Dr. Lucie Jeannotte is a regular researcher at the CHU Research Centre of Québec- Université Laval, Oncology Axis, and Professor in the Department of Molecular Biology, Medical Biochemistry and Pathology of the Faculty of Medicine at Université Laval. She is also a regular researcher at the Centre for Cancer Research at Université Laval. Her research aims at understanding the molecular mechanisms involved in the formation of the mammalian embryo with a specific interest for Hox genes. Hox genes encode transcriptional factors that play key roles in the developmental hierarchy leading to pattern formation of the embryo. Loss of Hox gene function in mice results in numerous malformations of skeleton and organs, among others, that can impair survival. The developmental origin of several diseases, including cancers, reveals how important it is to understand the mechanisms that control embryogenesis.
Function of the Hoxa5 gene in the formation of the respiratory system
Lung development implies a coordinated regulation of numerous molecules and factors. The team of Dr. Jeannotte has characterized the Hoxa5 mutant mouse line et revealed the critical and unique role of this gene in survival at birth. The loss of Hoxa5 function cause severe defects of the respiratory system that result in death of the mutants at birth. The malformations mimic pediatric congenital diseases, such as tracheal stenosis, lung hypoplasia and congenital diaphragmatic hernia as well as chronic obstructive pulmonary diseases (COPD), a major cause of death in the human population. Hoxa5 mutant mice thus provide a unique animal model to further study these pathologies. Dr. Jeannotte is interested in identifying the targets of HOXA5 transcriptional factor in the respiratory system in order to define the molecular mechanisms perturbed by the Hoxa5 mutation that underlie the phenotypes observed and may lead to future therapies.
Role of YY1 in the pathogenesis of the pleuropulmonary blastoma
The pleuropulmonary blastoma (PPB) is a rare pediatric lung tumor that arises during fetal life. It results from the progression of abnormal lung cysts to an aggressive sarcoma with poor survival. The team of Dr. Jeannotte has produced mutant mice devoid of Yy1 function in lung epithelium. This mutation causes lung cysts as those seen in PPB patients. YY1 is a transcription factor essential for embryo development and survival. YY1 expression is reduced in PPB lung tumors raising the hypothesis that the loss of Yy1 function is important for PPB pathogenesis. To determine the role and mechanisms of action of YY1 in PPB, Dr. Jeannotte aims at identifying the mechanisms of action of YY1 in lung formation in order to resolve its implication in PPB formation. These studies may reveal novel molecular targets for the design of effective and innovative therapies and better tools for the diagnosis and prognosis of this severe cancer.
9, rue McMahon
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- Houde, NicolasEmployeeL'Hôtel-Dieu de Québec+1 418-525-4444, extension 16936+1 418-691-5439Nicolas.Houde@crchudequebec.ulaval.ca
9, rue McMahon
Canada G1R 2J6
- Landry-Truchon, KimEmployeeL'Hôtel-Dieu de Québec+1 418-525-4444, extension 16936+1 email@example.com@firstname.lastname@example.org
9, rue McMahon
Canada G1R 2J6
Conditional Loss of Hoxa5 Function Early after Birth Impacts on Expression of Genes with Synaptic Function.Journal Article
Front Mol Neurosci, 10 , pp. 369, 2017.
Pathomechanisms of Congenital Cystic Lung Diseases: Focus on Congenital Cystic Adenomatoid Malformation and Pleuropulmonary Blastoma.Journal Article
Paediatr Respir Rev, 19 , pp. 62-8, 2016, ISSN: 1526-0542.
Hoxa5: A Key Player in Development and DiseaseJournal Article
J Dev Biol, 4 (2), pp. 13, 2016.
Perinatal induction of Cre recombination with tamoxifen.Journal Article
Transgenic Res, 24 (6), pp. 1065-77, 2015, ISSN: 0962-8819.
Epithelial inactivation of Yy1 abrogates lung branching morphogenesis.Journal Article
Development, 142 (17), pp. 2981-95, 2015, ISSN: 0950-1991.
Crucial requirement of ERK/MAPK signaling in respiratory tract development.Journal Article
Development, 141 (16), pp. 3197-211, 2014, ISSN: 0950-1991.
Hoxa5/Cre transgenic mice: novel tools for regional deletion along the anterior-posterior axis.Journal Article
Genesis, 52 (2), pp. 149-56, 2014, ISSN: 1526-954X.
YY1 acts as a transcriptional activator of Hoxa5 gene expression in mouse organogenesis.Journal Article
PLoS ONE, 9 (4), pp. e93989, 2014.
Hox5 interacts with Plzf to restrict Shh expression in the developing forelimb.Journal Article
Proc Natl Acad Sci U S A, 110 (48), pp. 19438-43, 2013, ISSN: 0027-8424.
Partial functional redundancy between Hoxa5 and Hoxb5 paralog genes during lung morphogenesis.Journal Article
Am J Physiol Lung Cell Mol Physiol, 304 (12), pp. L817-30, 2013, ISSN: 1040-0605.
- Centre de recherche du CHU de Québec - Université Laval, Subvention, Centre hospitalier universitaire de Québec - Université Laval, Centres de recherche affiliés, from 2017-01-01 to 2099-12-31
- Centre de recherche sur le cancer, Subvention, Institutionnel - BDR, BDR - Centres de recherche reconnus, from 1996-05-01 to 2023-04-30
- Characterization of the role of the Yin Yang1 (YY1) transcription factor in pleuropulmonary blastoma, Subvention, Société de recherche sur le cancer, Subvention de fonctionnement, from 2019-09-01 to 2021-08-31
Recently finished projects
- (FRSQ 78521)Soutien du projet de recherche dans l'axe oncologie, Subvention, Fondation du CHU de Québec, from 2017-06-12 to 2018-06-11
- Characterization of the role of the Yin Yang1 (YY1) transcription factor in pleuropulmonary blastoma (PPB), Subvention, Fondation de l'Université Laval, from 2016-09-15 to 2018-09-14
- Characterization of the role of the Yin Yang1 (YY1) transcription factor in pleuropulmonary blastoma, Subvention, Société de recherche sur le cancer, Subvention de fonctionnement, from 2017-09-01 to 2019-08-31
- Transcriptional complexity at the Hoxa5 locus: Characterization of the role of the Hoxa5associated., Subvention, Conseil de recherches en sciences naturelles et génie Canada, Subventions à la découverte SD (individuelles et d'équipe), from 2015-04-01 to 2020-03-31