The Atwood lab is interested in how cells choose their fate. We focus on protein kinase regulation of signaling pathways and transcription factors, using models of skin cancer and skin development, to determine how kinases influence fate by controlling the genetic landscape of the cell.
We define how the actin cytoskeleton, and actin cytoskeletal regulators, control primary cilia-mediated signaling. We show that Cdc42 recruits two distinct regulatory complexes, MIM and aPKC, to control Src activation and subsequent actin polymerization, which is necessary for primary cilia length and Hedgehog signaling. Disruption of the actin cytoskeleton promotes aPKC activity and its subsequent activation of Gli1, a process that cancer co-opts to promote chemotherapy resistance to Hedgehog pathway inhibitors.
Journal of Cell Biology. 217(9):3255-66. Link PDF