Profile
Research interest
My research is to understand genetic basis of disease that includes infectious and complex disease. Tuberculosis (TB) is potentially a serious infectious disease usually caused by a virulent bacteria Mycobacterium tuberculosis. The outcome of infection is manyfold. Only a minor group of people develop active tuberculosis upon exposure to Mycobacterium tuberculosis. A handful of individuals are able to clear the infection, whereas majority of infected individuals harbor the infection in latent condition. The ability to effectively restrict M.tb infection depends on the immune status of the individual. We are interested in deep mining of host genetic factors determining susceptibility to infection and understand pathogen and host interface using multiomics approach. The other aspect of my research is to understand genetic basis of congenital heart disease.
5 Selected Publications:
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Analysis of variants in mitochondrial genome and their putative pathogenicity in tuberculosis patients from Mizoram, North east India, Tonsinga MV, Sailoa CV, Zothansangab, Chhakchhuakb L, Chhakchhuakb Z, Pandit B, Kumar D, Majumder PP, Senthil NK, Mitochondrion, (2020)54:21-25
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An exome wide association study of pulmonary tuberculosis patients and their asymptomatic household contacts, Bhattacharyya C, Majumder PP, Pandit B, Infection Genetics & Evolution, (2019) 71:76-81.
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Sputum Proteomics Reveals a Shift in Vitamin D-binding Protein and Antimicrobial Protein Axis in Tuberculosis Patients Bishwal SC, Das MK, Badireddy VK, Dabral D, Das A et.al, Scientific Report, (2019) 31;9(1):1036.
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CXCL10 is overexpressed in active Tuberculosis patients compared to M. tuberculosis-exposed household contacts, Bhattacharyya C, Majumder PP, Pandit B, Tuberculosis (2018) 109:8-16.
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Dissecting host factors that regulate the early stages of tuberculosis infection, Agrawal N, Bhattacharyya C, Mukherjee A, Ullah U, Pandit B, Rao KVS, Majumder PP, Tuberculosis, (2016)100:102-113.
Research
Role of host genomics in determining susceptibility to tuberculosis
Traditionally, infectious diseases were textbook examples of “non-genetic diseases.” But now beyond doubt it has been proven that genetic factors determine the susceptibility to various infectious diseases and their clinical courses upon infection. About one third of world’s population is infected with M.Tb causing tuberculosis with India bout 1.8 million new cases annually. 5-10% of the infected individuals develop active disease at some point of his life, whereas 90% of infected individuals remain asymptomatic. Individual with latent form of disease serves as a reservoir for the disease and is a major obstacle for controlling the disease. Studies with twins and genome wide analysis suggest that host genetics has strong role in determining susceptibility towards TB.
To address the issue of inter individual differences to disease susceptibility we are performing genomic studies to identify host factors that independently or along with pathogen factors modulate course of infection, disease progression and response to treatment. High throughput genotyping and sequencing platforms are used to identify variations in innate immune genes and other cytokines. We have identified that CXCL10 a chemokine is the most significantly altered cytokines in tuberculosis and correlates with severity of disease. Stimulation of CXCL10 expression by ESAT6 compared to Rv2031c reinforced the importance of CXCL10 in the active stage of infection. CXCL10 may, therefore, be considered as a potential biomarker of active phase of infection. In an exom-wide study we have identified a novel locus HLA-DRA associated with protection from tuberculosis.
We intend to understand the disease from different angles which includes genomics, transcriptomics studies and findings are functionally validated. We have recently expanded our study to other regions of India and developed strong collaboration with institutes pan India.
Molecular mechanisms underlying Congenital heart disease
Congenital Heart Disease (CHD) is a group of diseases with various anomalies in heart that occur during embryonic development. Molecular mechanisms of such defects include mutations in transcription factors regulating cardiac gene network, regulatory signaling proteins or sarcomeric proteins. MicroRNA dysfunction, epigenetics also contribute to CHD. The molecular etiology of congenital heart disease has been explored in great details, but lot more remains unanswered. We are interested in understanding the genetic alteration and its cellular effects that leads to different abnormal phenotypes of CHD like septal defect, valve stenosis, hypertrophic cardiomyopathy and many more. Our research focus is to investigate role of genetic variations, dysregulation of microRNA leading to altered gene expression in case of ASD. Different genomic tools are used for exploring such mechanisms.
Projects:
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Genomics-driven Dissection of Susceptibility and Drug Resistance to Pulmonary Tuberculosis, with a Geographical Focus on NER (DBT funded)
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Understanding the regulatory dynamics of tubercular granulomas through genomic and proteomic analyses: implications for latency and re-activation (DBT funded, completed)
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Replication and Functional validation of genomic correlates of tuberculosis susceptibility (WB-DBT funded)
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Exploring underlying Molecular mechanisms of defects in congenital heart disease
CV
Name: BHASWATI PANDIT
Email: bp1nibmg.ac.in
Present Position: Associate Professor
Highest educational Qualification: Ph.D.
