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--- bacteria:t3e:xopag [2020/07/03 08:50] – rkoebnik
+++ bacteria:t3e:xopag [2025/02/12 23:22] (current) – jfpothier
@@ Line 1: / Line 1: @@
-====== XopAG ======
+====== The Type III Effector XopAG from //Xanthomonas// ======
-Author: Christian Vernière & Trainees from the 2<sup>nd</sup>  EuroXanth Training School\\
+Author: [[https://www.researchgate.net/profile/Christian_Verniere|Christian Vernière]] & Trainees from the 2<sup>nd</sup> EuroXanth Training School ([[https://www.researchgate.net/profile/Songul_Erken|Songül Erken]], [[https://www.researchgate.net/profile/Damla_Ertimurtas|Damla Ertimurtaş]], [[https://www.researchgate.net/profile/Jelena_Menkovic|Jelena Menković]], [[https://www.researchgate.net/profile/Andjelka_Prokic|Andjelka Prokić]])\\
-Internal reviewer: FIXME \\
+Internal reviewer: [[https://www.researchgate.net/profile/Tamas_Kovacs6|Tamás Kovács]]\\
-Expert reviewer: FIXME
+Expert reviewer: [[https://www.researchgate.net/profile/Nian-Wang|Nian Wang]]
-Class: Xop?\\
+Class: XopAG\\
-Family: XopAG\\
+Families: XopAG1, XopAG2\\
-Prototype: Xop? (//Xanthomonas//; strain)\\
+Prototype: AvrGf1 (//Xanthomonas citri// pv. //citri//; Xac‐A<sup>w</sup> strain 12879), AvrGf2 (//Xanthomonas fuscans// pv. //aurantifolii//; Xac‐A<sup>w</sup> strain Xfa-C51302)\\
-RefSeq ID: [[https://www.ncbi.nlm.nih.gov/protein/WP_080633702.1|WP_080633702.1]] (425 aa)\\
+GenBank ID (AvrGf1): [[https://www.ncbi.nlm.nih.gov/protein/ABB84189.1|ABB84189.1]] (532 aa)\\
-D structure:
+GenBank ID (AvrGf2): [[https://www.ncbi.nlm.nih.gov/protein/AIP90071.1|AIP90071.1]] (508 aa)\\
+RefSeq ID (XopAG1): [[https://www.ncbi.nlm.nih.gov/protein/WP_272820829.1|WP_272820829.1]] (511 aa)\\
+RefSeq ID (XopAG2): [[https://www.ncbi.nlm.nih.gov/protein/WP_007970248.1|WP_007970248.1]] (508 aa)\\
+Synonym: AvrGf1, AvrGf2\\
+D structure: Unknown
 ===== Biological function =====
@@ Line 15: / Line 19: @@
 === How discovered? ===
-//Xanthomonas citri// pv. //citri// (Xcc-A) causing citrus bacterial canker can infect most of the commercial citrus species and are worldwide distributed. Strains that were pathogenic on Key lime (//Citrus aurantifolia//), but that did not cause canker symptoms on grapefruit, were reported in Florida and designated as Xcc-AW. Three clones were selected from a genomic library of the 12879 strain of Xcc-Aw that caused rapid necrosis in grapefruit leaves, but not in tomato leaves when they were expressed in //X. perforans// (Rybak //et al//., 2009). A 1599-bp open reading frame (ORF) was found within the nucleotide sequence of DNA from a 2.3-kb subclone from pL799 that caused HR in grapefruit leaves. The complete sequence of the ORF, designated as //avrGf1// (Rybak //et al//., 2009). Genes //avrGf1// and //avrGf2// were found to share low sequence similarity at the nucleotide level, except for a small region in the last 200 nucleotides of the genes, which showed a high level of identity (68%) (Gochez //et al//., 2017). The alignment of translated proteins AvrGf1 (533 amino acids) and AvrGf2 (509 amino acids) determined that AvrGf2 had a low degree of sequence identity (45% amino acid identity) with the previously identified AvrGf1. The highest sequence similarities were observed between AvrGf1 and AvrGf2 in the C-terminal portions of the effector proteins (74.5% identity at the amino acid level over 51 amino acids) (Gochez //et al//., 2017).
