15th International Conference on Arabidopsis Research - TAIR

T05-017
Regulation of Cell Death in Arabidopsis by the LSD1-
Gene Family
Petra Epple(1), Charles C. Clover(1), Ben F. Holt III(1), Hironori Kaminaka(1), Jeffery
L. Dangl(1, 2)
1-Department of Biology, Coker Hall 108, CB#3280, University of North Carolina at Chapel Hill,
Chapel Hill, NC 27599-3280
2-Curriculum in Genetics, Coker Hall 108, CB#3280, University of North Carolina at Chapel Hill,
Chapel Hill, NC 27599-3280
LSD1, a negative regulator of oxidative stress-induced cell death, is a member
of a small gene family of zinc finger proteins. It shares a novel consensus
motif (CxxCRxxLMYxxGASxVxCxxC) with three other proteins designated LOL1
(LSD One Like 1, At1g32540), LOL2 (At4g21610) and LOL3 (At1g02170).
Analysis of a lol1-mutant demonstrated that LOL1 function is required for
lsd1 runaway cell death (rcd). Conversely, conditional over-expression of
LOL1 triggers cell death in Ws-0 and lsd1 backgrounds. Yeast two-hybrid
analysis demonstrated that LOL1 can interact with LSD1 and with additional
LSD1 interactors. We are now analyzing the in vivo interaction between LSD1
and LOL1. Conditional over-expression of LOL2 induces cell death in Ws-0
and lsd1 backgrounds as well. Although LOL2 doesn't interact with LSD1 or
LOL1, it does interact in yeast two-hybrid assays with AtTip49a, which itself
interacts with LSD1, but not LOL1. Thus regulation of cell death in Arabidopsis
might be dependent on complexes that contain LSD1 and it's different
interactors. We are now analyzing these complexes in vitro and in vivo.
Dietrich et al. (1997) Cell 99, 685-694
Holt et al. (2002) Dev. Cell 2,807-817
Epple et al. (2003) PNAS 100, 6831-6836
15 th <strong>International</strong> <strong>Conference</strong> on Arabidopsis Research 2004 · Berlin
T05-018
Structure / Function Analyses of Pseudomonas
syringae Type III Effectors
Darrell Desveaux(1), Alex U. Singer(2), Laurie Betts(2), Jeffrey H. Chang(1), Zachary
Nimchuk(1), Sarah R. Grant(1, 5), John Sondek(2, 4), Jeffery L. Dangl(1, 5)
1-Department of Biology University of North Carolina Chapel Hill
2-Department of Pharmacology University of North Carolina Chapel Hill
3-Department of Microbiology and Immunology University of North Carolina Chapel Hill
4-Department of Biochemistry and Biophysics University of North Carolina Chapel Hill
5-Lineberger Comprehensive Cancer Center University of North Carolina Chapel Hill
Many gram-negative bacterial pathogens of both plants and animals use an
evolutionarily conserved type-III secretion system (TTSS) to deliver virulence
proteins termed type III effectors directly into host cells. Once inside the cell,
these type III effectors manipulate signaling pathways in order to inhibit host
defense mechanisms and aid pathogen colonization. Importantly, recent
findings suggest that the plant immune system, mediated by plant disease
resistance (R) genes, recognizes the virulence activity of type III effectors,
supporting a general model suggesting that indirect recognition of the action
of pathogen virulence factors is the initiator of successful plant immune
responses. Recent genome-wide analyses for proteins secreted in a type
III system-dependent manner by phytopathogenic Pseudomonas syringae
pathovar tomato DC3000 have revealed ~50 confirmed or predicted type
III effectors. Furthermore, several type III effectors of P. syringae increase
virulence on genetically susceptible hosts. However, despite increasing
efforts, biochemical functions have been assigned to a paltry few P. syringae
type III effectors. Consequently, understanding the function of type III effector
proteins in virulence and resistance is currently a major goal in the study
of plant pathology. In response to this dearth of functional data, we have
initiated a focused structural proteomics approach to complement biochemical
and genetic techniques in order to further characterize P. syringae type III
effectors and to gain insight into their mechanisms of action.
T05 Interaction with the Environment 2 (Biotic)