Doctor of Philosophy (Ph.D.)
Zoology
University of Calcutta
1989
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Faculty
Faculty
Atanu Duttaroy, Ph.D.
Professor
Department/Office
- Biology
School/College
- College of Arts & Sciences
Biography
Atanu Duttaroy, Ph.D., is a professor in the Department of Biology at Howard University. He earned his doctorate from the University of Calcutta and holds both a master’s degree and bachelor’s degree from the University of Burdwan in India. Since joining Howard University, Duttaroy has built a distinguished career in molecular genetics, aging research and cellular biology, while contributing to the university’s mission of excellence in teaching, research and mentorship.
Duttaroy’s research focuses on the molecular mechanisms of aging, oxidative stress and neurodegeneration. His laboratory uses Drosophila melanogaster as a model organism to investigate the role of manganese superoxide dismutase and related cellular pathways in aging, longevity and disease. His work has been supported by the National Institutes of Health, the National Science Foundation and the American Federation for Aging Research, and he has published extensively on topics including oxidative stress, mitochondrial function, gene regulation and developmental biology.
At Howard University, Duttaroy teaches courses in molecular genetics and advanced molecular techniques and applications while mentoring undergraduate and graduate students in biological research. In addition to his teaching and scholarship, he has helped expand research opportunities for students through collaborative initiatives and federally funded programs aimed at increasing participation in aging and biomedical research. His work reflects a commitment to advancing scientific discovery while preparing the next generation of researchers in the biological sciences.
Education & Expertise
Education
Master of Science (M.Sc.)
Zoology
University of Burdwan
1980
Bachelor of Science (B.Sc).
Zoology (Honors)
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
Academics
Advanced Molecular Techniques and Application (BIOL462)
Molecular Genetics (BIOL450)
Research
Research
Specialty
Superoxide dismutase characterization in DrosophilaFunding
ACTIVE
1. National Institutes of health R25AG047843 (9/1/14- 8/31/2026). Role: Principal Investigator. Project Title: Advancing aging research through development of minority gerontologists. Award Total: $3.8 million.
2. National Institutes of health 1R25AG086106-01 The Howard University Expanding. Research in Alzheimer's Disease and Related Dementias Postbaccalaureate Research Education Program (HU-ERA-PREP). (5/15/2024 to 4/30/2029). Role: Multiple PI grant with Joanne Allard, Atanu Duttaroy, Sudha Sharma. Total cost: $2,142,090.
3. National Science Foundation: FAIN 2406155. Targeted Infusion Project: Advancing Computational Biology training for undergraduate students at Howard University. (12/01/24-11/30/27). Role: Coprincipal Investigator. Shaolei Teng- PI. Total Cost: $400,000.
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
"Peroxisome proliferator-activating receptor gamma coactivator 1 (PGC-1) is a key transcriptional coactivator in mammals, involved in a myriad of physiological functions, including energy homeostasis, gluconeogenesis, and fatty acid oxidation. PGC-1 can respond to environmental cues, such as nutrients, and to the regulation of thermal tolerance. The single Drosophila PGC-1 homolog, designated Spargel, shares significant homology with PGC-1 at the RNA recognition motif (RRM) and serine–arginine repeat (RS), as well as comparable subcellular localization, which may have greater functional significance.
Duttaroy Group has been a leading group working on spargel for 10+ years. During this time, we reported that Spargel is functionally involved in the nutrient-sensing pathway, oogenesis, chorion gene amplification, and, most recently, endoreplication and cell growth in developing somatic tissues. We generated many exclusive reagents to support these claims, including a Spargel monoclonal antibody (7A10), a spargel transgene tagged with a GFP reporter for overexpression in target tissue(s), a null mutant for the gene (srlnull), and RRM and RS deletion mutants (delta-RRM and delta-RS) created by precise deletion of the endogenous spargel using CRISPR/Cas9. Srlnull homozygotes are late-embryonic lethal, whereas both delta-RRM and delta-RS flies are less viable and poorly fertile due to limited egg production. These spargel mutants have enabled us to gather a wealth of information, but we are trying to understand the mechanistic aspects of Spargel action(s)."
