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Mol Plant Pathol. 2019 Feb;20(2):254-269. doi: 10.1111/mpp.12752. Epub 2018 Oct 31.

Plant responses underlying nonhost resistance of Citrus limon against Xanthomonas campestris pv. campestris.

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Instituto de Biología Molecular y Celular de Rosario (IBR)-Consejo Nacional de Investigaciones Científicas y Tecnológicas (CONICET), Ocampo y Esmeralda S/N, S2002LRK, Rosario, Argentina.
Área Virología, Facultad de Ciencias Bioquímicas y Farmacéuticas, Universidad Nacional de Rosario (UNR), Suipacha 590, S2002LRK, Rosario, Argentina.
Laboratorio de Fisiología Vegetal, Instituto de Investigaciones en Ciencias Agrarias de Rosario (IICAR)-UNR/CONICET, Parque Villarino S/N, 2125 Zavalla, Santa Fe, Argentina.
Facultad de Ciencias Agropecuarias, Universidad Católica de Santa Fe, Ludueña 612, S3560DYR Reconquista, Santa Fe, Argentina.
Facultad de Ciencias Agrarias, Universidad Nacional del Litoral, Producción Vegetal, Kreder 2805, 3080 HOF Esperanza, Santa Fe, Argentina.
Instituto de Biología Molecular y Celular de Plantas (IBMCP), Universidad Politécnica de Valencia-C.S.I.C, Ingeniero Fausto Elio, S/N, 46022, Valencia, España.


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.


PAMP-triggered immunity; biofilm formation; canker disease; glucosinolates; protection; salicylic acid; stomatal immunity


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