Curriculum Vitae:
Education
|
Year |
University |
Degree |
|
2001 |
University of Calcutta |
Ph.D |
|
1995 |
University of Calcutta |
M.Sc |
|
1993 |
University of Calcutta |
B.Sc |
Professional Appointments
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Assistant Professor, 2010-2019, National Institute of Biomedical genomics
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Assistant Professor, 2008-2010, SN. Pradhan Center for Neurosciences, University of Calcutta
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Post Doctoral fellow, 2005-2008 Center for Molecular Cardiology Department of Genetics and Genomic Sciences, Mount Sinai School of Medicine, NY, USA
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Post Doctoral Fellow, 2001-2005 Division of Endocrinology, Diabetes and Medical Genetics, Medical University of South Carolina, USA
Professional Memberships
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Indian Society for Human Genetics
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Calcutta Consortium of Human Genetics
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DNA Society of India
Awards/Honors
2007 Best publication of the year 2007, Mount Sinai School of Medicine
Invited/Special lectures
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2019 2nd International Conference on antimicrobial resistance, novel drug discovery and development: challenges and opportunities’ SRM University in association with Royal Society of Tropical Medicine and Hygiene
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2019 International Conference on Molecular Basis of Diseases and Therapeutics, School of Life Sciences, Central University of Rajasthan
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2018 18th ALL INDIA CONGRESS OF CYTOLOGY AND GENETICS, International Symposium on “Translating Genes and Genomes” jointly organized by CSIR-Indian Institute of Chemical Biology and Archana Sharma Foundation of Calcutta
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2009 Lady Brabourne College, Kolkata, Career workshop for young Biochemists, Roadmap of Genetic Diseases: Introduction to Genetic markers and gene mapping
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2008 Mount Sinai School of Medicine, NY, USA, “Meet the Author” series lecture
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2008 Bose Institute, New role of RAS/MAPK pathway: link to Cardiac hypertrophy
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2004 Dept. of Human Genetics, University of Michigan, Ann Arbor, USA Sitosterolemia: A Model for Dietary Sterol Absorption and Excretion
Past Major Projects
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Gene discovery of Noonan Syndrome
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Genetic and biochemical study of sterol metabolic disorder: Sitosterolemia and Smith Lemli Opitz syndrome
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Genetic instability in Chinese hamster V79 cells
Publications
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Analysis of variants in mitochondrial genome and their putative pathogenicity in tuberculosis patients from Mizoram, North east India, Tonsing MV, Sailo CV, Zothansang, Chhakchhuak L, Chhakchhuak Z, Pandit B, Kumar D, Majumder PP, Senthil NK. Mitochondrion, (2020) 54:21-25.
-
An exom-wide association study of pulmonary tuberculosis patients and their asymptomatic household contacts, Bhattacharyya C, Majumder PP, Pandit B. Infection Genetics Evolution. (2019) 71:76-81.
-
Sputum Proteomics Reveals a Shift in Vitamin D-binding Protein and Antimicrobial Protein Axis in Tuberculosis Patients, Bishwal SC, Das MK, Badireddy VK, Dabral D, Das A et.al. Scientific Report, (2019) 31;9(1):1036.
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CXCL10 is overexpressed in active Tuberculosis patients compared to M. tuberculosis-exposed household contacts, Bhattacharyya C, Majumder PP, Pandit B. Tuberculosis (2018) 109:8-16.
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Genes and Genetics of tuberculosis, Pandit B. International Journal of Pulmonary& Respiratory Sciences (2017) 1(4):55567.
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Dissecting host factors that regulate the early stages of tuberculosis infection, Agrawal N, Bhattacharyya C, Mukherjee A, Ullah U, Pandit B, Rao KVS, Majumder PP. Tuberculosis, (2016)100 :102-113.
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Roles for transcription factors Sp1, NF-kB, IRF3 and IRF7 in expression of the human IFNL4 gene, Chinnaswamy S, Bhusan A, Behera AK, Ghosh S, Rampurkar V, Chandra V, Pandit B, Kundu TK. Viral Immunology (2016)Jan-Feb 29(1)49-63.
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Deregulated tyrosine-phenylalanine metabolism in pulmonary tuberculosis patients- Das MK,Bishwal SC, Das A, DabralD, Badireddy VK, Pandit B, Varghese GM, Nanda RK. J Proteome Research (2015) 14(4): 1947-56.
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Gain-of-function RAF1 mutations cause Noonan and LEOPARD syndromes with hypertrophic cardiomyopathy- Pandit B, Sarkozy A, Pennacchio LA, Carta C, Oishi K,Martinelli S, Pogna EA, Schackwitz W, Ustaszewska A, Landstrom A, Bos JM, Ommen SR, Esposito G, Lepri F, Faul C, Mundel P, López Siguero JP, Tenconi R, Selicorni A, Rossi C, Mazzan L, Torrente I, Marino B, Digilio MC, Zampino G, Ackerman MJ, Dallapiccola B, Tartaglia M, Gelb BD, Nature Genetics (2007) 39(8):1007-1012.
