Minisymposium 25: Pathogen virulence mechanisms

Abs # 46004: 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, St Louis, MO 63130 (B): Institute for Genomic Research, Rockville, MD, 20850

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 several other JA signaling mutants, including jin1, jar1 and axr1. Of these, jin1 and axr1 mutants exhibit reduced susceptibility to Pst, while jar1 mutants exhibit normal levels of disease. To learn more about the role of JA signaling in Pst pathogenesis we are investigating the genetic and molecular basis of reduced susceptibility in jin1 plants. Similar to coi1, reduced susceptibility to Pst in jin1 is correlated with insensitivity to coronatine and elevated PR1 gene expression. To determine whether elevated SA responses contribute to reduced susceptibility of jin1 mutants, we created jin1 lines carrying the SA-degrading nahG transgene. These plants are fully susceptible to Pst infection, suggesting that reduced disease susceptibility in jin1 mutants is dependent on SA accumulation. Our results demonstrate that an intact JA signaling pathway is required for full susceptibility to virulent P. syringae and may serve as a virulence target through which the pathogen modulates plant defense. To further examine the role of JA signaling in Pst infection, we generated jin1jar1 double mutants. The disease resistance phenotype of the double mutant is identical to that of jin1 plants, suggesting that JIN1 and JAR1 are involved in different aspects of JA signaling and that susceptibility to Pst is mediated through a JIN1-dependent pathway independent of JAR1-facilitated JA modification. Work is underway to identify additional components of this signaling pathway that have an effect on the plant’s response to Pst infection.