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bacteria:t3e:xopi [2020/07/03 10:57] rkoebnik |
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- | ====== XopI ====== | ||
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- | Author: [[https:// | ||
- | Internal reviewer: Isabel Rodrigues\\ | ||
- | Expert reviewer: FIXME | ||
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- | Class: XopI\\ | ||
- | Family: XopI\\ | ||
- | Prototype: (// | ||
- | RefSeq ID: [[https:// | ||
- | 3D structure: Unknown | ||
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- | ===== Biological function ===== | ||
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- | === How discovered? === | ||
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- | Effector proteins (T3Es) can suppress the plant innate immunity and alter the plant metabolism to the pathogen’s advantage. The T3E XopI was identified in Xcv strain 85-10 due to a F-box motif based on the presence of a PIP (pathogen-inducible promoter) box in its promoter region. XopI secretion and translocation was shown during the interaction of Xcv with resistant pepper plants (Schulze //et al//., 2012). Moreover, interaction studies in yeast showed that XopI specifically interacts with one out of 21 // | ||
- | === (Experimental) evidence for being a T3E === | ||
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- | The transcripts of XopI were amplified from Xcv derivative 85* strain, which expresses a constitutively active HrpG point mutant resulting in constitutive expression of the T3S system, suggesting co‐expression with T3S genes (Schulze //et al//., 2012). To investigate whether //xopI// was indeed T3SS dependently secreted and translocated into the plant cell, a translational fusion with the reporter protein AvrBs3D2, a derivative of the TAL effector AvrBs3 which lacks a T3S and translocation signal, was performed. Fusion of a functional T3S signal to AvrBs3D2 enables its translocation and thus the induction of the HR in pepper cultivar ECW-30R plants that harbor the corresponding resistance gene Bs3. When the bacteria were incubated in T3S medium, XopI1–140-AvrBs3D2 was detected in the culture supernatant of strain 85*, but not of 85*DhrcV, by an AvrBs3-specific antibody. These results demonstrate that the XopI effector contained functional T3S signals in the N-terminal regions (Schulze //et al//., 2012) To test for T3SS dependent translocation, | ||
- | === Regulation === | ||
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- | XopI is presumably controlled by both HrpG and HrpX. The HrpX-dependent induction of //xopR// has been described previously (Koebnik //et al.//, 2006). HrpG‐ and HrpX‐dependent co‐regulation with the T3S system (+, co‐regulation; | ||
- | === Phenotypes === | ||
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- | Bacterial strains carrying deletions of XopI showed no difference in the induction of disease symptoms and the HR compared with wild-type strain 85-10 (Schulze //et al//., 2012). In tomato plants, virulence of xopI knockout strains is dramatically reduced. The stomatal aperture is as well reduced, suggesting that XopI is essential for Xcv entry into the host plant apoplast | ||
- | === Localization === | ||
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- | XopI is translocated by the 85*Δ// | ||
- | === Enzymatic function === | ||
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- | These phenotypes can be ascribed either to the virulence activity of the effectors in plant cells, or to their recognition by the plant surveillance system. As shown in [[https:// | ||
- | === Interaction partners === | ||
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- | XopR and XopS belong to //Xcv// translocation class A, comprising T3Es whose translocation into plant cells is completely dependent on HpaB, whereas XopB, XopG, **XopI**, XopK, XopM and XopV were assigned to class B, because they are still translocated in the absence of HpaB (Büttner //et al.//, 2006). Both new class A effectors lack homology to known proteins or motifs, so that their molecular function remains elusive. By contrast, the class B effectors comprise the putative enzyme XopG, a member of the HopH family of putative zinc metalloproteases. Other effectors possess interesting features, for example XopI contains an F‐box motif typical for eukaryotic proteins playing a role in the ubiquitin‐26S proteasome system (UPS). The UPS controls protein stability in eukaryotes and appears to be a favorable target for many T3Es, for example members of the GALA family, which strongly contribute to the virulence of //R. solanacearum// | ||
- | ===== Conservation ===== | ||
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- | === In xanthomonads === | ||
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- | Yes. | ||
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- | === In other plant pathogens/ | ||
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- | No. | ||
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- | ===== References ===== | ||
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- | <font 10.5pt/ | ||
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- | Nagel O, Bonas U (2018). The // | ||
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- | Salomon D, Dar D, Sreeramulu S, Sessa G (2011). Expression of // | ||
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- | Schulze S, Kay S, Büttner D, Egler M, Eschen-Lippold L, Hause G, Krüger A, Lee J, Müller O, Scheel D, Szczesny R, Thieme F, Bonas U (2012). Analysis of new type III effectors from // | ||
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- | Teper D, Sunitha S, Martin GB, Sessa G (2015). Five // | ||
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- | Üstün S, Börnke F (2014). Interactions of // | ||