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Functional analysis of CsMAF1, an RNA polymerase III repressor involved in cell growth control and pathogen response in plants

Grant number: 17/18570-9
Support Opportunities:Scholarships in Brazil - Post-Doctoral
Effective date (Start): December 01, 2017
Effective date (End): January 31, 2021
Field of knowledge:Biological Sciences - Biochemistry - Molecular Biology
Principal Investigator:Celso Eduardo Benedetti
Grantee:Maxuel de Oliveira Andrade
Host Institution: Centro Nacional de Pesquisa em Energia e Materiais (CNPEM). Ministério da Ciência, Tecnologia e Inovação (Brasil). Campinas , SP, Brazil
Associated research grant:11/20468-1 - Molecular mechanisms involved in pathogen adaptation and virulence, host resistance and symptom development in citrus-bacteria interactions, AP.TEM


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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Scientific publications (4)
(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
ANDRADE, MAXUEL OLIVEIRA; SFORCA, MAURICIO LUIS; HELENO BATISTA, FERNANDA APARECIDA; MIGLIORINI FIGUEIRA, ANA CAROLINA; BENEDETTI, CELSO EDUARDO. The MAF1 Phosphoregulatory Region Controls MAF1 Interaction with the RNA Polymerase III C34 Subunit and Transcriptional Repression in Plants. PLANT CELL, v. 32, n. 9, p. 3019-3035, . (17/18570-9, 18/08535-4, 14/50880-0)
ZOU, XIUPING; DU, MEIXIA; LIU, YUNUO; WU, LIU; XU, LANZHEN; LONG, QIN; PENG, AIHONG; HE, YONGRUI; ANDRADE, MAXUEL; CHEN, SHANCHUN. CsLOB1 regulates susceptibility to citrus canker through promoting cell proliferation in citrus. Plant Journal, v. 106, n. 4, . (17/18570-9)
PICCHI, SIMONE CRISTINA; GRANATO, LAIS MOREIRA; FRANZINI, MARIA JULIA FESTA; ANDRADE, MAXUEL OLIVEIRA; TAKITA, MARCO AURELIO; MACHADO, MARCOS ANTONIO; DE SOUZA, ALESSANDRA ALVES. Modified Monosaccharides Content of Xanthan Gum Impairs Citrus Canker Disease by Affecting the Epiphytic Lifestyle of Xanthomonas citri subsp. citri. MICROORGANISMS, v. 9, n. 6, . (13/10957-0, 17/18570-9, 14/50880-0, 13/01395-9, 19/01901-8)
MOREIRA MARTINS, PAULA MARIA; ANDRADE, MAXUEL DE OLIVEIRA; BENEDETTI, CELSO EDUARDO; DE SOUZA, ALESSANDRA ALVES. Xanthomonas citri subsp. citri: host interaction and control strategies. ROPICAL PLANT PATHOLOG, v. 45, n. 3, p. 24-pg., . (13/10957-0, 18/18550-0, 14/50880-0, 18/08535-4, 17/18570-9, 16/01273-9)

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