Abstract

Jasmonate signaling is critical for susceptibility of Arabidopsis thaliana to the bacterial pathogen Pseudomonas syringae, as demonstrated by the reduced susceptibility of coil mutant plants. The infection responses of another jasmonate-insensitive mutant, jinl, had previously been unknown. This work demonstrates that susceptibility to P. syringae requires activity of the transcription factor JTN1/MYC2. Reduced susceptibility correlates with reduced sensitivity to the P. syringae phytotoxin coronatine, a molecular mimic of the endogenous jasmonate JA-Ile. The reduced susceptibility of jinl mutant plants correlates with increased salicylic acid (SA)-dependent signaling. Analysis of jinl plants carrying the sidl mutation, resulting in decreased S A synthesis during infection, reveals that the decreased bacterial growth in jinl mutants requires SA signaling, while the decrease in disease symptom development does not. To identify additional jasmonate signaling mutants with altered responses to P. syringae infection, over 23,500 mutagenized seedlings were screened for altered sensitivity to coronatine. Seven mutants were identified. Four are less sensitive to coronatine and allelic to known jasmonate signaling mutants. Three exhibit enhanced sensitivity to coronatine. Two of these, coh-23 and coh-36, were further characterized and have increased sensitivity to both coronatine and jasmonate. The coh-23 mutant plants have an uncertain response to P. syringae infection, exhibiting reduced susceptibility that may result from a second unlinked mutation. The coh-36 mutant plants are more susceptible to P. syringae infection. They support slightly higher levels of bacterial growth early in infection. Later in infection, they develop more severe symptoms than wild-type plants, despite supporting similar levels of bacteria. This supports the observation from the jinl sid2 double mutants that bacterial growth and disease symptom development can be separated. The mutation in coh-36 plants was mapped to a region of chromosome 2 not previously implicated in jasmonate signaling, strongly suggesting that the coh-36 mutant represents a novel component in this pathway. A candidate gene has been identified. Tests are underway to determine whether its function is disrupted in coh-36 mutants. The gene affected by the coh-36 mutation is proposed to be a negative regulator of a jasmonate signaling pathway required primarily for symptom development.

Committee Chair

Barbara Kunkel

Committee Members

Barak Cohen, Tuan-hua Ho, Eric Richards, Craig Pikaard, James Skeath

Degree

Doctor of Philosophy (PhD)

Author's Department

Biology

Author's School

Graduate School of Arts and Sciences

Document Type

Dissertation

Date of Award

Summer 8-15-2008

Language

English (en)

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