Phytopathogenic bacteria utilizes several strategies to infect, colonize and cause disease in plants. Xanthomonas citri pv citri (Xcc), the causal agent of citrus canker, employs the type III secretion system to inject effector proteins of the PthA family into the host cell. Such proteins act as transcription factors activating target genes that would promote pathogen growth and contribute to disease development. Besides activating target genes in the plant, it was found that PthA4, required to elicit cankers on citrus, interact with citrus CsMaf1. CsMaf1 is an RNA polymerase (Pol) III repressor and negative regulator of cell growth. Our previous work shows that CsMaf1 inhibits cell growth during canker development and that CsMaf1 is regulated by PKA and TOR kinase, which control cell proliferation and defense responses in plants. In addition, we found that auxin prevented CsMaf1 from interacting with Pol III in the nucleolus. Since auxin is the principal hormone that controls cell growth and division in plants, and has been shown to promote canker formation, the aim of this proposal is to elucidate the auxin and TOR signaling pathway that converge into CsMaf1 phosphorylation and deactivation. We also intend to analyze post-transcriptional modifications such as phosphorylation and sumoylation of CsMaf1 which likely regulate CsMaf1 interaction with PthA4 and Pol III. Moreover, we plan to identify new citrus proteins that would be sumoylated or ubiquitinated in response to pathogen attack in two distinct types of interactions, i.e. in a compatible and incompatible interaction. We believe that this work will significantly contribute to a better understanding of the auxin and TOR signaling pathway that integrates several cell signals that lead to cell growth and proliferation in plants.
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