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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Transcriptional analysis of the sweet orange interaction with the citrus canker pathogens Xanthomonas axonopodis pv. citri and Xanthomonas axonopodis pv. aurantifolii

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Cernadas, Raul Andres [1] ; Camillo, Luciana Rodrigues [1] ; Benedetti, Celso Eduardo [1]
Total Authors: 3
[1] Brazilian Synchrotron Light Lab, Ctr Mol & Struct Biol, BR-13083970 Campinas, SP - Brazil
Total Affiliations: 1
Document type: Review article
Source: MOLECULAR PLANT PATHOLOGY; v. 9, n. 5, p. 609-631, SEP 2008.
Web of Science Citations: 52

Xanthomonas axonopodis pv. citri (Xac) and Xanthomonas axonopodis pv. aurantifolii pathotype C (Xaa) are responsible for citrus canker disease; however, while Xac causes canker on all citrus varieties, Xaa is restricted to Mexican lime, and in sweet oranges it triggers a defence response. To gain insights into the differential pathogenicity exhibited by Xac and Xaa and to survey the early molecular events leading to canker development, a detailed transcriptional analysis of sweet orange plants infected with the pathogens was performed. Using differential display, suppressed subtractive hybridization and microarrays, we identified changes in transcript levels in approximately 2.0% of the similar to 32 000 citrus genes examined. Genes with altered expression in response to Xac/Xaa surveyed at 6 and 48 h post-infection (hpi) were associated with cell-wall modifications, cell division and expansion, vesicle trafficking, disease resistance, carbon and nitrogen metabolism, and responses to hormones auxin, gibberellin and ethylene. Most of the genes that were commonly modulated by Xac and Xaa were associated with basal defences triggered by pathogen-associated molecular patterns, including those involved in reactive oxygen species production and lignification. Significantly, we detected clear changes in the transcriptional profiles of defence, cell-wall, vesicle trafficking and cell growth-related genes in Xac-infected leaves between 6 and 48 hpi. This is consistent with the notion that Xac suppresses host defences early during infection and simultaneously changes the physiological status of the host cells, reprogramming them for division and growth. Notably, brefeldin A, an inhibitor of vesicle trafficking, retarded canker development. In contrast, Xaa triggered a mitogen-activated protein kinase signalling pathway involving WRKY and ethylene-responsive transcriptional factors known to activate downstream defence genes. (AU)

FAPESP's process: 00/10266-8 - A structural biology laboratory network for the study of the 3D structures of proteins
Grantee:Nilson Ivo Tonin Zanchin
Support type: Genome Research Grants
FAPESP's process: 98/14138-2 - Center for Structural Molecular Biotechnology
Grantee:Glaucius Oliva
Support type: Research Grants - Research, Innovation and Dissemination Centers - RIDC