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bacteria:t3e:xopi [2025/02/21 13:08] – [Biological function] rkoebnik | bacteria:t3e:xopi [2025/07/04 23:35] (current) – jfpothier | ||
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====== The Type III Effector XopI from // | ====== The Type III Effector XopI from // | ||
- | Author: [[https:// | + | Author: [[https:// |
- | Internal reviewer: Isabel Rodrigues | + | Internal reviewer: |
Class: XopI\\ | Class: XopI\\ | ||
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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 // | 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 // | ||
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=== (Experimental) evidence for being a T3E === | === (Experimental) evidence for being a T3E === | ||
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XopI belongs to the translocation class of T3SS-secreted proteins, based on HpaB dependence (Büttner //et al.//, 2006). | XopI belongs to the translocation class of T3SS-secreted proteins, based on HpaB dependence (Büttner //et al.//, 2006). | ||
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=== 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. | ||
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=== Phenotypes === | === Phenotypes === | ||
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 | 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 | ||
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=== Localization === | === Localization === | ||
XopI is translocated by the 85*Δ// | XopI is translocated by the 85*Δ// | ||
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=== Enzymatic function === | === Enzymatic function === | ||
The T3Es XopE1, XopF2, XopH, **XopI**, XopM, XopQ, XopV, AvrBs1 and AvrXv4 partially or fully inhibited cell death triggered by at least one of the cell death inducers (Teper //et al.//, 2015). | The T3Es XopE1, XopF2, XopH, **XopI**, XopM, XopQ, XopV, AvrBs1 and AvrXv4 partially or fully inhibited cell death triggered by at least one of the cell death inducers (Teper //et al.//, 2015). | ||
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=== Interaction partners === | === Interaction partners === | ||