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Identification of alternative sensor(s) for DSF autoinducer, pathogenicity regulator in Xanthomonas citri subsp. citri

Grant number: 15/22473-3
Support type:Scholarships in Brazil - Post-Doctorate
Effective date (Start): April 01, 2016
Effective date (End): December 31, 2018
Field of knowledge:Agronomical Sciences - Agronomy
Principal Investigator:Jesus Aparecido Ferro
Grantee:Juan Carlos Caicedo Cepeda
Home Institution: Faculdade de Ciências Agrárias e Veterinárias (FCAV). Universidade Estadual Paulista (UNESP). Campus de Jaboticabal. Jaboticabal , SP, Brazil
Associated scholarship(s):17/10517-1 - Design and construction of novel bioreporter strains to identify alternative DSF receptors in Xanthomonas citri subsp. citri, BE.EP.PD

Abstract

Xanthomonas citri subsp. citri (Xcc) is the causal agent of citrus canker, a disease that affects almost all types of citrus crops. Production of particular pathogenicity factors in Xcc is regulated by rpf gene cluster, which encodes elements of a cell-cell communication system called Quorum Sensing (QS). The QS in Xcc is mediated by a diffusible signal factor (DSF). Recently we have shown that Pseudomonas spp. and Bacillus spp. isolated from citrus phylloplane disrupt DSF signaling in Xcc, leading to a drastic disease reduction in susceptible hosts, confirming the importance of QS in Xcc virulence. The synthesis and perception of DSF are dependent on several Rpf proteins. DSF synthesis requires RpfF synthase, while the perception and transduction depends on the sensor RpfC and the regulator RpfG. Detailed analysis of regulatory functions of the Rpf proteins, have suggested the occurrence of new sensors for DSF. In fact, diverse DSF sensors homologous to RpfC, have been evidenced in Burkholderia cenocepacia, Xanthomonas campestris, Pseudomonas aeuroginosa and Xylella fastidiosa, some genes regulated by these sensors are actively involved in virulence and interspecies signaling.The main goal of this project is to identify alternative sensors for DSF in Xcc using a mutagenesis approach coupled with a comparative analysis of the transcriptomes of Xcc wild-type and mutant strains ”rpfF, ”rpfC and ”rpfFC, to establish a subset of genes regulated by DSF but not by RpfC. A better understanding of new DSF signaling pathway(s) in Xcc, and the finding of additional components, would provide fundamental knowledge to define mechanistic details in the regulation of virulence in Xcc, besides favoring the rational development of virulence inhibitors.