Genetic Dissection of Signaling Hierarchy in Arabidopsis Disease Resistance (2006)
Undergraduate: Zafia Anklesaria
Faculty Advisor: Jeff Dangl
Department: Biology
The objective of this study was to investigate the genetics of the innate immune response of Arabidopsis thaliana to bacterial pathogens such as Pseudomonas Syringae. Plants have a class of proteins termed Nucleotide binding leucine rich repeat (NB LRR) proteins which are involved in the plants immune response to bacterial infection. Bacteria such as Pseudomonas Syringae inject their effectors into the plants via the type III secretion system. These effectors are termed Avr proteins. The R gene, RPS2 confers resistance against bacterial pathogens expressing the gene AvrRpt2. The protein RIN4 has been shown to physically interact with the product of the R gene RPS2 in such a way that it holds RPS2 in a non signaling conformation. When the plant is infected with bacteria, AvrRpt2 causes the disappearance of RIN4 and thus RPS2 gets activated. This is termed appropriate activation of RPS2. And results in a localized cell death at the site of the infection termed ?hypersensitive response? (HR). When RIN4 is genetically eliminated from the plant RPS2 is constitutively activated and this results in a generalized cell death that kills the entire plant. This is termed inappropriate activation of RPS2. In Arabidopsis two components of the RPS2 signaling pathway have been identified; NDR1 and RAR1. Through a series of genetic crosses we attempted to assign a precise genetic position to NDR1 and RAR1 during inappropriate activation of RPS2. This was done by observing whether or not a mutation in RAR1 or NDR1 could suppress the lethality of a rin4 knock out mutant and suppress the phenotype of a rin4 knock down mutant. It was found that a mutation in RAR1 was able to partially suppress the phenotype of the rin4 mutations and is therefore downstream of RPS2 during inappropriate activation of RPS2.A mutation in NDR1 had no effect on the phenotype of the rin4 mutants and can therefore be positioned upstream of RPS2 during inappropriate activation.