We study how gene expression, subcellular organization and cell signaling influence cellular homeostasis and cell fate in health and disease.
In response to stress, mammalian cells make one of three fundamental decisions – die, survive or thrive. Critical determinants of these seemingly distinct cell fates include the induction of cell signaling cascades and selective expression of perturbation-responsive genes, which together help restore (ribostasis, proteostasis and) cellular homeostasis. Emerging evidence suggests that the dynamic reorganization of functionally nebulous, RNA- and protein-bearing, membrane-less compartments is an evolutionarily conserved hallmark of stress. Dysregulation or misappropriation of these stress response mechanisms are directly linked to aging and are key contributors to (neuro)degenerative pathologies and cancer. We seek to understand how cells maintain homeostasis and how stress response programs influence cellular decisions in physiology and pathology.
To address these pressing questions, we use an interdisciplinary approach that lies at the cusp of physical and life sciences. Herein, we utilize in vitro, cultured cell, animal and human tissue models for our research. We probe these models with an arsenal of contemporary imaging- and omics-based technologies that we develop and deploy, and combine them with classical biochemical and biophysical tools. Notably, we use single-molecule imaging, super-resolution microscopy, high-throughput imaging, single-cell sequencing and spatial omics among other cutting-edge technologies for our investigations. The ultimate aim is to leverage our foundational and translational research for diagnostic and therapeutic applications.