scRNA-seq and RNA FISH revealed elevated expression of Cdc42ep1 in escapees in Chen's paper, "Rapidly induced drug adaptation mediates escape from BRAF inhibition in single melanoma cells." Yang C, Tian C, Hoffman TE, Jacobsen NK, Spencer SL. (2019). bioRxiv.
Spencer lab members on a hike near Dillon, Colorado. Left to right: Mingwei, Tim, Sabrina, Claire, Justin, Humza, Yao, Iain, and Jordan.
Using an mCitrine-p21 fusion protein in order to monitor p21 levels compared to CDK2 activity in cells in transient quiescence. Moser J, Miller I, Carter D, Spencer SL. (2018). "Control of the Restriction Point by Rb and p21." PNAS.
The Spencer Lab making dinner during the lab retreat in Keystone, Colorado.
Venn diagram of gene sets differentially regulated in five forms of quiescence. Min M, Spencer SL. (2019). "Spontaneously slow-cycling subpopulations of human cells originate from activation of stress-response pathways." PLOS Biology.
Welcome to the Spencer Lab!
Research in the lab is focused on understanding how signaling events control cell fate. Studying these processes in single cells reveals remarkable cell-to-cell variability in response to stimuli, even among genetically identical cells in a uniform environment. We seek to understand the sources and consequences of this heterogeneity in the cellular response to stimuli. The stimuli we study include growth factors, cell stress, and targeted cancer therapeutics. To do this, we develop genetically encoded fluorescent sensors for signaling events of interest. We then use long-term live-cell microscopy and cell tracking to quantify the dynamics of upstream signals and link them to cell fate (proliferation, quiescence, apoptosis, differentiation). Our long-term goal is to understand the normal mechanistic functioning of signaling pathways that control proliferation, to understand how these signals go awry in cancer, and eventually to alter the fate of individual cells.