Overarching theme: Our lab addresses fundamental questions in biomedical research concerning cellular morphogenesis—a process that controls the shape, size, number, and spatial distribution of biological cells as they collectively organize into multicellular communities. This process is subject to perturbations triggered by various stress signals, including mechanical injury, toxins (e.g., pharmaceutical drugs), and microbial infections. Cells sense these perturbations and adaptively alter their morphology, growth rate, and metabolic fluxes to maintain fitness under stress. 

 

However, the “molecular grammar” rules governing the ability of individual cells to detect stress signals and convert them into actionable forces—reshaping cells and limiting their growth under stress—remain only partially understood. This is a universal, scale-bridging problem that nearly all biological cells must solve. Deciphering how they achieve this task is the core objective of our research.

 

To this end, we employ an interdisciplinary approach that integrates molecular multi-omics and data analysis of cells before and after perturbation to uncover molecular-scale patterns capable of predicting a set of heuristic rules. These rules are then incorporated into a computer model to simulate a virtual, whole-cell-scale morphophenotype, which is experimentally validated using quantitative cell microscopy and bioimage informatics along with molecular, genetic, and physicochemical analyses.

 

We hope that this work will ultimately reveal new targetable mechanisms behind adaptations to perturbations in pathogenic cells living on or in the human body. This is especially important in the context of ever-increasing drug resistance, one of the main threats to global health.

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