GENETICS OF PROGRAMMED CELL DEATH IN ARABIDOPSIS

University Of North Carolina Chapel Hill, Chapel Hill NC

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Abstract

DESCRIPTION: This proposal aims at a molecular and genetic understanding of processes determining the timing and control of programmed cell death in the easily manipulated model higher plant, Arabidopsis thaliana. Results will be critical in building generalizable models of cell death control in higher eukaryotes. These experiments will begin to clarify the control of cell death during both plant disease resistance responses and normal development. Results from these experiments can be contrasted to emerging models of cell death regulation in other organisms to ask whether molecular mechanisms are related, or largely divergent. The specific aims rest on the previous identification of Arabidopsis mutants which exhibit aberrant cell death control. These mutations defined four loci (termed lsd1 and lsd3-lsd5 based on their Lesion Simulating Disease Resistance phenotype), and many new mutants are now available. The lsd mutant class can be divided into loci controlling the initiation of cell death and loci which determine the propagation of cell death once it is initiated. These mutants exhibit cell-type specificity for onset of cell death implying spatial and developmental control. We recently isolated the LSD1 gene, which defines the propagation class of loci involved in limiting the spread of cell death, and showed that it encodes a novel zinc finger subclass protein. We also recently demonstrated that wild type LSD1 has a dual function, both of which respond to a superoxide-dependent signal. The first function is to dampen constitutive flux through a cell death pathway, and the second is to prevent rampant propagation of cell death once it is initiated. This proposal contrasts the control of cell death propagation, as defined by lsd1, with the initiation of cell death, exemplified by lsd5. We propose four Specific Aims: The first is to understand at a cell biology level how LSD1 carries out its functions. Aim two is genetic dissection of the LSD1 signal transduction pathway, via isolation of extragenic suppressors of the lsd1 phenotype. These will be placed into complementation groups, mapped, and tested for their ability to suppress cell death caused by external triggers, such as pathogens, and by "initiation class" mutations. Aim three is to finish cloning of the lsd5 gene, and aim four is a detailed analysis of extragenic suppressors of lsd5 which will parallel the study of lsd1 supressors.