Sanyal, Amartya

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Sanyal, Amartya

Sanyal, Amartya
Nanyang Assistant Professor

Office: 05n-22
Telephone: +65 6513 8270
Email: asanyal@ntu.edu.sg

 

Education

  • PhD                  Indian Institute of Science, Bangalore, India                2008
  • MSc                  Zoology Banaras Hindu University, Varanasi, India      2002
  • BSc                  Zoology(Hons) University of Calcutta, Kolkata, India    2000

Professional Experience

  • Assistant Professor (2014-present): School of Biological Sciences and Lee Kong Chian School of Medicine (LKCMedicine), Nanyang Technological University, Singapore
  • Postdoctoral Research Associate (2008-2014): University of Massachusetts Medical School, Worcester, MA, USA

Research Interest

The main focus of our research is to understand 3D genome organization inside the nucleus and its impact on transcriptional regulatory code during mammalian development, differentiation and disease.

Human genome is organized in highly complex conformations inside the nucleus. How this three-dimensional organization of chromatin affects gene regulation is largely unknown. Genome-wide annotations of genes and functional regulatory elements do not give an insight into which regulatory elements control any given gene. Long-range looping interactions between gene promoters and distal genomic elements such as enhancers are known to be important for regulation of transcription. The advent of Chromosome Conformation Capture (3C)-based techniques and its high-throughput adaptations has made it possible to detect spatial proximity and high-resolution chromatin interactions between genomic elements.

We are particularly interested in understanding how non-coding sequence variants identified by genome-wide association studies (GWAS) contribute to human disease risk and pathogenesis. In the past decade, genome-wide scans of SNPs (single nucleotide polymorphisms) in populations have identified many genomic loci associated with the predisposition to disease. The observed associations are possibly driven by linkage disequilibrium with the disease-associated region in vicinity. However, >90% GWAS SNPs do not map to coding regions suggesting these variants may, in fact, affect gene regulatory mechanism and involved in controlling the expression of distal target genes, the identity of which remain unknown. Connecting the GWAS SNPs to their target genes would aid in understanding genotype-phenotype relationships in disease and in designing effective treatment and therapeutics.

In our lab, we intend using high-throughput genomic methods, genome-editing and imaging techniques in combination with bioinformatics and computational approaches to understand structure-function relationship of chromatin. Overall, we are trying to decipher the regulatory mechanisms of cell- and tissue-specific gene expression in relation to 3D chromatin architecture, epigenetic mechanisms (chromatin modifications) and binding of trans-acting factors to understand various biological processes in normal and disease conditions.