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--- bacteria:t3e:xopag [2026/10/29 12:38] – [References] rkoebnik
+++ bacteria:t3e:xopag [2026/10/29 12:46] (current) – [Biological function] rkoebnik
@@ Line 19: / 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-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).
+//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).
+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 5×10<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.
+All //xopAG//-containing strains of //X. citri// pv. //citri// (//Xcc//) induced the hypersensitive response (HR) on grapefruit (//Citrus paradisi//) and sweet orange (//C. sinensis//), but expressed 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>  Δ//avrGf1// 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.
+Deletion of XopAG in //X. phaseoli// pv. //manihotis// (//Xpm//) did not affect morphology or extracellular enzyme production of //Xpm// but significantly attenuated its virulence on cassava (Yang //et al.//, 2026). Silencing MeHSP26 compromised cassava resistance to //Xpm//, following reduced flavonoid content and suppression of flavonoid gene expression. It was concluded that XopAG promotes MeHSP26 degradation to suppress flavonoid biosynthesis, thereby attenuating cassava immunity during early //Xpm// inoculation (Yang //et al.//, 2026).
 === 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.
 === 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). 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.
+The cassava small heat shock protein MeHSP26 was identified as a host target of XopAG, and both proteins were found to interact in both the cytoplasm and nucleus in //Nicotiana benthamiana// (Yang //et al.//, 2026). Notably, a degradation assay revealed that XopAG promotes MeHSP26 degradation in //N. benthamiana// (Yang //et al.//, 2026).
 ===== Conservation =====

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