+//Xanthomonas citri// pv. //citri// (Xcc-A) causing citrus bacterial canker can infect most of the commercial citrus species and are worldwide distributed. Strains that were pathogenic on Key lime (//Citrus aurantifolia//), but that did not cause canker symptoms on grapefruit, were reported in Florida and designated as Xcc-A<sup>w</sup>. Three clones were selected from a genomic library of the 12879 strain of Xcc-A<sup>w</sup> that caused rapid necrosis in grapefruit leaves, but not in tomato leaves when they were expressed in //X. perforans// (Rybak //et al.//, 2009). A 1599-bp open reading frame (ORF) was found within the nucleotide sequence of DNA from a 2.3-kb subclone from pL799 that caused HR in grapefruit leaves. The complete sequence of the ORF, designated as //avrGf1// (Rybak //et al.//, 2009). Genes //avrGf1// and //avrGf2// were found to share low sequence similarity at the nucleotide level, except for a small region in the last 200 nucleotides of the genes, which showed a high level of identity (68%) (Gochez //et al.//, 2017). The alignment of translated proteins AvrGf1 (533 amino acids) and AvrGf2 (509 amino acids) determined that AvrGf2 had a low degree of sequence identity (45% amino acid identity) with the previously identified AvrGf1. The highest sequence similarities were observed between AvrGf1 and AvrGf2 in the C-terminal portions of the effector proteins (74.5% identity at the amino acid level over 51 amino acids) (Gochez //et al.//, 2017).
 === (Experimental) evidence for being a T3E ===
+An active TTSS is necessary for HR produced by AvrGf1 in grapefruit leaves, as it was proven by transconjugation experiments (Rybak //et al.//, 2009).
 === Regulation ===
+No data available. The effector gene //xopAG// was however shown to be induced in XVM2 medium compared to NB medium in //X//. //citri// subsp. //citri// A<sup>W</sup> 12879 strain, a variant strain restricted to Mexican lime (Jalan et al., 2013).
 === Phenotypes ===
-All //xopAG//-containing strains of //X. citri// pv. //citri// induced the hypersensitive response (HR) on grapefruit (//Citrus paradisi//) and sweet orange (//C. sinensis//) but express canker symptoms on Key lime (Escalon //et al//., 2013). After infiltration of grapefruit leaves with inoculum adjusted to 5×108 cfu/mL, internal bacterial populations of Xcc-A (strain A 40) and Xcc-Aw (strain 12879) were similar through the second day, but populations of Xcc-A were significantly greater than those of Xcc-Aw after six days. The symptoms caused by the Xac-AwΔavrGf1 strain that was mutated on avrGf1 were more similar to those produced by the wild-type Xac-A strain than to those produced by the wild-type Xac-Aw strain (Rybak //et al//., 2009). So the whole pathogenicity was not restored.
+All //xopAG//-containing strains of //X. citri// pv. //citri// induced the hypersensitive response (HR) on grapefruit (//Citrus paradisi//) and sweet orange (//C. sinensis//) but express canker symptoms on Key lime (Escalon //et al.//, 2013). After infiltration of grapefruit leaves with inoculum adjusted to 5×10<sup>8</sup> cfu/mL, internal bacterial populations of Xcc-A (strain A 40) and Xcc-A<sup>w</sup>  (strain 12879) were similar through the second day, but populations of Xcc-A were significantly greater than those of Xcc-A<sup>w</sup> after six days. The symptoms caused by the Xac-A<sup>w</sup> ΔavrGf1 strain that was mutated on avrGf1 were more similar to those produced by the wild-type Xac-A strain than to those produced by the wild-type Xac-A<sup>w</sup> strain (Rybak //et al.//, 2009). So the whole pathogenicity was not restored.
 === Localization ===
-AvrGf1 (Figueiredo //et al//., 2011) and AvrGf2 (Gochez //et al//., 2017) possess a N-terminal chloroplast localization signal. The signal is not shared by all members of the XopAG effector family (Gochez //et al//., 2017). Transient expression of the protein with the first 116 amino acids deleted in grapefruit leaves resulted in the elimination of the HR and a lack of accumulation of the protein in the chloroplast.
