Project Details

Aerobic organisms have evolved cellular responses against reactive oxygen species (ROS) over the coures of 3 billion years, since the Earth's atmosphere became oxygenated. ROS targets macromolecules and metal cofactors, which can impair cellular function. ROS is generated as a by-product of normal metabolic operation. It is also used as an offensive tool by competing microbes and the human immune system.

Adaptation against ROS stress can require system-level responses, including metabolic shifts, use of alternative cofactors, and change in macromolecular composition. Adaptation against other stresses (e.g., thermal, pH, osmotic) requires similar system level responses.

Such system-level stress responses can be modeled using genome-scale models that integrate the processes of metabolism and macromolecule expression (ME models). By extending these models with the thermodynamic and kinetic processes associated with stress-related damage and repair of cellular components, it is possible to model microbial stress response. These extended models are collectively termed StressME models.

Our lab aims to:

  • model additional key stress responses (e.g., osmotic stress)
  • investigate the role of stress tolerance in infectious disease
  • model cellular response to osmotic, oxidative, and pH stress in bioprocess environments


Laurence Yang

Assistant Professor

Jiao Zhao

Research Associate

Sanjeev Dahal

Postdoctoral Fellow

Hao Xu

Research Assistant

  • Funding
  • 2020-2022: subaward of NIH Grant R01GM057089 (PI: Bernhard O. Palsson, UCSD)