SUMMARYTaxonomy: Bacteria; Proteobacteria, Gammaproteobacteria; Xanthomonadales; Xanthomonadaceae, Xanthomonas.Microbiological properties: Gram-negative, obligately aerobic, straight rods, motile by a single polar flagellum, yellow pigment.Related species: X. campestris , X. axonopodis , X. oryzae , X. albilineans .Host range: Affects Rutaceous plants, primarily Citrus spp., Fortunella spp., and Poncirus spp., world-wide. Quarantined pathogen in many countries. Economically important hosts are cultivated orange, grapefruit, lime, lemon, pomelo and citrus rootstock.Disease symptoms: On leaves, first appearance is as oily looking, 2-10 mm, similarly sized, circular spots, usually on the abaxial surface. On leaves, stems, thorns and fruit, circular lesions become raised and blister-like, growing into white or yellow spongy pustules. These pustules then darken and thicken into a light tan to brown corky canker, which is rough to the touch. On stems, pustules may coalesce to split the epidermis along the stem length, and occasionally girdling of young stems may occur. Older lesions on leaves and fruit tend to have more elevated margins and are at times surrounded by a yellow chlorotic halo (that may disappear) and a sunken centre. Sunken craters are especially noticeable on fruit, but the lesions do not penetrate far into the rind. Defoliation and premature abscission of affected fruit occurs on heavily infected trees.
Silicon increases the resistance of rice (Oryza sativa) to the rice blast pathogen Magnaporthe oryzae. This study described the relationship between silicon and M. oryzae in terms of whole‐genome gene expression. By assessing gene expression patterns in the rice cultivar Monko‐to using microarray technology, the physiological basis for silicon‐induced resistance was investigated. Silicon amendment resulted in the differential regulation of 221 genes in rice without being challenged with the pathogen. This means that silicon had an observable effect on rice metabolism, as opposed to playing a simple passive role in the resistance response of rice. Compared with control plants, silicon‐amended rice differentially regulated 60% less genes, implying that silicon affects the rice response to rice blast infection at a transcriptional level.
Citrus canker disease is caused by five groups of Xanthomonas citri strains that are distinguished primarily by host range: three from Asia (A, A*, and A(w)) and two that form a phylogenetically distinct clade and originated in South America (B and C). Every X. citri strain carries multiple DNA fragments that hybridize with pthA, which is essential for the pathogenicity of wide-host-range X. citri group A strain 3213. DNA fragments that hybridized with pthA were cloned from a representative strain from all five groups. Each strain carried one and only one pthA homolog that functionally complemented a knockout mutation of pthA in 3213. Every complementing homolog was of identical size to pthA and carried 17.5 nearly identical, direct tandem repeats, including three new genes from narrow-host-range groups C (pthC), A(w) (pthAW), and A* (pthA*). Every noncomplementing paralog was of a different size; one of these was sequenced from group A* (pthA*-2) and was found to have an intact promoter and full-length reading frame but with 15.5 repeats. None of the complementing homologs nor any of the noncomplementing paralogs conferred avirulence to 3213 on grapefruit or suppressed avirulence of a group A* strain on grapefruit. A knockout mutation of pthC in a group C strain resulted in loss of pathogenicity on lime, but the strain was unaffected in ability to elicit an HR on grapefruit. This pthC- mutant was fully complemented by pthA, pthB, or pthC. Analysis of the predicted amino-acid sequences of all functional pthA homologs and nonfunctional paralogs indicated that the specific sequence of the 17th repeat may be essential for pathogenicity of X. citri on citrus.
Xanthomonas citri pv. citri is a clonal group of strains that causes citrus canker disease and appears to have originated in Asia. A phylogenetically distinct clonal group that causes identical disease symptoms on susceptible citrus, X. citri pv. aurantifolii, arose more recently in South America. Genomes of X. citri pv. aurantifolii strains carry two DNA fragments that hybridize to pthA, an X. citri pv. citri gene which encodes a major type III pathogenicity effector protein that is absolutely required to cause citrus canker. Marker interruption mutagenesis and complementation revealed that X. citri pv. aurantifolii strain B69 carried one functional pthA homolog, designated pthB, that was required to cause cankers on citrus. Gene pthB was found among 38 open reading frames on a 37,106-bp plasmid, designated pXcB, which was sequenced and annotated. No additional pathogenicity effectors were found on pXcB, but 11 out of 38 open reading frames appeared to encode a type IV transfer system. pXcB transferred horizontally in planta, without added selection, from B69 to a nonpathogenic X. citri pv. citri (pthA::Tn5) mutant strain, fully restoring canker. In planta transfer efficiencies were very high (>0.1%/recipient) and equivalent to those observed for agar medium with antibiotic selection, indicating that pthB conferred a strong selective advantage to the recipient strain. A single pathogenicity effector that can confer a distinct selective advantage in planta may both facilitate plasmid survival following horizontal gene transfer and account for the origination of phylogenetically distinct groups of strains causing identical disease symptoms.The genus Xanthomonas is comprised of strains that exhibit a high level of host specificity; over 125 different pathogenic variants (pathovars) of X. campestris that differ primarily in host range have been described (29). Host specificity in Xanthomonas can be due to gene-for-gene interactions involving avirulence genes that act in a negative fashion to limit host range (18,29,38) but also can be due to positive acting pathogenicity factors that condition host range in a host-specific manner, e.g., pthN and avrb6 of X. campestris pv. malvacearum (6, 70), opsX of X. campestris pv. citrumelo (32), and pthA of X. citri (60, 61).A highly clonal population structure is typical of many Xanthomonas pathovars that cause serious diseases (22). Surprisingly, some pathovars are comprised of clonal groups that are phylogenetically distinct but have similar or identical host ranges and cause identical disease symptoms. Examples of this phenomenon are observed for (i) common bean blight, caused by two major groups of strains within X. campestris pv. phaseoli that are only 20% related by DNA-DNA hybridization (28); (ii) bacterial spot of tomato and pepper, caused by two major groups of strains within X. campestris pv. vesicatoria (30) that are less than 50% related by DNA-DNA hybridization (53); and (iii) citrus canker disease, caused by two major groups of strains within X. citri (5) that a...
Although strawberry is an economically important fruit crop worldwide, production of strawberry is limited by its susceptibility to a wide range of pathogens and the lack of major commercial cultivars with high levels of resistance to multiple pathogens. The objective of this study is to ectopically express the Arabidopsis thaliana NPR1 gene (AtNPR1) in the diploid strawberry Fragaria vesca L. and to test transgenic plants for disease resistance. AtNPR1 is a key positive regulator of the long-lasting broad-spectrum resistance known as systemic acquired resistance (SAR) and has been shown to confer resistance to a number of pathogens when overexpressed in Arabidopsis or ectopically expressed in several crop species. We show that ectopic expression of AtNPR1 in strawberry increases resistance to anthracnose, powdery mildew, and angular leaf spot, which are caused by different fungal or bacterial pathogens. The increased resistance is related to the relative expression levels of AtNPR1 in the transgenic plants. In contrast to Arabidopsis plants overexpressing AtNPR1, which grow normally and do not constitutively express defense genes, the strawberry transgenic plants are shorter than non-transformed controls, and most of them fail to produce runners and fruits. Consistently, most of the transgenic lines constitutively express the defense gene FvPR5, suggesting that the SAR activation mechanisms in strawberry and Arabidopsis are different. Nevertheless, our results indicate that overexpression of AtNPR1 holds the potential for generation of broad-spectrum disease resistance in strawberry.
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