Poster: Plant-pathogen interactions

Abs # 530: Jasmonic acid signaling mutants of Arabidopsis exhibit reduced susceptibility to the bacterial pathogen Pseudomonas syringae

Presenter:	Laurie-Berry, Neva L, nllaurie@artsci.wustl.edu
Authors	Laurie-Berry, Neva L (A)   Joardar, Vinita  (B)   Kunkel, Barbara N (A)
Affiliations:	(A): Department of Biology, Washington University (B): The Institute for Genomic Research

We are interested in disease susceptibility and the mechanisms by which virulent pathogens modify host cell processes to promote tissue colonization and disease development. In a screen for Arabidopsis mutants with reduced susceptibility to the bacterial pathogen Pseudomonas syringae pv. tomato (Pst) we isolated an allele of the coronatine insensitive locus (COI1). coi1 mutants are insensitive to the plant hormone methyl jasmonate (JA) and to the phytotoxin coronatine, a P. syringae virulence factor believed to act as a molecular mimic of JA. We demonstrated that reduced susceptibility to Pst in coi1 plants is correlated with sensitization of the salicylic acid (SA)-dependent defense response pathway and that that SA-mediated defenses are required for restriction of Pst growth in coi1 plants. To determine whether reduced susceptibility is a common feature of JA signaling mutants, we assayed disease responses in other mutants, including jin1, jar1 and axr1. jin1 and axr1 mutants exhibit reduced susceptibility to Pst, while jar1 mutants exhibit normal levels of disease. To examine the role of JA signaling in Pst pathogenesis we are investigating the genetic and molecular basis of reduced susceptibility in jin1 plants. Reduced susceptibility to Pst in jin1, like coi1, is correlated with insensitivity to coronatine and elevated PR1 gene expression and is dependent on SA. Thus, intact JA signaling is required for full susceptibility to virulent P. syringae and may serve as a virulence target through which the pathogen modulates plant defense. Analysis of jin1jar1 double mutants suggests that susceptibility to Pst is mediated through a JIN1-dependent, JAR1-independent pathway. Work is underway to identify additional components of this signaling pathway.