Education

Ph.D.
University of Calcutta
1989

M.Sc
University of Burdwan
1980

B.Sc.
University of Burdwan
1978

Expertise

Superoxide dismutase characterization in Drosophila

Cell signaling events related to oxidative stress

Neuroimmunological role of Microglial cells

Relationship between MnSOD and neuromuscular degeneration

Academics

Advanced Molecular Techniques and Application (BIOL462)

Molecular Genetics (BIOL450)

Research

Specialty

Superoxide dismutase characterization in Drosophila

Funding

Current
National Institutes of Heath.  Title:  Advancing Aging Research Through the Development of Minority gerontologists.  1 R25AG047843-01. 9/1/14 to 8/31/19.
PI ($1.9 million).
Completed
National Science Foundation.  Title: Centre for Environmental Implications of Nanotechnology (CEIN) with Duke University. 2008-2013.Co-PI. ($450,000)
National Institutes of Health.  Title: Manganese superoxide dismutase in mechanisms of aging and neurodegeneration. 2 U54 NS039407-06A1. ($750,000) 
National Institutes of Health.  Title: ROS induced cellular toxicity and tissue damage assessment.  1R15 AG025754-01. PI. ($300,000)
National Institutes of Health. Manganese superoxide dismutase and in vivo aging. 1R15 AG 17846-01. 9/01/00 to 8/31/03. PI ($150,000)
National Institutes of Health 1R15 AG 17846-01 and 1R15 AG 17846-01S1 (supplement) "Manganese Superoxide Dismutase and In Vivo Aging." 9/01/2000 to 8/31/2003. PI. ($52,000)
American Federation for Aging Research. "Genomic Regions Involved in Manganese Superoxide Dismutase Regulation in Drosophila. 7/1/01 to 6/30/03. PI. ($50,000)

Group Information

Aerobic organisms employ a family of metalloenzymes known as Superoxide Dismutase (SOD) to scavenge superoxide anions (O2-); the highly reactive oxygen species generated by univalent reduction of molecular oxygen during cellular respiration. SODs essentially dismutate O2- to hydrogen peroxide (H2O2) that is converted to H2O by Catalase and Peroxidase. O2- radicals are damaging to cellular constituents because these radicals attack proteins, nucleic acids and membrane lipids, thereby disrupting cellular function and integrity. The cumulative effect of this cellular damage contributes to many cellular pathologies including mutagenesis, carcinogenesis, diabetes, neurodegenerative disease, inflammatory diseases, as well as to the overall process of cellular senescence organismal aging proces. I am using the fruitfly, Drosophila melanogaster as a model organism in my laboratory, since Drosophila offers a well-defined reproductive, developmental, behavioral and molecular genetic system. Drosophila carries two forms of SOD: the copper-zinc SOD (Cu-ZnSOD), which is cytoplasmic, and the Manganese SOD (MnSOD), which acts in mitochondria. Null mutants for Cu-ZnSOD in Drosophila show reduced viability and most importantly, Cu-ZnSOD null mutants have neuropathology and reduced motor activity. The DrosophilaMnSOD gene is now well characterized (Duttaroy et al., 1994; Duttaroy et al., 1997; Duttaroy et al., 2003) although the biological role of MnSOD remains virtually unexplored. MnSOD function must be vital to the cell, since MnSOD activity is restricted to the principal cellular radical generating organelle, the mitochondria. The interest of my laboratory will be geared towards understanding MnSOD gene function by using following molecular genetic tools available in Drosophila: