantly related XopC2 has homologs in //X. citri//, //X. euvesicatoria//, | ||
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- | === In other plant pathogens/ | ||
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- | XopC1: //Ralstonia solanacearum// | ||
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- | XopC2: // | ||
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- | ===== References ===== | ||
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- | Adlung N, Prochaska H, Thieme S, Banik A, Blüher D, John P, Nagel O, Schulze S, Gantner J, Delker C, Stuttmann J, Bonas U (2006). Non-host resistance induced by the // | ||
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- | Büttner D, Lorenz C, Weber E, Bonas U (2006). Targeting of two effector protein classes to the type III secretion system by a HpaC- and HpaB-dependent protein complex from // | ||
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- | Herzfeld EM (2013). Identifizierung und Charakterisierung von dem pflanzlichen Interaktionspartner OAS-TL des Typ-III-Effektors XopC. Doctoral Thesis, Martin-Luther-Universität Halle-Wittenberg, | ||
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- | Liu Y, Long J, Shen D, Song C (2016). // | ||
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- | Noël L, Thieme F, Gäbler J, Büttner D, Bonas U (2003). XopC and XopJ, two novel type III effector proteins from // | ||
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- | Noël L, Thieme F, Nennstiel D, Bonas U (2001). cDNA-AFLP analysis unravels a genome-wide // | ||
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- | Roden JA, Belt B, Ross JB, Tachibana T, Vargas J, Mudgett MB (2004). A genetic screen to isolate type III effectors translocated into pepper cells during // | ||
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- | Salomon D, Dar D, Sreeramulu S, Sessa G (2011). Expression of // | ||
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- | Szurek B, Rossier O, Hause G, Bonas U (2002). Type III-dependent translocation of the // | ||