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
  [email protected]
• Ms.Hitika Gulabani
  Senior Research Fellow
  [email protected]
• Mr. Ingole Kishore Dnyaneshwar
  Senior Research Fellow
  [email protected]
• Mr. Mritunjay Kasera
  Senior Research Fellow
  [email protected]
• Mr. Krishendu Goswami
  Junior Research Fellow
  [email protected]
• Shreeshail Sonyal
  Young Investigator
  [email protected]
• Dahale Shraddha Kantilal
  Junior Research Fellow
  [email protected]

1. Bhattacharjee S, Noor JJ, Gohain B, Gulabani H, Dnyaneshwar IK, Singla A. (2015)  Post-translational modifications in regulation of pathogen surveillance and signaling in plants: The inside- (and perturbations from) outside story. IUBMB Life 67:524
2. Kim SH, Son GH, Bhattacharjee S, Kim HJ, Nam JC, Nguyen PD, Hong JC, Gassmann W. (2014) The Arabidopsis immune adaptor SRFR1 interacts with TCP transcription factors that redundantly contribute to effector-triggered immunity.
   Plant J 78:978.
3. Bhattacharjee S, Garner CM, Gassmann W. (2013) New clues in the nucleus: transcriptional reprogramming in effector-triggered immunity. Front Plant Sci 4:364.
4. Kim TH, Hans-Henning K, Bhattacharjee S, Hauser F, Park JY, Engineer C, Liu A, Ha T, Parker JE, Gassmann W, Schroeder JI. (2012) Natural Variation in Small Molecule-Induced TIR-NB-LRR Signaling Induces Root Growth Arrest via EDS1 and PAD4-Co-complexed R Protein VICTR. The Plant Cell 24:5177.
5. Gassmann W, Bhattacharjee S. (2012) Effector-triggered immunity signaling: From gene-for-gene pathways to protein-protein interaction networks. Mol. Plant Microbe Interact. 25:862.
6. Bhattacharjee S, Halane MK, Kim SH, Gassmann W. (2011). Pathogen effectors target Arabidopsis EDS1 and alter its interactions with immune regulators. Science 334(6061):1405.
7. Jaubert MJ, Bhattacharjee S, Mello AFS, Perry KL, Moffett P. (2011) AGO2 mediates RNA silencing anti-viral defenses against Potato virus X in Arabidopsis. Plant Physiol156:1556.
8. Kim SH, Gao F, Bhattacharjee S, Adiasor JA, Nam JC, Gassmann W. (2010) The Arabidopsis resistance-like gene SNC1 is activated by mutations in SRFR1 and contributes to resistance to the bacterial effector AvrRps4. PLoS Pathogens 6:e1001172.
9. Liu PP, Bhattacharjee S, Klessig D, Moffett P. (2010) Systemic acquired resistance is induced by R gene-mediated responses independent of cell death. Mol. Plant Pathol. 11155.
10. Bhattacharjee S, Zamora A, Azhar MT, Sacco MA, Lambert LH, Moffett P. (2009) Virus resistance induced by NB-LRR proteins involves Argonaute4-dependent translational control. Plant J 58:940.
11. Kim SH, Kwon SI, Bhattacharjee S, Gassmann W. (2009) Regulation of defense gene expression by Arabidopsis SRFR1. Plant Signaling and Behavior 4:149.
12. Kwon SI, Kim SH, Bhattacharjee S, Noh JJ, Gassmann W. (2009) SRFR1, a suppressor of effector-triggered immunity, encodes a conserved tetratricopeptide repeat protein with similarity to transcriptional repressors. Plant J 57:109.
13. Bhattacharjee S, Lee LY, Oltmanns H, Cao H, Veena, Cuperus J, Gelvin SB. (2008) IMPa-4, an Arabidopsis importin isoform, is preferentially involved in Agrobacterium-mediated plant transformation. Plant Cell 20:2661.
14. Zhu Y, Nam J, Humara JM, Mysore KS, Lee LY, Cao H, Valentine L, Li J, Kaiser A, Kopecky A, Hwang HH, Bhattacharjee S, Rao P, Tzfira T, Rajagopal J, Yi H, Veena,Yadav BS, Crane Y, Lin K, Larcher Y, Gelvin M, Knue M, Ramos C, Zhao X, Davis S, Kim SI, Ranjith-Kumar CT, Choi YJ, Hallan V, Chattopadhyay S, Sui X, Ziemienowicz A, Matthysse AG, Citovsky V, Hohn B, Gelvin SB. (2003) Identification of Arabidopsis rat mutants. Plant Physiol 132:494.
15. Tao Y, Rao PK, Bhattacharjee S, Gelvin S.B. (2004) Expression of a plant protein phosphatase 2C interferes with nuclear import of the Agrobacterium T-complex protein VirD2. Proc Natl Acad Sci USA 101:5164.