Taxonomic status: Bacteria; Phylum Proteobacteria; Class Gammaproteobacteria; Order Xanthomonadales; Family Xanthomonadaceae; Genus Xanthomonas; Species Xanthomonas citri ssp. citri (Xcc). Host range: Compatible hosts vary in their susceptibility to citrus canker (CC), with grapefruit, lime and lemon being the most susceptible, sweet orange being moderately susceptible, and kumquat and calamondin being amongst the least susceptible. Microbiological properties: Xcc is a rod-shaped (1.5-2.0 × 0.5-0.75 µm), Gram-negative, aerobic bacterium with a single polar flagellum. The bacterium forms yellow colonies on culture media as a result of the production of xanthomonadin. Distribution: Present in South America, the British Virgin Islands, Africa, the Middle East, India, Asia and the South Pacific islands. Localized incidence in the USA, Argentina, Brazil, Bolivia, Uruguay, Senegal, Mali, Burkina Faso, Tanzania, Iran, Saudi Arabia, Yemen and Bangladesh. Widespread throughout Paraguay, Comoros, China, Japan, Malaysia and Vietnam. Eradicated from South Africa, Australia and New Zealand. Absent from Europe.
BackgroundXanthomonas citri, a causal agent of citrus canker, has been a well-studied model system due to recent availability of whole genome sequences of multiple strains from different geographical regions. Major limitations in our understanding of the evolution of pathogenicity factors in X. citri strains sequenced by short-read sequencing methods have been tracking plasmid reshuffling among strains due to inability to accurately assign reads to plasmids, and analyzing repeat regions among strains. X. citri harbors major pathogenicity determinants, including variable DNA-binding repeat region containing Transcription Activator-like Effectors (TALEs) on plasmids. The long-read sequencing method, PacBio, has allowed the ability to obtain complete and accurate sequences of TALEs in xanthomonads. We recently sequenced Xanthomonas citri str. Xc-03-1638-1-1, a copper tolerant A group strain isolated from grapefruit in 2003 from Argentina using PacBio RS II chemistry. We analyzed plasmid profiles, copy number and location of TALEs in complete genome sequences of X. citri strains.ResultsWe utilized the power of long reads obtained by PacBio sequencing to enable assembly of a complete genome sequence of strain Xc-03-1638-1-1, including sequences of two plasmids, 249 kb (plasmid harboring copper resistance genes) and 99 kb (pathogenicity plasmid containing TALEs). The pathogenicity plasmid in this strain is a hybrid plasmid containing four TALEs. Due to the intriguing nature of this pathogenicity plasmid with Tn3-like transposon association, repetitive elements and multiple putative sites for origins of replication, we might expect alternative structures of this plasmid in nature, illustrating the strong adaptive potential of X. citri strains. Analysis of the pathogenicity plasmid among completely sequenced X. citri strains, coupled with Southern hybridization of the pathogenicity plasmids, revealed clues to rearrangements of plasmids and resulting reshuffling of TALEs among strains.ConclusionsWe demonstrate in this study the importance of long-read sequencing for obtaining intact sequences of TALEs and plasmids, as well as for identifying rearrangement events including plasmid reshuffling. Rearrangement events, such as the hybrid plasmid in this case, could be a frequent phenomenon in the evolution of X. citri strains, although so far it is undetected due to the inability to obtain complete plasmid sequences with short-read sequencing methods.Electronic supplementary materialThe online version of this article (10.1186/s12864-017-4408-9) contains supplementary material, which is available to authorized users.
Citrus canker is an important bacterial disease of citrus in several regions of the world. Strains of Xanthomonas citri type-A (Xc-A) group are the primary pathogen where citrus canker occurs. After Xc-A entered the Northeast of Argentina in 1974, the disease spread rapidly from 1977 to 1980 and then slowed down and remained moving at slow pace until 1990 when it became endemic. Citrus canker was detected in Northwest Argentina in 2002. This paper presents the main steps in the fight of the disease and the management strategies that have been used to control citrus canker at this time. We think the process might be usefull to other countries with the same situation. Results from more than 40 years of research in Northeast (NE) Argentina indicate that we are at the limit of favorable environment for the disease. The severity of citrus canker is greatly affected by the environment and El Niño Southern Oscillation (ENSO) phenomenon which causes cyclic fluctuations on the disease intensity in the NE region. Weather-based logistic regression models adjusted to quantify disease levels in field conditions showed that the environmental effect was strongly modulated by the distance from a windbreak. Production of healthy fruits in citrus canker endemic areas is possible knowing the dynamics of the disease. A voluntary Integrated Plan to Reduce the Risk of Canker has been in place since 1994 and it allows growers to export unsymptomatic, uninfested fresh fruit to countries which are free of the disease and require healthy, pathogen free fruits. The experience from Argentina can be replicated in other countries after appropriate trials.
