ABSTRACT
The most recent major advances in the study of programmed cell death (PCD) in plants include the observation that peptide inhibitors of caspases inhibit the hypersensitive response. Nitric oxide has been shown to be required for the induction of disease related PCD. Mutant analysis has led to the cloning of the first genes involved in PCD related disease resistance, LSD1 and MLO.
Subject(s)
Apoptosis/genetics , Arabidopsis Proteins , Apoptosis/drug effects , Arabidopsis/cytology , Arabidopsis/genetics , DNA-Binding Proteins/genetics , Mutation , Plant Proteins/genetics , Salicylic Acid/pharmacology , Signal Transduction , Transcription Factors/geneticsABSTRACT
Arabidopsis Isd1 mutants are hyperresponsive to cell death initiators and fail to limit the extent of cell death. Superoxide is a necessary and sufficient signal for cell death propagation. Thus, LSD1 monitors a superoxide-dependent signal and negatively regulates a plant cell death pathway. We isolated LSD1 via its map position. The predicted LSD1 protein contains three zinc finger domains, defined by CxxCxRxxLMYxxGASxVxCxxC. These domains are present in three additional Arabidopsis genes, suggesting that LSD1 defines a zinc finger protein subclass. LSD1 is constitutively expressed, consistent with the mutant phenotype. Alternate splicing gives rise to a low abundance mRNA encoding an extra five amino-terminal amino acids. We propose that LSD1 regulates transcription, via either repression of a prodeath pathway or activation of an antideath pathway, in response to signals emanating from cells undergoing pathogen-induced hypersensitive cell death.
