Open AccessPlant responses underlying nonhost resistance of Citrus limon against Xanthomonas campestris pv. campestris
Author(s) -
Chiesa María A.,
Roeschlin Roxana A.,
Favaro María A.,
Uviedo Facundo,
CamposBeneyto Laura,
D’Andrea Rodrigo,
Gadea José,
Marano María R.
Publication year - 2019
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/mpp.12752
Subject(s) - xanthomonas citri , citrus canker , biology , xanthomonas campestris , callose , xanthomonas , pseudomonas syringae , canker , plant disease resistance , botany , salicylic acid , xanthomonas campestris pv. campestris , host (biology) , bacterial disease , microbiology and biotechnology , defence mechanisms , pathogen , bacteria , gene , genetics , cell wall
Summary Citrus is an economically important fruit crop that is severely afflicted by citrus canker, a disease caused by Xanthomonas citri ssp. citri ( X. citri ); thus, new sustainable strategies to manage this disease are needed. Although all Citrus spp. are susceptible to this pathogen, they are resistant to other Xanthomonas species, exhibiting non‐host resistance (NHR), for example, to the brassica pathogen X. campestris pv. campestris ( Xcc ) and a gene‐for‐gene host defence response (HDR) to the canker‐causing X. fuscans ssp. aurantifolii ( Xfa ) strain C. Here, we examine the plant factors associated with the NHR of C. limon to Xcc . We show that Xcc induced asymptomatic type I NHR, allowing the bacterium to survive in a stationary phase in the non‐host tissue. In C. limon , this NHR shared some similarities with HDR; both defence responses interfered with biofilm formation, and were associated with callose deposition, induction of the salicylic acid (SA) signalling pathway and the repression of abscisic acid (ABA) signalling. However, greater stomatal closure was seen during NHR than during HDR, together with different patterns of accumulation of reactive oxygen species and phenolic compounds and the expression of secondary metabolites. Overall, these differences, independent of Xcc type III effector proteins, could contribute to the higher protection elicited against canker development. We propose that Xcc may have the potential to steadily activate inducible defence responses. An understanding of these plant responses (and their triggers) may allow the development of a sustained and sustainable resistance to citrus canker.