Swasti Raychaudhuri

Biography

Swasti obtained his MSc in Biotechnology from Dr. B C Guha Centre for Genetic Engineering and Biotechnology, University of Calcutta in 2002 and PhD from the Crystallography and Molecular Biology Division, Saha Institute of Nuclear Physics, Kolkata in 2008. He was a postdoctoral research fellow at the Max Planck Institute for Biochemistry, Martinsried, Germany from 2008-2013. During his PhD with Prof. Nitai P Bhattacharyya, Swasti characterized a novel huntingtin interacting protein HYPK as an intrinsically unstructured chaperone-like protein. At the MPI Biochemistry Swasti worked with Prof. F. Ulrich Hartl. There he discovered several novel modulators of heat shock response and studied the implication of acetylation in HSF1 protein stability and function. He also designed a set of "Proteostasis Sensor" proteins which could be successfully used in wide range of model organisms.

Research Interest

With the increasing average life expectancy of the population, developing effective treatments for numerous degenerative, age-related diseases becomes of enormous medical, social and economic relevance. Hence, research on the processes of cellular and organismal aging is now the focus of several leading laboratories of the world and has provided different hypotheses about the causes of aging. One prominent hypothesis suggests that a gradual, age-dependent decline of protein homeostasis, or proteostasis is an underlying cause of aging. Protesostasis is maintained by a highly complex but organized molecular network and this network is now considered as an attractive target for pharmacological intervention in age-related diseases. In our lab we plan to perform systemic analysis of proteostasis network in models of aging and age-related diseases. We shall use modern cell biology and state-of-the-art proteomics arsenal to address our questions. This work, in principle, should lead to a deeper understanding of protein homeostasis and simultaneously should provide us with the mechanistic knowledge on the regulatory mechanism of loss of proteostasis capacity in aging diseases.