Differences

This shows you the differences between two versions of the page.

--- bacteria:t3e:xopf [2020/08/07 14:33]
kalyanmondal [XopF]
+++ — (current)
@@ Line 1: / Line 1: @@
-====== XopF ======
-Author: [[https://www.researchgate.net/profile/Leonor_Martins|Leonor Martins]]\\
-Internal reviewer: [[https://www.researchgate.net/profile/Jaime_Cubero|Jaime Cubero]]\\
-Expert reviewer: FIXME
-Class: XopF\\
-Family: XopF1, XopF2, XopF3\\
-Prototype: XopF (//Xanthomonas euvesicatoria// pv. //euvesicatoria//, ex //Xanthomonas campestris //pv. //vesicatoria//; strain 85-10)\\
-RefSeq ID: XopF1_Xe [[https://www.ncbi.nlm.nih.gov/protein/WP_011346095.1|WP_011346095.1]] (670 aa), XopF1_Xoo AHK80891.1 (661 aa), XopF2 [[https://www.ncbi.nlm.nih.gov/protein/56121735|AAV74205.1]] (667 aa)\\
-Synonym: Hpa4\\
-D structure: Unknown
-===== Biological function =====
-=== How discovered? ===
-XopF1 and XopF2 were identified in a genetic screen, using a Tn//5//-based transposon construct harboring the coding sequence for the HR-inducing domain of AvrBs2, but devoid of the effectors' T3SS signal, that was randomly inserted into the genome of //X. campestris// pv. //vesicatoria// (//Xcv//)strain 85-10. The XopF1::AvrBs2 and XopF2::AvrBs2 fusion proteins triggered a //Bs2//-dependent hypersensitive response (HR) in pepper leaves (Roden //et al//., 2004).
-=== (Experimental) evidence for being a T3E ===
-Type III-dependent secretion of XopF1 and XopF2 was confirmed using a calmodulin-dependent adenylate cyclase reporter assay, with a Δ//hrpF// mutant strain serving as negative control (Roden //et al.//, 2004, Mondal et al, 2016).
-Fragments of the //xopF1// gene are located within the //hrp// cluster of many //Xanthomonas// spp., although a complete ORF is present only in the //Xcv// and //Xanthomonas oryzae// pv. //oryzae// (//Xoo//) //hrp// clusters (Roden //et al//., 2004).
-XopF1 belongs to the class A effectors (Büttner //et al//., 2006). XopF2 is 59% identical and 68% similar to XopF1 when analysed with the pairwise BLAST algorithm. //xopF2// appears to be co-transcribed with ORF1. ORF1 analysis revealed characteristics shared by type III chaperones, and is suggested to encode an Xcv chaperone (Roden //et al//., 2004).
-=== Regulation ===
-RT-PCR analysis revealed //xopF1// is regulated by //hrpG// and //hrpX// and that //xopF1//, //hpaD//, //hpaI// belong to the same operon. Upstream there is a PIP box which provides binding site for HrpX (Büttner //et al//., 2007).
-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 //xopF//, were significantly reduced in the //Xanthomonas oryzae// pv. //oryzae// Δ//xrvC// mutant compared with those in the wild-type strain PXO99<sup>A</sup>  (Liu //et al.//, 2016).
-=== Phenotypes ===
-  * Roden et al. did not find significant growth defects of a //Xcv//  Δ//xopF1//  or Δ//xopF2//  mutant in susceptible pepper and tomato leaves (Roden et al., 2004)
-  * To study the possible virulence function of the putative //xopF1//  operon encoding HpaD, HpaI, and XopF1 these three genes were deleted from the genome of //X. campestris//  pv. //vesicatoria//  85-10. The resultant mutant strain 85-10Δ//EF//  displayed a wild-type phenotype when infiltrated into susceptible and resistant plants. To investigate a possible functional redundancy due to homologous genes, //xopF2//  and the flanking ORF //XCV2943//  were also deleted in strain 85-10Δ//EF//. Since the resulting multiple mutant strain 85-10Δ//EF//Δ//xopF2//  also behaved like the wild type in infection tests//, xopF1//  and //xopF2//  regions did not seem to play an obvious role in the bacterial interaction with the host plant. (Büttner //et al//., 2007).
-  * Later, //Xoo//  XopF1 was proven to contribute to virulence in rice, as infection with //xopF1//  mutant has shown a reduced lesion size comparing to wild type (Mondal //et al//., 2016).
