Abstract

Xanthomonas campestris pv. vesicatoria (Xcv) is the causal agent of bacterial spot disease in tomato (Solanum lycopersicum) plants. We recently identified a MAPKKK gene, SlMAPKKKε, which is required for tomato resistance to Xcv strains and encodes a positive regulator of cell death. We also provided evidence that the MEK2 MAPKK, and the WIPK and SIPK MAPKs act downstream to MAPKKKε in Nicotiana benthamiana plants. Here, we used the virus-induced gene silencing technique to assess whether tomato homologs of MEK2 (SlMKK2), SIPK (SlMPK1 and SlMPK2), WIPK (SlMPK3), and other components of MAP kinase cascades (SlNPK1, SlMEK1 and SlNTF6), which were previously implicated in plant immunity, are involved in disease resistance to Xcv. Silencing of none of the tested genes caused the appearance of disease symptoms in tomato leaves challenged with an avirulent Xcv strain. However, bacterial populations were significantly higher in leaves of plants silenced for SlMKK2 and SlMPK2, as compared to control plants, suggesting that these two genes contribute to disease resistance to Xcv. It remains to be established whether SlMKK2 and SlMPK2 are activated by SlMAPKKKε directly or through a distinct MAPKKK.

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