About Fellow

Purdue University, USA

National Centre for Biological Sciences, Bangalore

National Centre for Biological sciences, Bangalore

My career in science began as a masters' student at the Birla Institute of Technology and Science, Pilani, consistently ranked among the top 10 undergraduate institutions in India. Since engineering and science students were required to take many of the same courses, BITS initiated me to cross disciplinary training, a theme that has persisted throughout my career.

For graduate studies, I joined Dr. Claudio Aguilar's lab at Purdue University when he had just begun his tenure track. I received multidisciplinary training in genetics, cell biology and biochemistry, with a focus on the interplay between vesicle trafficking and cellular signaling pathways. I demonstrated that endocytic proteins, in addition to their classical functions, could also initiate Rho-GTPase mediated signaling cascades. On the other hand, GTPase regulators could also utilize vesicle trafficking pathways for localization to distinct cellular domains. My most notable achievement at Purdue was being named the H. E. Umbarger Outstanding Graduate Student in Research – the highest award granted to a graduate student in the Department of Biological Sciences at Purdue and in the same year, being included in the Teaching Assistantship Honor Roll.

I was excited about returning to India after my PhD, especially after a discussion on a project on Fragile X Syndrome initiated in Prof. SumantraChattarji's lab at NCBS. The study interested me because I realized that I could use my expertise on vesicle trafficking to understand the molecular basis of the synaptic defects his lab had identified in a mouse model of FXS. I also realized that by bringing together my experience in cell biology and biochemistry with the expertise in electrophysiology and animal behaviour in Prof. Chattarji's lab, my project would not only foster interdisciplinary science, but was bound to have a big impact.

FXS is the leading heritable cause of intellectual disability and autism, caused by silencing of the FMR1 gene. The widely accepted mGluR theory of FXS successfully explains several of its phenotypes; however, the supporting evidence is largely based on studies in the hippocampus and cortex – brain areas that can only explain the cognitive aspects of the disease. But FXS being an autism spectrum disorder, has equally debilitating emotional deficits. The amygdala encodes the emotional phenotypes of FXS - the molecular basis of which is completely unknown.

My proposal aims to address two fundamental questions about the neurobiology of FXS. The first question stems from the intriguing observation that activation of the mGluR5 receptor leads to weakening of synapses in the hippocampus while strengthening them in the amygdala. The mechanism underlying this difference is not known. Furthermore, in the mouse model of FXS, synaptic plasticity is impaired in both the brain areas. Hippocampal synapses are further weakened, but synaptic strengthening in the amygdala is completely abolished. It is believed that this phenotype is caused by excessive removal of AMPA receptors from the cell surface. Hence, my second goal is to understand the underlying receptor trafficking defects that cause this reduction, with a future aim of reversing it.

I developed an interest in public health research while considering long term career goals and the exciting potential of transforming basic science innovations into public health interventions and tools. Currently, I am an INSPIRE Faculty at the Public Health Foundation of India, Gurgaon, where I am collaborating with the Centre for Chronic Disease Control and the Centre for Mental Health on several projects, including investigating the potential of using cognitive, neural activity and blood based biomarkers for community based detection of autism spectrum disorders (ASD) in young children; developing scalable assessment tools for identifying cognitive delays in pre-school children; and exploring the mechanistic basis of depression-diabetes co-morbidity through the identification of common biomarkers.