Christian E. Rocheleau, Ph.D.
Associate Professor, Department of Medicine
Tel: 514-934-1934 x76207
christian.rocheleau [at] mcgill.ca
A native of Massachusetts, I attended undergraduate at Assumption College in Worcester (1990-94), where I developed an interest in cell biology and signal transduction. I further pursued these interests earning a Ph.D. (2000) at the University of Massachusetts Medical School (Worcester) working with Dr. Craig Mello in the Department of Cell Biology. There I used the then new technique of RNA-mediated interference (RNAi) and the emerging genome sequence to elucidate a novel Wnt/MAPK-like pathway as establishing polarity and cell fates in the early C. elegans embryo. As a Jane Coffin Childs Memorial Fund Postdoctoral fellow I continued studies in signal transduction in the Department of Genetics at the University of Pennsylvania (Philadelphia) working with Dr. Meera Sundaram (2000-05). There I characterized the role of scaffold proteins in the Ras/MAPK pathway and identified numerous novel regulators of Ras/MAPK signaling via mutagenesis screens and RNAi. In 2005 I established my own lab in the Division of Endocrinology and Metabolism, Department of Medicine at McGill University and the MUHC Research Institute as an Assistant Professor and Canada Research Chair. In 2011 I was promoted to Associate Professor with tenure and joined the Department of Anatomy and Cell Biology as an associate member.
Vesicular trafficking, signal transduction, cell biology, genetics, Caenorhabditis elegans
Research or Clinical Activities
Our laboratory studies the molecular mechanisms of endocrinology using the model organism Caenorhabditis elegans. Hormones and Growth Factors act as signals from one cell to another to control various cellular behaviors such as proliferation, differentiation, and migration. These signals can activate receptors on the cell surface to initiate a cascade of molecular events that transduce the signal to the cell interior to elicit a cellular response. The Ras/MAPK pathway can transduce signals from a variety of receptors to control numerous cellular responses and inappropriate activation of this pathway can lead to cancer. Vesicular trafficking plays an important role in endocrine signaling, in both the secretion of hormone signals and in the regulation of downstream signaling events. Our research focuses on understanding the mechanisms that regulate vesicular trafficking and signal transduction as well as understanding how these two processes intersect. These fundamental cellular processes are evolutionarily conserved between humans and the nematode C. elegans. Therefore, we can apply the rapid forward and reverse genetic approaches available in C. elegans to identify and characterize new regulators relevant to the development of therapeutics to treat human cancers and endocrine diseases caused by unregulated signaling and/or vesicular trafficking.
Selected Recent Publications
The VPS-34 PI3 kinase negatively regulates RAB-5 during endosome maturation.
Law F, Seo J-H, Wang Z, DeLeon JL, Bolis Y, Brown A, Zong W-X, Du G and Rocheleau CE (2017) Journal of Cell Science, 130, 2007-2017.
Dynein-mediated trafficking negatively regulates LET-23 EGFR signaling.
Skorobogata O, Meng J, Gauthier K and Rocheleau CE (2016) Molecular Biology of the Cell, 27, 3771-3779.
An AGEF-1/Arf GTPase/AP-1 ensemble antagonizes LET-23 EGFR basolateral localization and signaling during C. elegans vulva induction.
Skorobogata O, Escobar-Restrepo JM and Rocheleau CE (2014) PLoS Genetics,10, e1004728.
RAB-7 antagonizes LET-23 EGFR signaling during vulva development in Caenorhabditis elegans.
Skorobogata O and Rocheleau CE (2012). PLoS ONE, 7, e36489.
TBC-2 regulates RAB-5/RAB-7-mediated endosomal trafficking in C. elegans.
Chotard L, Mishra AK, Sylvain MA, Tuck S, Lambright DG and Rocheleau CE (2010) Molecular Biology of the Cell, 21, 2285-2296.