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Doron Teper
Jin Xu
Sheo Shankar Pandey
Nian Wang

Citrus canker disease caused by Xanthomonas citri subsp. citri (Xcc) is one of the most destructive diseases in citrus. XccA causes canker disease in most commercial citrus varieties, whereas XccAW, which is genetically similar to XccA, infects only lime and alemow. Understanding the mechanism that determines the host range of pathogens is critical to investigating and utilizing host resistance. We hypothesized that XccAW would undergo mutations in genes that restrict its host range when artificially inoculated into incompatible citrus varieties. To test this hypothesis, we used an experimental evolution approach to identify phenotypic traits and genetic loci associated with the adaptation of XccAW to incompatible sweet orange. Repeated inoculation and re-isolation cycles improved the ability of three independent XccAW strains to colonize sweet orange. Adapted XccAW strains displayed increased expression of type III secretion system and effector genes. Genome sequencing analysis indicated that two of the adapted strains harbored mutations in pthAW1, a transcription activator-like effector (TALE) gene, that corresponded to the removal of one or two repeats from the central DNA binding repeat region. Introduction of the original but not the adapted pthAW1 variants into XccA abolished its ability to cause canker symptoms in sweet orange, Meyer lemon, and clementine but not in other XccAW-resistant citrus varieties. The original pthAW1, when expressed in XccA, induced ion leakage and the expression of PR genes, but had no effect on CsLOB1 expression of sweet orange. Our study has identified a novel host-specific avirulence TALE.

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PthAW1, a transcription activator-like effector of Xanthomonas citri subsp. citri, promotes host specific immune responses

Doron Teper
Jin Xu
Sheo Shankar Pandey
Nian Wang

PthAW1, a transcription activator-like effector of Xanthomonas citri subsp. citri, promotes host specific immune responses

Citrus canker disease caused by Xanthomonas citri subsp. citri (Xcc) is one of the most destructive diseases in citrus. XccA causes canker disease in most commercial citrus varieties, whereas XccAW, which is genetically similar to XccA, infects only lime and alemow. Understanding the mechanism that determines the host range of pathogens is critical to investigating and utilizing host resistance. We hypothesized that XccAW would undergo mutations in genes that restrict its host range when artificially inoculated into incompatible citrus varieties. To test this hypothesis, we used an experimental evolution approach to identify phenotypic traits and genetic loci associated with the adaptation of XccAW to incompatible sweet orange. Repeated inoculation and re-isolation cycles improved the ability of three independent XccAW strains to colonize sweet orange. Adapted XccAW strains displayed increased expression of type III secretion system and effector genes. Genome sequencing analysis indicated that two of the adapted strains harbored mutations in pthAW1, a transcription activator-like effector (TALE) gene, that corresponded to the removal of one or two repeats from the central DNA binding repeat region. Introduction of the original but not the adapted pthAW1 variants into XccA abolished its ability to cause canker symptoms in sweet orange, Meyer lemon, and clementine but not in other XccAW-resistant citrus varieties. The original pthAW1, when expressed in XccA, induced ion leakage and the expression of PR genes, but had no effect on CsLOB1 expression of sweet orange. Our study has identified a novel host-specific avirulence TALE.

Scientific Publication
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