Tomato Protein Kinase 1b Mediates Signaling of Plant Responses to Necrotrophic Fungi and Insect Herbivory

Abstract

The tomato protein kinase 1 (TPK1b) gene encodes a receptor-like cytoplasmic kinase localized to the plasma membrane. Pathogen infection, mechanical wounding, and oxidative stress induce expression of TPK1b, and reducing TPK1b gene expression through RNA interference (RNAi) increases tomato susceptibility to the necrotrophic fungus Botrytis cinerea and to feeding by larvae of tobacco hornworm (Manduca sexta) but not to the bacterial pathogen Pseudomonas syringae. TPK1b RNAi seedlings are also impaired in ethylene (ET) responses. Notably, susceptibility to Botrytis and insect feeding is correlated with reduced expression of the proteinase inhibitor II gene in response to Botrytis and 1-aminocyclopropane-1-carboxylic acid, the natural precursor of ET, but wild-type expression in response to mechanical wounding and methyl-jasmonate. TPK1b functions independent of JA biosynthesis and response genes required for resistance to Botrytis. TPK1b is a functional kinase with autophosphorylation and Myelin Basis Protein phosphorylation activities. Three residues in the activation segment play a critical role in the kinase activity and in vivo signaling function of TPK1b. In sum, our findings establish a signaling role for TPK1b in an ET-mediated shared defense mechanism for resistance to necrotrophic fungi and herbivorous insects.

Botrytis cinerea Manipulates the Antagonistic Effects between Immune Pathways to Promote Disease Development in Tomato

“…The lesion size on leaves of the def1 and Spr2 mutants inoculated with isolate B8403 was approximately twofold that of wild-type plants (see Supplemental Figures 1B and 1D online). These results suggest that JA signaling is involved in tomato resistance to B. cinerea isolate B8403, which is consistent with previous reports (AbuQamar et al, 2008).…”

“…related to the activation of defense responses. Resistance to B. cinerea has been known to be JA dependent (Farmer and Ryan, 1992;Li et al, 2003;AbuQamar et al, 2008). Therefore, we examined the expression levels of two JA-dependent genes, proteinase inhibitors I and II (PI I and PI II).…”

“…The polypeptide systemin is a known elicitor of JA signaling in tomato (Farmer and Ryan, 1992;Li et al, 2003;AbuQamar et al, 2008). We evaluated whether or not systemin is involved in tomato resistance to B. cinerea.…”

Polyamines Attenuate Ethylene-Mediated Defense Responses to Abrogate Resistance to Botrytis cinerea in Tomato

“…Fungal culture and preparation of conidial spore suspension were as described previously . B. cinerea disease assays were done on detached leaves by drop inoculation of a conidial suspension on tomato leaves (3 3 10 5 spores/mL; AbuQamar et al, 2008), and lesion diameter was determined (n = 60). Wild-type and transgenic leaves were inoculated with 300 mg/mL Alternaria solani cultures, and lesion diameter was calculated 7 d after inoculation.…”

“…Botrytis cinerea, a necrotrophic fungal pathogen that infects .200 plant species, is the causal agent of the gray mold disease, resulting in significant economic losses. Information on how plants combat necrotrophic pathogens such as B. cinerea and what signaling molecules are involved in such interactions is beginning to emerge (Abuqamar et al, 2008;Laluk et al, 2011). Host immune response to infection is mediated by diverse regulatory processes, of which, plant hormone functions have been studied extensively in relation to disease (Spoel and Dong, 2008;Bari and Jones, 2009;Pieterse et al, 2009).…”