This shows you the differences between two versions of the page.
Both sides previous revision Previous revision Next revision | Previous revision | ||
bacteria:t3e:xops [2020/06/30 19:07] rkoebnik [References] |
— (current) | ||
---|---|---|---|
Line 1: | Line 1: | ||
- | ====== XopS ====== | ||
- | |||
- | Author: Gabor Rakhely\\ | ||
- | Internal reviewer: Fernando Tavares\\ | ||
- | Expert reviewer: FIXME | ||
- | |||
- | Class: XopS\\ | ||
- | Family: XopS\\ | ||
- | Prototype: XopS (// | ||
- | RefSeq ID: -\\ | ||
- | 3D structure: Unknown | ||
- | |||
- | ===== Biological function ===== | ||
- | |||
- | === How discovered? === | ||
- | |||
- | Although no homology was found between XopS and other T3E effectors, //xopS //was putatively identified by the presence of a plant-inducer promoter (PIP) box, a lower GC content suggesting acquisition by HGT, and co-expression with other T3E genes (Schulze //et al.//, 2012). Deficient mutants and overexpression studies revealed that XopB and XopS contribute to disease symptoms and bacterial growth, and suppress plant defense gene expression (Schulze //et al.//, 2012). | ||
- | === (Experimental) evidence for being a T3E === | ||
- | |||
- | Type III secretion (T3S) assays of XopS-AvrBs3Δ2 fusion proteins indicated that XopS is secreted and translocated into the plant cells through T3S, inducing HR in pepper leaves. Further supporting XopS identity as a T3E it was shown that deletion mutants (ΔxopS) cause a considerable attenuation of disease symptoms (Schulze //et al.//, 2012). | ||
- | |||
- | For expression in Xcv, //xopS// was amplified from strain 85-10 and cloned into the Golden Gate‐compatible expression vector pBRM (Schulze //et al//., 2012). To generate // | ||
- | === Regulation === | ||
- | |||
- | HrpG- and HrpX-dependent co-regulation with the T3S system (Schulze //et al//., 2012). Presence of a PIP and -10 box (TTCGB‐N< | ||
- | === Phenotypes === | ||
- | |||
- | To study the contribution of the T3Es to bacterial virulence, the effector gene was individually deleted in Xcv strain 85‐10, and the mutant was inoculated into leaves of susceptible ECW pepper plants. In addition, induction of the HR in pepper ECW‐10R was analyzed, which is based on the recognition of the T3E AvrBs1 by the Bs1 resistance gene (Schulze //et al//., 2012). Deletion of //xopB// or //xopS// led to significantly reduced disease symptoms, whereas the HR induction was not impaired. The mutant phenotypes of 85-10ΔxopB and 85-10ΔxopS were complemented by ectopic expression of the respective effector gene, suggesting that reduced virulence was not caused by polar effects of the deletions on downstream genes. Although the growth of both individual effector mutants in ECW plants did not differ significantly from that of the wild‐type strain), multiplication of an 85‐10ΔxopBΔxopS double mutant was reduced significantly, | ||
- | === Localization === | ||
- | |||
- | Unknown. | ||
- | |||
- | === Enzymatic function === | ||
- | |||
- | Unknown. | ||
- | |||
- | === Interaction partners === | ||
- | |||
- | Unknown. | ||
- | |||
- | ===== Conservation ===== | ||
- | |||
- | === In xanthomonads === | ||
- | |||
- | Yes (//e.g.//, // | ||
- | |||
- | === In other plant pathogens/ | ||
- | |||
- | Unknown | ||
- | |||
- | ===== References ===== | ||
- | |||
- | Barak JD, Vancheva T, Lefeuvre P, Jones JB, Timilsina S, Minsavage GV, Vallad GE, Koebnik R (2016). Whole-genome sequences of // | ||
- | |||
- | 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 // | ||