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bacteria:t3e:xopi [2020/06/30 22:08] irodrigues |
bacteria:t3e:xopi [2020/07/09 10:16] rkoebnik |
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====== XopI ====== | ====== XopI ====== | ||
- | Author: Trainees from the EuroXanth | + | Author: |
Internal reviewer: Isabel Rodrigues\\ | Internal reviewer: Isabel Rodrigues\\ | ||
Expert reviewer: FIXME | Expert reviewer: FIXME | ||
Class: XopI\\ | Class: XopI\\ | ||
- | Family: | + | Family: |
- | Prototype: (// | + | Prototype: (// |
RefSeq ID: [[https:// | RefSeq ID: [[https:// | ||
- | 3D structure: | + | 3D structure: |
===== Biological function ===== | ===== Biological function ===== | ||
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=== How discovered? === | === How discovered? === | ||
- | 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 // | + | 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 === | === (Experimental) evidence for being a T3E === | ||
- | 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 | + | 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 |
+ | |||
+ | Translocation class; classification based on HpaB dependence (Büttner //et al.//, 2006). | ||
=== Regulation === | === Regulation === | ||
- | 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 | + | 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. |
=== Phenotypes === | === Phenotypes === | ||
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=== Localization === | === Localization === | ||
- | According to Büttner //et al.// (2006)), | + | XopI is translocated by the 85*Δ// |
=== Enzymatic function === | === Enzymatic function === | ||
- | 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:// | + | 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 === | === Interaction partners === | ||
- | 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 | + | 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 ===== | ===== Conservation ===== | ||
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===== References ===== | ===== References ===== | ||
- | Nagel O, Bonas U (2018). The // | + | <font 10.5pt/ |
+ | |||
+ | Nagel O, Bonas U (2018). The // | ||
Salomon D, Dar D, Sreeramulu S, Sessa G (2011). Expression of // | Salomon D, Dar D, Sreeramulu S, Sessa G (2011). Expression of // | ||
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Üstün S, Börnke F (2014). Interactions of // | Üstün S, Börnke F (2014). Interactions of // | ||
+ | |||
+ | ===== Further reading ===== | ||
+ | |||
+ | Thieme F (2006). Genombasierte Identifizierung neuer potentieller Virulenzfaktoren von // | ||