Ph.D., University of Calcutta, India (1989)
Graduate Seminar (501)
Advanced Molecular Techniques and Application (462)
Molecular Genetics (450)
Superoxide dismutase characterization in Drosophila
Cell signaling events related to oxidative stress
Relationship between MnSOD and neuromuscular degeneration
Neuroimmunological role of Microglial cells
Awards, Grants and Service
NIH U54 | MnSOD in aging and neurodegeneration
NSF | Center for Environmental implications of Nanotechnology
NIH R15 | ROS induced cellular toxicity and tissue damage assessment
NIH R15 | Maganese superoxide dismutase and in vivo imaging
American Federation for Aging Research (AFAR)
The Duttaroy Lab:
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 Drosophila MnSOD 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:
Genetic characterization of the Mn SOD gene functions in Drosophila.
Both Loss of function mutation as well as hypomorphic mutations for
MnSOD function were isolated. MnSOD mutants will be important to explore
the biology of this primary defense system against oxidative stress.
over expression, tissue specific misexpression, and tissue specific
loss of MnSOD function will help us to explore the biology of this
primary defense system against oxidative stress.
· Does oxidative stress activates cell signaling event? I am attempting to answer this question by measuring the effects of oxidative stress on mutants in the signal transduction pathways.
· Relationship between MnSOD function and neuromuscular degeneration
||Spargel/dPGC-1 Is a New Downstream Effector in the Insulin–TOR Signaling Pathway in Drosophila. Subhas Mukherjee and Atanu Duttaroy. Genetics October 2013 195:433-441; Early online August 9, 2013.
||Armstrong N, Ramamoorthy M, Lyon D, Jones K, and Duttaroy A (2013) Mechanism of Silver Nanoparticles Action on Insect Pigmentation Reveals Intervention of Copper Homeostasis. PLoS One 8(1):e53186
||Vrailas-Mortimer A, delRivero, T, Mukherjee S, Nag S, Giatanidis A, Consoulas C, Duttaroy A, and Sanyal S (2011) A muscle-specific p38 MAPK/Mef-2/MnSOD pathway regulates stress, motor function, and life span in Drosophila. Developmental Cell 21:783-795.
Mukherjee S, Forde R*, Belton A*, and Duttaroy A. (2011) SOD2, the principal scavenger of superoxide, is dispensable for embryogenesis and imaginal tissue development but essential for adult survival. FLY 5: 39 (see also cover photograph)
Godenschwege T, Forde R*, Davis C*, Paul A, Beckwith K*, Duttaroy A. (2009) Mitochondrial Superoxide Radicals Differentially Impacts Muscle Activity and Neural Functions in Drosophila. Genetics 183: 175-184.
Piazza N, Hayes M, Martin I, Duttaroy A, Grotewiel M, Wessells R (2009) Multiple measures of functionality exhibit progressive decline in a parallel, stochastic fashion in Drosophila Sod2 null mutants. Biogerontology 10(5): 637-48.
Wicks S, Bain N, Duttaroy A, Hilliker AJ, Phillips JP (2009) Hypoxia rescues early mortality conferred by superoxide dismutase deficiency. Free Radic Biol Med. 46:176-81
Paul A, Belton A*, Nag S, Martin I, Grotewiel MS and DuttaroyA (2007) Reduced mitochondrial SOD displays mortality characteristics reminiscent of natural aging. Mechanisms of Aging and Development 128: 706-716.
Dora Dias-Santagata, Atanu Duttaroy and Mel B. Feany (2007) Tau-induced neurodegeneration is modulated by oxidative stress and activates the JNK pathway in Drosophila. Journal of Clinical Investigation 117:236–245.
Belton A*, Paul A, and Duttaroy A (2006) Deletions encompassing the Manganese Superoxide Dismutase gene in the Drosophila melanogaster. Genome 49: 746-749.