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

1. Townley R, Deniaud A, Stacy KS, Rodriguez Torres CS, Cheraghi F, Wicker NB, de la Cova CC. The E3/E4 ubiquitin ligase UFD-2 suppresses normal and oncogenic signaling mediated by a Raf ortholog in Caenorhabditis elegans. Sci Signal. 2023 Aug 29;16(800):eabq4355. DOI: 10.1126/scisignal.abq4355.
2. de la Cova CC. The Highs and Lows of FBXW7: New Insights into Substrate Affinity in Disease and Development. Cells. 2023 Aug 24;12(17):2141. DOI: 10.3390/cells12172141.
3. de la Cova CC, Townley R, Greenwald I. Negative feedback by conserved kinases patterns the degradation of Caenorhabditis elegansRaf in vulval fate patterning. Development. 2020 Dec 23;147(24):dev195941. DOI: 10.1242/dev.195941.
4. Kodra A, de la Cova C, Gerhold AR, Johnston LA. Widely Used Mutants of eiger, Encoding the DrosophilaTumor Necrosis Factor, Carry Additional Mutations in the NimrodC1 Phagocytosis Receptor. G3 Genes Genomes Genetics (Bethesda). 2020 Dec 3;10(12):4707-4712. DOI: 1534/g3.120.401800.
5. de la Cova C, Townley R, Regot S, and Greenwald I. A real-time biosensor for ERK activity reveals signaling dynamics during elegans cell fate specification. Developmental Cell. 2017 Vol. 42(5):542-553. DOI: 10.1016/j.devcel.2017.07.014.
6. Meyer SN, Amoyel M, Bergantiños C, de la Cova C, Schertel C, Basler K, Johnston LA. An ancient defense system eliminates unfit cells from developing tissues during cell competition. Science. 2014 Vol. 346(6214):1258236. DOI: 10.1126/science.1258236.
7. de la Cova C, Senoo-Matsuda N, Ziosi M, Wu DC, Bellosta P, Quinzii CM, Johnston LA. Supercompetitor status of Drosophila Myc cells requires p53 as a fitness sensor to reprogram metabolism and promote viability. Cell Metabolism. 2014 Vol. 19(3):470-483. DOI: 10.1016/j.cmet.2014.01.012.
8. de la Cova C and Greenwald I. SEL-10/Fbw7-dependent negative feedback regulation of LIN-45/Braf signaling in C. elegans via a conserved phosphodegron. Genes and Development. 2012 26(22):2524-2535. DOI: 10.1101/gad.203703.112.
9. de la Cova C and Johnston LA. Myc in model organisms: a view from the flyroom. Seminars in Cancer Biology. 2006 Vol. 16 (4): 303-312. DOI: 10.1016/j.semcancer.2006.07.010.
10. de la Cova C, Abril M, Bellosta P, Gallant P, Johnston LA. Drosophila Myc regulates organ size by inducing cell competition. 2004 Cell. Vol. 117(1):107-116. DOI: 10.1016/s0092-8674(04)00214-4.