Bio


As an undergraduate at UC Berkeley, I studied physics and applied mathematics, while developing interest in using imaging to study biological phenomena. As a graduate student in the Computational and Systems Biology PhD program at MIT, I became interested in the shapes of animal tissues: how cells self-organize and cooperate to sculpt tissue shape and function. I worked with Dr. Adam C. Martin in the Biology department to study how cells of the fruitfly embryo collectively generate force using their actin cytoskeleton and facilitate the folding of the embryonic tissue. I developed computational methods to quantitatively analyze the spatiotemporal dynamics of myosin contractions in four-dimensional data. I uncovered cooperative interactions between cells which facilitates the coordinated force-generation in this complex system.

Currently, I am working with Dr. Jan Skotheim to examine how cell growth and cell division is coupled in a living tissue.

Professional Education


  • Bachelor of Arts, University of California Berkeley (2010)
  • Doctor of Philosophy, Massachusetts Institute of Technology (2016)

Stanford Advisors


Current Research and Scholarly Interests


The coordination between cell growth and cell cycle in vivo.

All Publications


  • Loss of G(alpha 12/13) exacerbates apical area dependence of actomyosin contractility MOLECULAR BIOLOGY OF THE CELL Xie, S., Mason, F. M., Martin, A. C. 2016; 27 (22): 3526-3536

    Abstract

    During development, coordinated cell shape changes alter tissue shape. In the Drosophila ventral furrow and other epithelia, apical constriction of hundreds of epithelial cells folds the tissue. Genes in the Gα12/13 pathway coordinate collective apical constriction, but the mechanism of coordination is poorly understood. Coupling live-cell imaging with a computational approach to identify contractile events, we discovered that differences in constriction behavior are biased by initial cell shape. Disrupting Gα12/13 exacerbates this relationship. Larger apical area is associated with delayed initiation of contractile pulses, lower apical E-cadherin and F-actin levels, and aberrantly mobile Rho-kinase structures. Our results suggest that loss of Gα12/13 disrupts apical actin cortex organization and pulse initiation in a size-dependent manner. We propose that Gα12/13 robustly organizes the apical cortex despite variation in apical area to ensure the timely initiation of contractile pulses in a tissue with heterogeneity in starting cell shape.

    View details for DOI 10.1091/mbc.E16-05-0305

    View details for Web of Science ID 000387391400014

    View details for PubMedID 27489340