Jean Greenberg, Ph.D.

Research Summary

My broad interest is in how organisms adapt to a changing environment. I study this in the context of host-pathogen interactions using the model system of the plant Arabidopsis thaliana and the gram negative pathogen Pseudomonas syringae. In response to infection, plants mount a complex defense response involving cell suicide, the crosslinking of cell wall components, antibiotic production and defense gene activation. We discovered that infection also activates cell growth and the cell cycle. We study how Arabidopsis regulates its defense and cell death response to pathogens using mutants, which express one or more aspects of the defense response in the absence of pathogens. We focus on a particular class of mutants, which show cell suicide and defense responses when no pathogen is present. We call these mutants acd for accelerated cell death. We use a collection of these mutants in two ways. First, we try to learn about defense signaling and cell death control using these mutants in combination with other mutations that affect specific aspects of plant defense. Second, we clone the genes identified by the mutations in order to gain insights into the molecular basis for the mutant phenotypes and as reagents for doing biochemical and cell biological studies on the mechanism of gene action. We also studying virulence proteins secreted by pathogenic bacteria by a specialized type III secretion system directly into plant cells. We do structure-function analysis on known secreted proteins (called effectors) to determine how they function to exert their virulence, we study the role of effectors in host range restriction and we study the localization and host targets of effectors.

Selected Papers

Guttman DS, Vinatzer BA, Sarkar SF, Ranall MV, Kettler G and Greenberg JT. (2002). "A functional screen for the type III (Hrp) secretome of the plant pathogen Pseudomonas syringae." Science 295: 1722-6.

Lu, H., Rate, D. N., Song, J. T. and Greenberg, J. T. (2003). "ACD6, a novel ankyrin protein, is a regulator and an effector of salicylic acid signaling in the Arabidopsis defense response." Plant Cell 15: 2408-20.

Liang H, Yao N, Song JT, Luo S, Lu H and Greenberg JT. (2003). "Ceramides modulate programmed cell death in plants." Genes Dev 17: 2636-41.

Greenberg JT and Yao N. (2004). "The role and regulation of programmed cell death in plant-pathogen interactions." Cell Microbiol 6: 201-11.

Song JT, Lu H and Greenberg JT. (2004). "Divergent roles in Arabidopsis thaliana development and defense of two homologous genes, aberrant growth and death2 and AGD2-LIKE DEFENSE RESPONSE PROTEIN1, encoding novel aminotransferases." Plant Cell 16: 353-66.

Song JT, Lu H, McDowell JM and Greenberg JT. (2004). "A key role for ALD1 in activation of local and systemic defenses in Arabidopsis." Plant J 40: 200-12.

Yao N, Eisfelder BJ, Marvin J and Greenberg JT. (2004). The mitochondrion, an organelle commonly involved in programmed cell death in Arabidopsis thaliana. Plant J. 40:596-610.

Yao N and Greenberg JT. (2005). Arabidopsis ACCELERATED CELL DEATH2 Modulates Programmed Cell Death. Plant Cell. Dec 30.

Vinatzer BA, Jelenska J, and Greenberg JT. (2005). Bioinformatics correctly identifies many type III secretion substrates in the plant pathogen Pseudomonas syringae and the biocontrol isolate P. flurescens SBW25.  MPMI 18:877-888.

Vinatzer BA, Teitzel GM, Lee M-W, Jelenska J, Hotton S, Fairfax K, Jenrette J, and Greenberg JT.  (2006). The Type III effector repertoire of Pseudomonas syringae pv. syringae B728a and its role in survival and disease on host and non-host plants.  Mol. Micro. 62:26-44.