+AvrGf1 (Figueiredo //et al.//, 2011) and AvrGf2 (Gochez //et al.//, 2017) possess a N-terminal chloroplast localization signal. The signal is not shared by all members of the XopAG effector family (Gochez //et al.//, 2017). Transient expression of the protein with the first 116 amino acids deleted in grapefruit leaves resulted in the elimination of the HR and a lack of accumulation of the protein in the chloroplast.
 === Enzymatic function ===
+AvrGf2 elicited rapid cell death in grapfruit leaves (Gonchez //et al.//, 2015), detailed enzymatic function has not been determined yet.
 === Interaction partners ===
-The XopAG AvrGf2 effector contains a Cyp-binding site that is essential for the elicitation of HR in citrus (Gochez //et al//., 2017).
+The XopAG AvrGf2 effector contains a Cyp-binding site that is essential for the elicitation of HR in citrus (Gochez //et al.//, 2017). Yeast two-hybrid experiments showed strong interaction of AvrGf2 with grapefruit cyclophilin (GfCyp), whereas mutation of the GPLL motif in the cyclophilin-binding domain abolished the interaction.
 ===== Conservation =====
 === In xanthomonads ===
-Yes (e.g. //X.c.// pv. //vasculorum//, //X.c.// pv. //musacearum//, //X.c.// pv. //campestris//) (Gochez //et al//., 2017).
+Yes (//e.g.//, //X. campestris//, //X. vasicola//) (Gochez //et al//., 2017).
 === In other plant pathogens/symbionts ===
-Yes (e.g. //P.s.// pv. //phaseolicola// (HopG1), //P.s.// pv. //tomato// (HopG1), //Ralstonia solanacearum//, //Acidovorax citrulli//) (Gochez //et al//., 2017).
+Yes (//e.g.//, //P. syringae.// pv. //phaseolicola// (HopG1), //P. syringae// pv. //tomato// (HopG1), //Ralstonia solanacearum//, //Acidovorax citrulli//) (Gochez //et al//., 2017).
 ===== References =====
@@ Line 44: / Line 51: @@
 Figueiredo JF, Romer P, Lahaye T, Graham JH, White FF, Jones JB (2011). //Agrobacterium//-mediated transient expression in citrus leaves: a rapid tool for gene expression and functional gene assay. Plant Cell Rep. 30: 1339-1345. DOI: [[https://doi.org/10.1007/s00299-011-1045-7|10.1007/s00299-011-1045-7]]
+Gochez AM, Minsavage GV, Potnis N, Canteros BI, Stall RE, Jones JB (2015). A functional XopAG homologue in //Xanthomonas fuscans// pv. //aurantifolii// strain C limits host range. Plant Pathol, 64: 1207-1214. DOI: [[https://doi.org/10.1111/ppa.12361|10.1111/ppa.12361]]
 Gochez AM, Shantharaj D, Potnis N, Zhou X, Minsavage GV, White FF, Wang N, Hurlbert JC, Jones JB (2017). Molecular characterization of XopAG effector AvrGf2 from //Xanthomonas fuscans// ssp. //aurantifolii// in grapefruit. Mol. Plant Pathol. 18: 405-419. DOI: [[https://doi.org/10.1111/mpp.12408|10.1111/mpp.12408]]
+Jalan N, Kumar D, Andrade MO, Yu F, Jones JB, Graham JH, White FF, Setubal JC, Wang N (2013). Comparative genomic and transcriptome analyses of pathotypes of //Xanthomonas citri// subsp. //citri// provide insights into mechanisms of bacterial virulence and host range. BMC Genomics 14: 551. DOI: [[https://doi.org/10.1186/1471-2164-14-551|10.1186/1471-2164-14-551]]
 Rybak M, Minsavage GV, Stall RE, Jones JB (2009). Identification of //Xanthomonas citri// ssp. //citri// host specificity genes in a heterologous expression host. Mol. Plant Pathol. 10: 249-262. DOI: [[https://doi.org/10.1111/j.1364-3703.2008.00528.x|10.1111/j.1364-3703.2008.00528.x]]
+===== Acknowledgements =====
+This fact sheet is based upon work from COST Action CA16107 EuroXanth, supported by COST (European Cooperation in Science and Technology).

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