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Gain-of-function SOS1 mutations cause a distinctive form of Noonan syndrome, Tartaglia M, Pennacchio LA, Zhao C, Yadav KK., Fodale V, Sarkozy A, Pandit B, Oishi K, Martinelli S, Schackwitz W, Ustaszewska A, Martin J, Bristow J, Carta C, Lepri F, Neri C, Vasta I, Gibson K, Curry CJ, López Siguero JP, Digilio MC, Zampino G, Dallapiccola B, Bar-Sagi D, Gelb BD. Nature Genetics (2007) 39(1):75-79.
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Increased expression of genes in a radioresistant cell strain: modulation of hnRNP E2, Hsp90 and SSBP2 genes in γ-irradiated Chinese hamster V79 cells Roychoudhury P, Pathak R, Pandit B, Chaudhuri K, Bhattacharyya NP. Int J of Low Radiation (2007) 4(4), 313-331.
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Loss of Apolipoprotein E exacerbates the neonatal lethality of the Smith-Lemli-Opitz Syndrome mouse-Solca C*, Pandit B*, Yu H, Tint GS, Patel SB. Molecular Genetics and Metabolism (2007) 91(1):7-14.* equal contribution.
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A detailed Hapmap of the STSL locus spanning 69kb; Differences between Caucasians and African-Americans, Pandit B, Ahn GS, Hazard SE, Gordon D, Patel SB. BMC Medical Genetics (2006)7(1): 13.
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Sitosterolemia in Switzerland: Molecular genetics links to the US Amish Mennonites to their European roots, Solca C, Stanga Z, Pandit B, Diem P, Greeve J, Patel SB. Clinical Genetics (2005) 68:174-178.
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Induction of apoptosis by Benzamide and its inhibition by Aurin triboxylic Acid (ATA) in Chinese hamster V79 cells, Ghosh U, Pandit B, Dutta J, Bhattacharyya NP. Mutation Research (2004) 554:121-129.
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Identification of two differentially expressed mitochondrial genes in a methotrexate – resistant chinese hamster cell derived from V79 cells using RNA fingerprinting by arbitrary primed polymerase chain reaction, Chaudhuri K, Banerjee R, Pandit B, Mukherjee A, Das S, Sengupta S, Roychoudhury S, Bhattacharyya NP. Radiation Research (2003) Jul; 160(1):77-85.
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The rat STSL locus: characterization, chromosomal assignment, genetic variations in sitosterolemic hypertensive rats, Yu H, Pandit B, Klett EL, Lee MH, Lu K, Helou K, Ikeda I, Egashira N, Sato M, Klein RL, Batta A, Salen G, Patel SB. BMC Cardiovascular Disorders (2003) 3:4, 1-19.
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Co-amplification of dhfr and a homologue of hmsh3 in a Chinese hamster methotrexate-resistant cell line correlates with resistance to a range of chemotherapeutic drugs, Pandit B, Roy M, Dutta J, Padhi BK, Bhowmik G, Bhattacharyya NP. Cancer Chemotherapy & Pharmacology (2001) 48:312-318.
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In vitro and in vivo inhibition of telomerase activity from Chinese hamster V79 cells, Pandit B & Bhattacharyya NP. Indian Journal of Biochemistry & Biophysics (2001) 38,42-47.
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Detection of telomerase activity in Chinese hamster V79 cells and its inhibition by 7 deaza deoxy guanosine triphosphate and (TTAGGG)4 in vitro Pandit B & Bhattacharyya NP. Biochemical and Biophysical Research Communications (1998), 251:620-624.
Monographs
Radiation resistance in a cell strain derived from Chinese Hamster V79 cells, B Pandit & N.P Bhattacharyya. Trends in Radiation and Cancer Biology (1998), edited by R. N. Sharan, 104-110.
Mutator phenotype in Chinese hamster cell strain? B Pandit, G. Bhaumik and N.P. Bhattacharyya. Recent Aspects of Cellular and Applied Radiobiology (1999), edited by R. N. Sharan, 165-169.
Review
Sitosterolemia: of mice and man, Patel SB, Klett EL, Ahn GS, Yu H, Chen J, Pandit B, Lee MH, Salen G. International Congress Series (2004)1262:300-304.
Book Chapters:
GC×GC-TOFMS Measurement of Actively Sampled Indoor Air VOCs Mrinal Kumar Das, Aleena Das, Subasa Chandra Bishwal, Ankur Varshney, Satish Pendurthi, I. Ibungo Singh, W. Asoka Singh, George M. Varghese, Bhaswati Pandit and Ranjan Kumar Nanda. (2016): 78-88
Lab members
PhD Students
Anuradha Gautam
Samadrita Ojha
Project personnel
Ahana Dasgupta
Anindita Roy
Integrated PhD student
Kaveri Srivastav
