Claire de la Cova

Assistant Professor
Biological Sciences

Education and Experience

Post-doctoral Training/Associate, Columbia University, New York, NY, 2008-2018
PhD, Genetics and Development, Columbia University, New York, NY, 2008
BA, Biology, Macalester College, Saint Paul, MN, 1999

Lab Website

https://sites.uwm.edu/delacova/

Courses Taught

BIO SCI 325: Genetics (Spring semesters)

BIO SCI 498/498G: Genetics of Development and Cancer (Fall semesters)

Research Interests

My research focuses on cell communication mediated by the Ras-MAP kinase cascade, a conserved signal transduction pathway that acts in a diverse set of cellular processes, including neuronal function, membrane organization, cell proliferation, fate specification, and aging. In animals, a growing body of research suggests that Ras signaling is modulated by inhibitory and negative feedback mechanisms, but our understanding of this network is incomplete.

My laboratory takes both genetic and quantitative imaging approaches to understand the regulatory logic of Ras signaling in animal development. We utilize the small worm Caenorhabditis elegans (C. elegans) as an experimental model to understand the consequences of mutations that perturb Ras signaling in human diseases, and to genetically identify novel regulators that inhibit signal transduction.

Selected Publications

de la Cova, Claire C., Townley, Robert, and Greenwald, Iva. “Negative feedback by conserved kinases patterns the degradation of Caenorhabditis elegans Raf in vulval fate patterning.” Development/Oxford University Press for The Company of Biologists Limited 147.24 Ed. Thomas Lecuit. (2020): 14.
de la Cova, Claire, Townley, R, Regot, S, and Greenwald, I. “A Real-Time Biosensor for ERK Activity Reveals Signaling Dynamics during C. elegans Cell Fate Specification.” Developmental Cell 42.5 (2017): 542-553.e4.
Meyer, S N., Amoyel, M, Bergantiños, C, de la Cova, Claire, Schertel, C, Basler, K, and Johnston, L A. “An ancient defense system eliminates unfit cells from developing tissues during cell competition.” Science 346.6214 (2014): 1258236.
de la Cova, Claire, Senoo-Matsuda, N, Ziosi, M, Wu, D C., Bellosta, P, Quinzii, C M., and Johnston, L A. “Supercompetitor status of Drosophila Myc cells requires p53 as a fitness sensor to reprogram metabolism and promote viability.” Cell Metabolism 19.3 (2014): 470-83.
de la Cova, Claire, and Johnston, L A. “Myc in model organisms: a view from the flyroom.” Seminars in Cancer Biology 16.4 (2006): 303-12.
de la Cova, Claire, Abril, M, Bellosta, P, Gallant, P, and Johnston, L A. “Drosophila myc regulates organ size by inducing cell competition.” Cell 117.1 (2004): 107-16.