Tomato protein kinase 1b mediates signaling of plant responses to necrotrophic fungi and insect herbivory

Synan AbuQamar, Mao Feng Chai, Hongli Luo, Fengming Song, Tesfaye Mengiste

Research output: Contribution to journalArticlepeer-review

120 Citations (Scopus)

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 methyljasmonate. 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.

Original languageEnglish
Pages (from-to)1964-1983
Number of pages20
JournalPlant Cell
Volume20
Issue number7
DOIs
Publication statusPublished - Jul 2008
Externally publishedYes

ASJC Scopus subject areas

  • Plant Science
  • Cell Biology

Fingerprint

Dive into the research topics of 'Tomato protein kinase 1b mediates signaling of plant responses to necrotrophic fungi and insect herbivory'. Together they form a unique fingerprint.

Cite this