Accomplishments
Accomplishments
Member Peer review Panel, Hevolution, an international effort to accelerate progress in healthy aging research
NIMHD Specialized Centers of Excellence on Minority Health and Health Disparities (U54), 2017
NIH/NIGMS Pathway to independence award (K99/R00) panel, 2015
NSF Physiological Mechanisms and Biomechanics Program panel, 2014
American Federation for Aging Research Review Panel, 2011-2012
NIH Challenge Grants review panel in Health and Science Research, 2009
F31 NIH/NRSA Pre-doctoral Fellowship, 2008, NIH Special Emphasis Panel, 2007
NIH Peer Review Panel, CMAD/NIA, 2007
NIH Peer Review Panel, CMAD/NIA, 2006
E. E. Just Research Achievement Award, Sigma-Xi Scientific Research Society. Howard University chapter, 2004.
Publications and Presentations
Publications and Presentations
Maternal Spargel/dPGC-1 is critical for embryonic development and influences chorion gene amplification via Cyclin E activity
The function of spargel/dPGC-1 in Drosophila oogenesis has been unequivocally established. Here, we sought to assess whether Spargel protein or RNA is essential for developmentally competent eggs. The trans-heterozygotic combination of two spargel mutant alleles allowed us to decrease Spargel expression to very low levels. Using this model, we now demonstrated the requirement for Spargel in eggshell patterning and embryonic development, which led us to establish that spargel is a maternal effect gene. Further examination of Spargel's potential mechanism of action in eggshell biogenesis revealed that low levels of Spargel in the adult ovary cause diminished Cyclin E activity, resulting in reduced chorion gene amplification levels, leading to eggshell biogenesis defects. Thus, another novel role for spargel/dPGC-1 is exposed whereby, through Cyclin E activity, this conserved transcriptional coactivator regulates the chorion gene amplification process.
Spargel/dPGC-1 is essential for oogenesis and nutrient-mediated ovarian growth in Drosophila
Spargel/dPGC-1 is essential for oogenesis and nutrient-mediated ovarian growth in Drosophila
Dietary proteins are crucial for oogenesis. The Target of Rapamycin (TOR) is a major nutrient sensor controlling organismal growth and fertility, but the downstream effectors of TOR signaling remain largely uncharacterized. We previously identified DrosophilaSpargel/dPGC-1 as a terminal effector of the TOR-TSC pathway, and now report that Spargel connects nutrition to oogenesis. We found that Spargel is expressed predominantly in the ovaries of adult flies, and germline spargel knockdown inhibits cyst growth, ultimately leading to egg chamber degeneration and female sterility. In situ staining demonstrated nuclear localization of Spargel in the nurse cells and follicle cells of the ovariole. Furthermore, Spargel/dPGC-1 expression is influenced by dietary yeast concentration and TOR signaling, suggesting Spargel/dPGC-1 might transmit nutrient-mediated signals into ovarian growth. We propose that potentiating Spargel/dPGC-1 expression in the ovary is instrumental in nutrient-mediated regulation of oogenesis.
The essential requirement of an animal heme peroxidase protein during the wing maturation process in Drosophila
Thus far, a handful of genes have been shown to be related to the wing maturation process in insects. A novel heme peroxidase enzyme known as curly suppressor (Cysu)(formerly CG5873), have been characterized in this report because it is involved in wing morphogenesis. Using bioinformatics tools we found that Cysu is remarkably conserved in the genus Drosophila (>95%) as well as in invertebrates (>70%), although its vertebrate orthologs show poor homology. Time-lapse imaging and histochemical analyses have confirmed that the defective wing phenotype of Cysu is not a result of any underlying cellular alterations; instead, its wings fail to expand in mature adults.
SOD2, the principal scavenger of superoxide
Definitive evidence on the impact of MnSOD/SOD2-deficiency and the consequent effects of high flux of mitochondrial reactive oxygen species (ROS) on pre-natal/pre-adult development has yet to be reported for either Drosophila or mice. Here we report that oocytes lacking maternal SOD2 protein develop into adults just like normal SOD2-containing oocytes suggesting that maternal SOD2-mediated protection against mitochondrial ROS is not essential for oocyte viability. However, the capacity of SOD2-null larvae to undergo successful metamorphosis into adults is negatively influenced in the absence of SOD2. We therefore determined the impact of a high superoxide environment on cell size, progression through the cell cycle, cell differentiation, and cell death and found no difference between SOD2-null and SOD2+ larva and pupa.
