Signaling pathways in effector triggered immunity of plant

Plants mount highly elaborate, layered, and complex defenses against constantly invading pathogens. These multilayered defenses broadly termed as PAMP-triggered immunity (PTI) and effector triggered immunity (ETI), account for responses on perception of conserved molecular patterns present on a pathogen surface or to a specific pathogen effector secreted and sensed within the plant cell by a cognate resistance (R) protein, respectively. Although genetic screens and subsequent molecular approaches have identified several key immune players, our present understanding clearly suggests that signaling in ETI defy the conventional step-wise linear arrangements of signal receivers and transducers. Previously, we have proposed that effector activities that cause alterations in dynamics of protein interactomes between the R protein with positive and negative regulators directly mediate the sensing and transduction of signals. The broad goal of our research group is to unravel this mystery at a molecular level.

We utilize the Pseudomonas syringae-Arabidopsis thaliana model system, advantageous due to completely sequenced genomes of both organisms, to identify routes for immune signaling. Macromolecular associations of most defense players are assembled on lipid interfaces via unknown mechanisms. We have obtained preliminary evidences that indicate a role of inositol compounds in this assembly and in plant defenses in general. Inositol derivatives, initially identified as a source of phosphate storage in seeds, direct several key cellular processes such as mRNA export, apoptosis, plant hormone signaling and control of transcription. Inositol-modified lipids (phosphatidylinositols, PtdIns) determine architecture of most eukaryotic membranes. Inositol phosphates (InsPs) function as key secondary messengers. The significance of inositols is clearly elaborated in several human diseases such as Huntington disease and sickle cell disease. Our research aims to transcend the plant/anim al species barrier and further highlight the fundamental similarities in defense responses of higher eukaryotes.

In order to elucidate inositol signaling in immune responses we have divided our approach in several broad directions:

• Identifying steady-state protein-protein interactions platforms of resistance proteins and defense modulators on cellular interfaces and how pathogen effectors directly/indirectly affect this assembly.
• Elucidation of inositol metabolite profiles in plant mutants altered in defense responses in order to identify specific signaling routes
• Identifying inositol compound-dependent synergistic and antagonistic cross-talk between hormonal pathways and how pathogen effectors or induced ETI impinge of this network.

Our investigations utilize a combination of genetic, cell biology, advanced microscopic, metabolic profiling approaches, among others, to gain a comprehensive understanding in this area. In addition we are also developing effector-independent inducible-ETI systems that will facilitate identification of signaling routes during initiation and execution of ETI responses.

• Ramalingaswami Re-entry Fellowship (2012-2013)

• Dr. Jewel Jameeta Noor
  Research Associate
  jewelj@rcb.res.in
• Ms.Hitika Gulabani
  Senior Research Fellow
  hitika.gulabani@rcb.res.in
• Mr. Ingole Kishore Dnyaneshwar
  Senior Research Fellow
  kishor.ingole@rcb.res.in
• Mr. Mritunjay Kasera
  Senior Research Fellow
  mritunjay@rcb.res.in
• Mr. Krishendu Goswami
  Junior Research Fellow
  krishnendu@rcb.res.in
• Shreeshail Sonyal
  Young Investigator
  shresshail@rcb.res.in
• Dahale Shraddha Kantilal
  Junior Research Fellow
  shraddha@rcb.res.in

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