| Abstract Detail
Plant-Pathogen Interactions Ma, Wei [1], Smigel, Andries [2], Tsai, Yu-Chang [3], Braam, Janet [3], Berkowitz, Gerald [1]. CNGC-mediated Ca conductance, cytosolic Ca/CaM rise and resulting activation of nitric oxide generation are critical steps in plant innate immunity. Plant innate immunity involves cytosolic Ca rise and nitric oxide (NO) generation that lead to hypersensitive response (HR) to avirulent pathogens. The specific proteins involved in this pathogen perception signaling cascade are unknown, as is the mechanism by which Ca rise is linked to NO generation. Arabidopsis dnd1 mutants lack a functional Ca-conducting cyclic nucleotide gated channel (CNGC2) and do not undergo HR. We find that application of the NO donor SNP restores HR (to avirulent Pseudomonas syringae pv. tomato (Pst)) in dnd1 plants. In wild type Arabidopsis plants, application of the Ca-channel blocker Gd or the calmodulin (CaM) antagonist W7 prevents HR to Pst. Using the guard cell of leaf epidermal peels as a model system to study this pathogen perception signaling at a cellular level, we find that chelation of external Ca with EGTA and block of CaM and CaM-like proteins with W7 prevents NO generation. These results are consistent with a model involving (a) NO rise as a signal leading to HR, (b) Ca conductance into the cytosol through CNGC2 as an early event in pathogen perception, and (c) the resulting increase in Ca binding to CaM or a CaM-like protein activating NO generation. Ca/CaM activates animal NO synthase; plant NO synthesis in this cascade may require a similar signal. We tested this model using a genetic approach as well. CML24 is one of many Arabidopsis CaM-like proteins (CMLs). We find that loss-of-function cml24 mutant plants have impaired HR to Pst. Thus, work presented here identifies external Ca influx into the cytosol through CNGC2, and the resulting rise in Ca bound to a CML (and/or CaM) as a signal to activate NO synthesis, and downstream NO generation as intermediary steps in pathogen perception signaling leading to HR. Supported by NSF awards 0344141 and 0321532.
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1 - University of Connecticut, Storrs, CT 06269-4163, Department of Plant Science
2 - University of Connecitcut, Storrs, CT 06269-4163, Department of Plant Science
3 - Rice University, Houston, TX 77251, Department of Biochemistry and Cell Biology
Keywords:
Calcium, CAM, ion channel
nitric oxide
hypersensitive response.
Presentation Type: Plant Biology Abstract
Session: P
Location: Exhibit Hall (Northeast, Southwest & Southeast)/Hilton
Date: Sunday, July 8th, 2007
Time: 8:00 AM
Number: P15049
Abstract ID:1258 |