Since citrus canker was first described in the early 1900's, four major types and three species of pathogenic xanthomonads associated to citrus were identified based on the characteristic symptoms and host range. Type A, caused by X. citri subsp. citri, develops typical raised cankered lesions and is pathogenic on most commercial citrus species and cultivars. Types B and C are caused by X. citri pv. aurantifolii which elicits canker lesions. Besides the typical type A, the more aggressive and most widely spread type, other subtypes have been described, such as type A*, type A w , type A-Manatee, type A-Miami, type A-minus pthA, and type-A etrog. The type B strains are found only in Argentina and are more pathogenic on lemon and less aggressive on sweet orange, tangerines and grapefruit. The type C strains are found only in Brazil and are pathogenic only on Key lime. X. alfalfae subsp. citrumelonis, formerly known as type E, causes citrus bacterial spot and is more aggressive on trifoliate citrus and its hybrids. Lesions caused by citrus bacterial spot are flat or sunken and not raised. Several subtypes of X. citri subsp. citri have also been identified. Besides the differences in pathogenicity, xanthomonads may also vary in their sensitivity to copper. Copper resistance has been reported for strains of X. citri subsp. citri and X. alfalfae subsp. citrumelonis and is conferred by the gene clusters copLAB or copABCD. Resistance to copper has serious implications for the use of copper-based bactericides, which are the most important chemicals for the control of diseases caused by Xanthomonas on citrus. Keywords Citrus bacterial spot. Citrus canker. Xanthomonas alfalfae subsp. citrumelonis. X. citri pv. aurantifolii. X. citri subsp. citri. copABCD. copLAB
Xanthomonas fuscans ssp. aurantifolii group C strains exhibit host specificity on different citrus species. The strains possess a type III effector, AvrGf2, belonging to the XopAG effector gene family, which restricts host range on citrus. We dissected the modular nature and mode of action of AvrGf2 in grapefruit resistance. XopAG effectors possess characteristic features, such as a chloroplast localization signal, a cyclophilin-binding domain characteristic amino acid sequence motif (GPLL) and a C-terminal domain-containing CLNAxYD. Mutation of GPLL to AASL in AvrGf2 abolished the elicitation of the hypersensitive response (HR), whereas mutation of only the first amino acid to SPLL delayed the HR in grapefruit. Yeast two-hybrid experiments showed strong interaction of AvrGf2 with grapefruit cyclophilin (GfCyp), whereas AvrGf2-SPLL and AvrGf2-AASL mutants showed weak and no interaction, respectively. Molecular modelling and in silico docking studies for the cyclophilin-AvrGf2 interaction predicted the binding of citrus cyclophilins (CsCyp, GfCyp) to hexameric peptides spanning the cyclophilin-binding domain of AvrGf2 and AvrGf2 mutants (VAGPLL, VASPLL and VAAASL) with affinities equivalent to or better than a positive control peptide (YSPSA) previously demonstrated to bind CsCyp. In addition, the C-terminal domain of XopAG family effectors contains a highly conserved motif, CLNAxYD, which was identified to be crucial for the induction of HR based on site-directed mutagenesis (CLNAxYD to CASAxYD). Our results suggest a model in which grapefruit cyclophilin promotes a conformational change in AvrGf2, thereby triggering the resistance response.
Citrus canker is caused by two Xanthomonas species, Xanthomonas citri, which has become the primary pathogen where citrus canker occurs (type A citrus canker, Xc‐A), and X. fuscans pv. aurantifolii (Xfa), which consists of strains B and C. The B strain is less pathogenic than the A strain, but produces symptoms in all citrus species. The C‐type cankers only infect Key lime (Citrus aurantifolia) and produce a hypersensitive reaction (HR) in grapefruit (Citrus paradisi) leaves. An avirulence gene, avrGf2, was identified in a C strain that was responsible for the HR in grapefruit. AvrGf2 is a member of XopAG effector family and shares 45% identity at amino acid level with another member of the same family, AvrGf1 from strain Xc‐Aw, which was previously shown to elicit an HR in grapefruit. AvrGf2 shares sequence identity with other XopAG effectors present in Xanthomonas vasculorum, Xanthomonas campestris pv. musacearum and Pseudomonas syringae pv. tomato. Mutagenesis of avrGf2 in C strain resulted in a compatible reaction in grapefruit. There was no observable effect on virulence when Xc‐A transconjugants containing either avirulence gene were inoculated on Key lime. Expression of avrGf1 or avrGf2 in Xc‐A resulted in a similar phenotype following infiltration into grapefruit leaves, although the avrGf2 transconjugant elicited a faster HR and lower populations than the transconjugant containing avrGf1. Also, it was shown that all Xfa‐B strains tested contain a transposon in avrGf2 that helps to explain the differences in host range between B and C strains.
This review summarizes the current status of citrus canker in the United States. The disease is present in Florida, Louisiana, and Texas. In Florida, the eradication program ended in 2006 and now citrus canker is endemic to many citrus-growing areas, although it is still possible to find canker-free groves. In endemic areas, the disease is controlled using windbreaks, applying copper-based bactericides, controlling the citrus leafminer, and applying systemic plant activators. In Louisiana, citrus canker was identified in 2013, the first time since the 1940s, and has since been identified in 10 of the parishes where plant material and fruit are not allowed to leave the quarantine areas. There are no eradication efforts in Louisiana and removal of trees is voluntary. Finally, citrus canker resurfaced in Texas in 2015 and has been detected in several locations. Currently only the type A W strain is present in Texas and quarantine efforts are being taken to mitigate the risk of introduction of the type A strain into the state.
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