DEPARTMENT OF BIOLOGY FACULTY PROFILE
RESEARCH ATANU DUTTAROY PUBLICATIONS
Contact Information
E-mail: aduttaroy@howard.edu
Office Location: EE Just Hall Room 336
Office Telephone: 202-806-5362
Laboratory Location: EE Just Hall Room 317

Education
Ph.D., University of Calcutta, India (1989)


Teaching
Graduate Seminar (501)
Advanced Molecular Techniques and Application (462)
Molecular Genetics (450)

Research
Superoxide dismutase characterization in Drosophila
Cell signaling events related to oxidative stress
Relationship between MnSOD and neuromuscular degeneration
Neuroimmunological role of Microglial cells


Laboratory Personnel
Tomilowl Abijo - Graduate Student
MD Adul Basar - Undergraduate Student

Research Detailed

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:

Selected Publications:

  The essential requirement of an animal heme peroxidase protein during the wing maturation process in Drosophila. Bailey D, Basar MA, Nag S, Bondhu N, Teng S, Duttaroy A. BMC Dev Biol. 2017 Jan 11;17(1)
  Mukherjee S, Basar MA, Davis C, Duttaroy A. Emerging functional similarities and divergences between Drosophila Spargel/dPGC-1 and mammalian PGC-1 protein. Front Genet. 2014 Jul 10;5:216. doi: 10.3389/fgene.2014.00216. eCollection 2014.
  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.
  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.