Open AccessContribution of a harpin protein from X anthomonas axonopodis pv. citri to pathogen virulence
Author(s) -
Sgro Germán G.,
Ficarra Florencia A.,
Dunger Germán,
Scarpeci Telma E.,
Valle Estela M.,
Cortadi Adriana,
Orellano Elena G.,
Gottig Natalia,
Ottado Jorgelina
Publication year - 2012
Publication title -
molecular plant pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.945
H-Index - 103
eISSN - 1364-3703
pISSN - 1464-6722
DOI - 10.1111/j.1364-3703.2012.00814.x
Subject(s) - citrus canker , xanthomonas citri , xanthomonas , biology , hypersensitive response , virulence , nicotiana benthamiana , microbiology and biotechnology , pseudomonas syringae , mutant , pathogen , canker , arabidopsis , botany , bacteria , gene , plant disease resistance , genetics
Summary X anthomonas axonopodis pv. citri ( X ac), the bacterium that causes citrus canker, contains a gene in the hrp [for hypersensitive response (HR) and pathogenicity] cluster that encodes a harpin protein called H pa1. H pa1 produced HR in the nonhost plants tobacco, pepper and A rabidopsis, whereas, in the host plant citrus, it elicited a weak defence response with no visible phenotype. Co‐infiltrations of X ac with or without the recombinant H pa1 protein in citrus leaves produced a larger number of cankers in the presence of the protein. To characterize the effect of H pa1 during the disease, an X acΔhpa1 mutant was constructed, and infiltration of this mutant caused a smaller number of cankers. In addition, the lack of H pa1 hindered bacterial aggregation both in solution and in planta . Analysis of citrus leaves infiltrated with H pa1 revealed alterations in mesophyll morphology caused by the presence of cavitations and crystal idioblasts, suggesting the binding of the harpin to plant membranes and the elicitation of signalling cascades. Overall, these results suggest that, even though H pa1 elicits the defence response in nonhost plants and, to a lesser extent, in host plants, its main roles in citrus canker are to alter leaf mesophyll structure and to aggregate bacterial cells, and thus increase virulence and pathogen fitness. We expressed the N ‐terminal and C ‐terminal regions and found that, although both regions elicited HR in nonhost plants, only the N ‐terminal region showed increased virulence and bacterial aggregation, supporting the role of this region of the protein as the main active domain.