Focus areas

Cell fate circuits and mechanobiology of the alveolus

How do alveolar progenitors decide between AT2 and AT1 fates and what prevents these transitions in disease? To answer this question, we combine single-cell genomics, membrane biophysics and genetically engineered mouse models to dissect the molecular and mechanical circuits that govern epithelial identity and plasticity. A major focus is understanding how membrane tension, growth factor signaling (FGF–ERK) and mechanotransduction (YAP-TAZ) integrate to orchestrate lineage decisions across development, homeostasis and injury.

Key approaches include:

  • Fluorescence lifetime imaging microscopy (FLIM) membrane tension imaging.
  • Optical trapping.
  • CRISPR and mosaics.
  • scRNA-seq lineage trajectories.
  • AT2→AT1 differentiation models.

Niche signals and mechanical context in lung development and repair

Intrinsic programs alone do not determine epithelial fate. Fibroblasts, smooth muscle, endothelial cells and matrix architecture provide potent physical and biochemical cues that shape progenitor competence.

We investigate how niche signals and mechanical context — from fibroblast wrapping to extracellular confinement — regulate membrane tension, signaling dynamics and differentiation outcomes.

Key questions include:

  • How do mesenchymal interactions gate or block AT1-AT2 differentiation?
  • What mechanical features define "permissive" versus "nonpermissive" niches?
  • Can engineered microenvironments restore regenerative capacity?

Approaches include:

  • 3D co-culture mechanics.
  • Organoid niche engineering.
  • Spatial imaging.
  • Biophysical manipulation.

Development, aging and injury: Conserved mechanisms across the lifespan

Development, aging and injury: Conserved mechanisms across the lifespan

We explore how developmental programs are reused, modified or destabilized during adult injury and aging. By comparing fetal, adult and regenerating alveoli, our lab identifies conserved principles that govern successful epithelial transitions — and why these same pathways are disrupted in diseases such as pulmonary fibrosis or severe viral injury.

Interests include:

  • Age-dependent differences in epithelial competence.
  • Reactivation of developmental signatures during repair.
  • Emergence and resolution of transitional states.

Approaches include:

  • Developmental time courses.
  • Human fetal tissue.
  • Organoid aging models.
  • Multi-omic integration.

Translational regeneration: Restoring lung function after injury

Our mechanistic insights guide efforts to develop regenerative therapies that repair or replace damaged epithelium. We model pathological "stuck" transitional states, such as KRT8⁺ populations in fibrosis, and test strategies to overcome them by modulating membrane tension, niche cues or circuit-level regulators.

We also collaborate on translational systems, including donor lung conditioning, ex vivo perfusion and organoid-based therapeutic discovery.

Goals include:

  • Identify actionable nodes that unlock AT2→AT1 conversion.
  • Engineer pro-regenerative microenvironments.
  • Develop interventions that reverse epithelial arrest in chronic injury.

What unites our research

Across all projects, our lab seeks to define the fundamental rules by which cells integrate mechanical forces and molecular cues to make fate decisions and leverage those rules to improve outcomes in lung disease.

Our trainees work at the interface of developmental biology, mechanobiology, regenerative medicine and high-content single-cell analysis, supported by a collaborative and interdisciplinary environment.