My current research primarily focus on how plants regulate immune responses. My part of the research involves the characterization of SRFR1, a negative regulator of effector-triggered immunity in the model plant system Arabidopsis thaliana. I have demonstrated that SRFR1 forms protein complexes with multiple R proteins and possibly determines the specificity of immune responses. Additionally, this complex also contains EDS1, the central regular of basal and TNL class of R protein-specific innate immunity. Multiple bacterial avirulence effectors target EDS1 in their attempt to dampen basal resistance. Because of tight association of EDS1 with the cognate R proteins in resistant host genotypes, this targeting of EDS1 is the trigger for initiation of effector triggered immunity.

See my current research.

My research exploited plant molecular mechanisms that recognize viruses as "non-self" entities and prevent virus accumulation. Previous systems were limited by the localized cell death, termed hypersensitive response (HR) that prevented thorough molecular analysis of the resistance mechanisms. I developed a novel agrobacterium-based transient experimental system that is HR-independent and separates the recognition phase from the execution of the virus. Utilizing this system and by polysome fractionation and northern analysis, I demonstrated that the induced anti-viral response allows accumulation of viral transcripts but these transcripts are not translated into proteins. The translational control of virus during gene for gene resistance is mediated by AGO4, a member of class of proteins called Argonautes. Collaborative experiments with Dr. Daniel Klessig's lab at BTI led additional important finding that HR is dispensable for R protein-mediated induction of systemic acquired resistance (SAR).

Among several plant proteins that play key roles in affecting the transformation process by Agrobacterium tumefaciens, the importin * members guide the nuclear import of the invading T-strands. I investigated the roles of 7 of the Arabidopsis importin * isoforms in a series of experimental approaches. Mainly these involved testing for direct protein-protein interaction assays via yeast two-hybrid and in vitro assays with two known T-strand-associated agrobacterium proteins. In planta assays included quantitative and qualitative root-based transient and stable transformation assays on T-DNA tagged mutant lines of each of the above members. Tissue specific expression patterns and relative transcript levels of these importin * isoforms were investigated by promoter-reporter fusions and quantitative real-time PCR approaches. The results revealed a unique property of the invading T-strands to utilize the most proficient of the importin * isoform in order to gain access to the nucleus. Subsequent manipulation in expression pattern/level of identified essential importin * member provides improved approaches to genetically engineer recalcitrant plant species by agrobacterium.

Set-up Transgenic mice facility.