The arabidopsis ALF3-1 mutation causes autoimmunity in the root and identifies a TIR domain protein
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Plant defense responses vary depending on the pathogen and intensity of attack. These responses are mediated through two levels of defense, with the first level being pathogen-triggered immunity (PTI) that is triggered by host recognition of microbe-associated molecular patterns (MAMPs). Successful pathogens are able to evade PTI by secreting effector molecules into host cells. These effectors are designed to suppress host defenses. In turn, effectors are inhibited by the second level of plant defense called effector-triggered immunity (ETI). In ETI, intracellular resistance proteins recognize and block effector dampening of host defenses. ETI results in gene expression changes that can lead to localized cell death known as the hypersensitive response (HR) as well as a plant-wide systemic acquired resistance. The Arabidopsis thaliana mutant alf3-1 (aberrant lateral root formation 3-1) was characterized as the first and only case of HR in the root system. The alf3-1 mutant’s primary and lateral roots die unless they are grown in auxin-supplemented medium or at elevated ambient temperature. This thesis describes further characterization of the mutant phenotype and identifies a candidate gene for ALF3. Consistent with an autoimmune response, we found that the alf3-1 mutant has increased production of phenylalanine- and tryptophan-derived defense compounds, as well as increased production of salicylic acid (SA), a plant hormone that mediates innate immunity. Based on gene expression profiling, we found that many immune and defense response genes were expressed highly in alf3-1 compared to wild type (WT). These genes include the SA-responsive PR1 and PBS3 as well as several WRKY transcription factors, a gene family implicated in plant defense. Importantly, we found that the vast majority of defense-related phenotypes dysregulated in alf3-1 returned to WT levels when the mutant was grown at elevated temperatures or in medium supplemented with auxin, conditions that suppress innate immunity. To determine the identity of ALF3, we used whole genome re-sequencing to identify a candidate gene that encodes an uncharacterized TIR domain protein. Because characterized plant TIR domain proteins have been shown to function in plant innate immunity, we hypothesize that alf3-1 is a gain-of-function mutation that causes an autoimmune phenotype in roots.