Rachel Turn
Department of Comparative Bioscience
Assistant Professor
School of Veterinary Medicine
2015 Linden Drive- SVM South Building Office Room #: 3466; Lab Room #: 3421
University of Wisconsin, Madison Madison, WI 53706
Education
Postdoc, Department of Microbiology and Immunology, Stanford University School of Medicine
PhD in Biochemistry, Cell, and Developmental Biology, Emory University
BA in Biology, Harriet L. Wilkes Honors College of FAU
Research Areas
- Membrane and Cellular Biophysics
- Protein folding, design & function
- Spectroscopy, Microscopy, Imaging
Deciphering the Temporal-Spatial Mechanisms Driving Cell Cycle Exit and Fate Change
Our research is driven by a fundamental question: what exactly is G0? Nearly every cell in the human body exits the cell cycle either as quiescent, stem-like cells poised to differentiate upon the correct signal or as terminally-differentiated cells with fate-specific functions. Disruption of quiescence contributes to diverse pathologies, including loss of regenerative capacity in pancreatic β cells in type 2 diabetes, uncontrolled proliferation, and stem cell dysfunction during aging. Yet, the cellular mechanisms that license cell cycle exit and fate commitment (and whether a universal marker of G0 even exists) remain unclear. We seek to define how G0 is regulated across molecular and cellular scales. By establishing a systems-level understanding of G0, we aim to uncover the time-resolved biophysical mechanisms governing cell fate decisions and what changes are required to reprogram function (e.g, energetics, cell architecture/morphology, compartmentalization).
Our research has revealed a critical role for tight temporal-spatial regulation of the cell signaling landscape in establishing a healthy G0 program. To do so, we integrate advanced live- and fixed-cell imaging with time-resolved proteomics and phosphoproteomics in synchronized, homogeneous mammalian cell culture systems in an approach termed STAMP (Synchronized Temporal-Spatial Analysis via Microscopy and Proteomics). Thus, we can cleanly resolve biophysical mechanisms underlying signaling dynamics in time and space. As a framework for tracking G0 progression, we leverage the ordered assembly of the primary cilium, a signaling organelle that forms specifically in quiescent cells and provides a well-defined sequence of phenotypic signposts for keeping track of our progression. This strategy enables detailed cataloging of transient, spatially-restricted signaling events that may function as checkpoints during cell cycle exit and fate commitment.
As part of the Turn lab, trainees from the Biophysics Program would leverage diverse interdisciplinary approaches to get at the heart of fundamental cellular mechanisms and how they are disrupted in disease: high-throughput data acquisition through mass spectrometry as well as computational analysis, advanced superresolution and time-resolved microscopy, structural modeling of transient, context-specific protein complexes and post-translational modifications, and more. We are question-driven and employ whatever approaches necessary to address our overarching research goals.