-  * Additionally, XopF1 and XopF2 of //X. euvesicatoria//  and //Xoo//  seem to have a role in PTI suppression //in planta//, namely by inhibiting callose deposition and by suppressing the induction of PTI marker genes, overall contributing to development of symptoms (Mondal //et al//., 2016; Popov //et al//., 2016).
-  * //Xoo//  XopF1 triggered an HR in non-host plants (Li //et al//., 2016).
-=== Localization ===
-XopF2 localizes in the Golgi apparatus, while XopF1 has been found in cytoplasm (Popov //et al//., 2016) and plasma membrane (Mondal //et al//., 2016). XopF1 is encoded within //hrp//  region, between //hpaB//  and //hrpF//, while XopF2 is encoded elsewhere in the bacterial chromosome (Roden //et al//., 2004; Büttner //et al//., 2007).
-=== Enzymatic function ===
-Unknown.
-=== Interaction partners ===
-XopF1 secretion and translocation is T3SS-dependent; HpaH, HpaC and T3S chaperone HpaB are required for efficient secretion XopF1 (Büttner //et al//., 2006, 2007).
-===== Conservation =====
-=== In xanthomonads ===
-Yes (//e.g.//, //X. arboricola, X. bromi//, //X. citri, X. oryzae//, //X. euvesicatoria//, //X. translucens//, //X. vasicola//). Since the G+C content of the //xopF1//  gene is similar to that of the //Xcv//  //hrp//  gene cluster, it may be a member of a “core” group of //Xanthomonas//  spp. effectors (Roden et al., 2004).
-=== In other plant pathogens/symbionts ===
-Unknown.
-===== References =====
-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 //Xanthomonas campestris//  pv. //vesicatoria//. Mol. Microbiol. 59: 513-527. DOI: [[https://onlinelibrary.wiley.com/doi/full/10.1111/j.1365-2958.2005.04924.x|10.1111/j.1365-2958.2005.04924.x]]
-Büttner D, Noël L, Stuttmann J, Bonas U (2007). Characterization of the nonconserved //hpaB//-//hrpF//  region in the //hrp//  pathogenicity island from //Xanthomonas campestris//  pv. //vesicatoria.//  Mol. Plant Microbe Interact. 20: 1063-1074. DOI: [[https://apsjournals.apsnet.org/doi/10.1094/MPMI-20-9-1063|10.1094/MPMI-20-9-1063]]
-Li S, Wang Y, Wang S, Fang A, Wang J, Liu L, Zhang K, Mao Y, Sun W (2015). The type III effector AvrBs2 in //Xanthomonas oryzae//  pv. //oryzicola//  suppresses rice immunity and promotes disease development. Mol. Plant Microbe Interact. 28: 869-880. DOI: [[https://apsjournals.apsnet.org/doi/10.1094/MPMI-10-14-0314-R|10.1094/MPMI-10-14-0314-R]]
-Liu Y, Long J, Shen D, Song C (2016). //Xanthomonas oryzae//  pv. //oryzae//  requires H-NS-family protein XrvC to regulate virulence during rice infection. FEMS Microbiol. Lett. 363: fnw067. DOI: [[https://doi.org/10.1093/femsle/fnw067|10.1093/femsle/fnw067]]
-Mondal K K, Verma G, Manju, Junaid A, Mani C (2016). Rice pathogen //Xanthomonas oryzae//  pv. //oryzae//  employs inducible hrp-dependent XopF type III effector protein for its growth, pathogenicity and for suppression of PTI response to induce blight disease. Eur. J. Plant Pathol. 144: 311-323. DOI: [[https://link.springer.com/article/10.1007/s10658-015-0768-7|10.1007/s10658-015-0768-7]]
-Popov G, Fraiture M, Brunner F, Sessa G (2016). Multiple //Xanthomonas euvesicatoria//  type III effectors inhibit flg22-triggered immunity. Mol. Plant Microbe Interact. 29: 651-660. DOI: [[https://apsjournals.apsnet.org/doi/10.1094/MPMI-07-16-0137-R|10.1094/MPMI-07-16-0137-R]]
-Roden J, Belt B, Ross J, Tachibana T, Vargas J, Mudgett M (2004). A genetic screen to isolate type III effectors translocated into pepper cells during //Xanthomonas//  infection. Proc. Natl. Acad. Sci. USA 101: 16624-16629. DOI: [[https://www.pnas.org/content/101/47/16624|10.1073/pnas.0407383101]]
-===== Further reading =====
-Salomon D, Dar D, Sreeramulu S, Sessa G (2011). Expression of Xanthomonas campestris pv. //vesicatoria//  type III effectors in yeast affects cell growth and viability. Mol. Plant Microbe Interact. 24: 305-314. DOI: [[https://doi.org/10.1094/MPMI-09-10-0196|10.1094/MPMI-09-10-0196]]

EuroXanth DokuWiki

User Tools

Site Tools

Differences

Page Tools