Emerging functional similarities and divergences between Drosophila Spargel/dPGC-1and mammalian PGC-1 protein
Peroxisome Proliferator Activated Receptor Gamma Co-activator-1 (PGC-1) is a well-conserved protein among all chordates. Entire Drosophila species subgroup carries a PGC-1 homolog in their genome called spargel/dPGC-1 showing very little divergence. Recent studies have reported that significant functional similarities are shared between vertebrate and invertebrate PGC-1's based on their role in mitochondrial functions and biogenesis, gluconeogenesis, and most likely in transcription and RNA processing. With the help of genetic epistasis analysis, we established that DrosophilaSpargel/dPGC-1 affects cell growth process as a terminal effector in the Insulin-TOR signaling pathway. The association between Spargel/dPGC-1 and Insulin signaling could also explain its role in the aging process. Here we provided a further comparison between Spargel/dPGC-1 and PGC-1 focusing on nuclear localization, oxidative stress resistance, and a possible role of Spargel/dPGC-1 in oogenesis reminiscing the role of Spargel in reproductive aging like many Insulin signaling partners. This led us to hypothesize that the discovery of newer biological functions in DrosophilaSpargel/dPGC-1 will pave the way to uncover novel functional equivalents in mammals.
Mechanism of Silver Nanoparticles Action on Insect Pigmentation Reveals Intervention of Copper Homeostasis
Silver nanoparticles (AgNPs), like almost all nanoparticles, are potentially toxic beyond a certain concentration because the survival of the organism is compromised due to scores of pathophysiological abnormalities past that concentration. However, the mechanism of AgNP toxicity remains undetermined. Instead of applying a toxic dose, we attempted to monitor the effects of AgNPs at a nonlethal concentration on wild type Drosophila melanogaster by exposing them throughout their development.
Spargel/dPGC-1 is a new downstream effector in the Insulin-TOR signaling pathway in Drosophila
Spargel/dPGC-1 is a new downstream effector in the Insulin-TOR signaling pathway in Drosophila
Insulin and target of rapamycin (TOR) signaling pathways converge to maintain growth so a proportionate body form is attained. Insufficiency in either insulin or TOR results in developmental growth defects due to low ATP level. Spargel is the Drosophila homolog of PGC-1, which is an omnipotent transcriptional coactivator in mammals. Like its mammalian counterpart, Spargel/dPGC-1 is recognized for its role in energy metabolism through mitochondrial biogenesis. An earlier study demonstrated that Spargel/dPGC-1 is involved in the insulin–TOR signaling, but a comprehensive analysis is needed to understand exactly which step of this pathway Spargel/PGC-1 is essential. Using genetic epistasis analysis, we demonstrated that a Spargel gain of function can overcome the TOR and S6K mediated cell size and cell growth defects in a cell autonomous manner.
A muscle-specific p38 MAPK/Mef-2/MnSOD pathway regulates stress, motor function, and life span in Drosophila
Molecular mechanisms that concordantly regulate stress, life span, and aging remain incompletely understood. Here, we demonstrate that in Drosophila, a p38 MAP kinase (p38K)/Mef2/MnSOD pathway is a coregulator of stress and life span. Hence, overexpression of p38K extends life span in a MnSOD-dependent manner, whereas inhibition of p38K causes early lethality and precipitates age-related motor dysfunction and stress sensitivity, that is rescued through muscle-restricted (but not neuronal) add-back of p38K. Additionally, mutations in p38K are associated with increased protein carbonylation and Nrf2-dependent transcription, while adversely affecting metabolic response to hypoxia. Mechanistically, p38K modulates expression of the mitochondrial MnSOD enzyme through the transcription factor Mef2, and predictably, perturbations in MnSOD modify p38K-dependent phenotypes. Thus, our results uncover a muscle-restricted p38K-Mef2-MnSOD signaling module that influences life span and stress, distinct from the insulin/JNK/FOXO pathway. We propose that potentiating p38K might be instrumental in restoring the mitochondrial detoxification machinery and combating stress-induced aging.