Sarah Jenna


Ph.D., Directrice adjointe Biochimie
Université du Québec à Montréal
Page web personnelle

Research field

Rho GTPase regulatory machinery forms a dynamic protein network and plays a critical role in cell signaling integration processes. The research program developed in my lab seeks to identify the composition, the structure and the dynamics of this protein network throughout Caenorhabditis elegans development and life cycle. To do so we use integrative genomics, reverse genetics, molecular and cell biology approaches This program will largely contribute to the acquisition of a Systems-level understanding of cell signaling integration events required for development and survival of multicellular organisms. In addition, this program will provide a better understanding of Rho GTPase implications in pathogenic processes leading to mental retardation. The “Rho regulome” of C. elegans embryogenesis In multicellular organisms, embryonic development is dependent on a continuous flow of information through a complex network of cells. The ability of signaling machinery to transduce and integrate multiple upstream signals is critical in the control of cellular behavior. Rho GTPases are key signaling proteins controlling cell adhesion, cell morphology, gene expression, membrane trafficking and playing a critical role in cell signaling integration. To fulfill their multiple tasks, Rho GTPases function in a coordinated manner. This coordination depends on proteins regulating their activation level called regulators. To date, mechanisms enabling coordination of Rho GTPases during morphogenic events in multicellular organisms is far to be understood. The research program proposed here is designed to significantly improve our understanding of these mechanisms using Caenorhabditis elegans embryonic development as a model system and to extend this knowledge to other multicellular organisms using a systems biology approach. Rho regulation and cognitive disorders: what can we learn from worms Mental Retardation (MR) occurs in 2-3% of the general population and is one of the five highest sources of healthcare cost in the world. However, MR pathologies are still not therapeutically addressed and remain largely considered as 'untreatable' disorders. Finding a cure for these pathologies is therefore on the priority list of health research organizations. Number of non-syndromic forms of mental retardation are associated with mutations in Rho GTPase regulators that are highly conserved between human and C. elegans. We use a combination of integrative genomics, microfluidic engineering, reverse genetics, molecular and cellular biology techniques to characterize the neuronal function of these regulators in C. elegans.

Publications récentes

  1. Harel S. and Jenna S.* (2010) : Soigner la déficience intellectuelle : la recherche d’équilibre. Médecine Sciences. In press

  2.  Lee A.Y., Perrault R., Harel S., Boulier E., Suderman M., Hallett M.T. and Jenna S.* (2010): Searching for signaling balance through the identification of genetic interactors of the Rab Guanine-nucleotide Dissociation Inhibitor, gdi-1. PLoS One. 13;5(5):e10624.

  3. Chartrand E., Arnold A. A., Gravel A., Jenna S. and Marcotte I. (2010): Investigating the role of the loop segment Ile583-Y597 of the hERG channel in its functioning and drug-induced LQTS. Biochim Biophys Acta. 2010 May 24. [Epub ahead of print].

  4. Boulier E. and Jenna S.* (2009): Genetic dissection of Caenorhabditis elegans embryogenesis using RNA interference and flow-cytometry. Human Embryogenesis : Methods and Protocols. Methods in Molecular Biology. 550:181-94.

  5. Caruso M.-E., Jenna S., Baillie D., Boismenu D., Halawani D., Latterich M. and Chevet E*.(2008): GTPase-mediated regulation of the Unfolded Protein Response in Caenorhabditis elegans is dependent on the AAA+ ATPase CDC-48. Molecular and Cellular Biology. 28(13):4261-74.

  6. Jenna S*. and Chevet E.* (2008): High-throughput RNAi in Caenorhabditis elegans – from molecular phenotypes to pathway analysis. RNA interference (RNAi), edited by Martin Latterich, Taylor & Francis Group.