Viger, Robert PhD- Regular researcher


Full professor - Université Laval

(1) Reproduction, mother and child health axis, Centre de recherche du CHU de Québec

(2) Obstetrics, gynaecology and reproduction axis, Faculty of Medicine

CRDSI Director

Research interest

Dysfunctions of the reproductive system are common medical conditions. Problems range for differences in the sexual determination process to male and female infertility. Research is therefore essential to better understand, diagnose, treat and eventually prevent these problems which, for many individuals and couples, can be devastating. My research program thus aims to better understand the molecular mechanisms that control the animal and human reproductive function. Our goal is to provide the basis required for the development of new therapies that will eventually be used to improve reproductive health and thus quality of life of everyone. 

See details of research interests under "complementary information"Voir détails des intérêts de recherche sous l'onglet ¨information complémentaire ¨

Expertise

Sex determination Gene expression Hormone Reproduction Transcription

Centre de recherche du CHU de Québec (CHUL)

2705 boul. Laurier
Québec (QC) Canada
G1V 4G2
(418) 656-4141 extension : 46159
Fax : (418) 654-2783
robert.viger@crchudequebec.ulaval.ca

Postdoctoral fellowship: Molecular Endocrinology, Institut de recherches clinique de Montréal (Montréal, QC, Canada)

PhD: Pharmacology and Therapeutics, Université McGill (Montréal, QC, Canada)

Undergraduate: Biochemistry, Université McGill (Montréal, QC, Canada)




codirection
Nenonene, Karen - Master - Studies in progress
Subject :

Détermination du rôle de la protéine du X-fragile (FMRP) dans l’ovaire  


1 Latest projects

  • Regulation and mechanism of action of transcription factor GATA4 in reproduction

More precisely, my laboratory is interested in the transcriptional regulation of genes involved in sexual determination processes (i.e. the development of testis or ovaries) and secular differentiation (i.e. the establishment of internal and external genital tracts and thus the establishment of the male or female phenotypic sex) in mammals. We are also interested in understanding the transcriptional control of gonadic gene expression, especially in testis somatic cells (Sertoli and Leydig cells) where we have great expertise. During the pas years, our main objective was to understand the physiological roles played by the transcription factor family, GATA. Because of their well-established role in other tissues such as the heart and digestive system, we proposed that GATA factors could play roles of the same importance in the developmental and functional regulation of gonads. Using classic molecular biology methods (gene promoter characterization) and the use of various cell line models, we have contributed significantly to a better understanding of the genes and network of genes targeted by GATA factors. In fact, the range of action of GATA factors now includes gonads where they control the early development of testis and ovaries, sexual differentiation and steroidogenesis. During these processes, GATA factors, namely GATA4, regulate a wide range of genes. These includes those that are expressed early in gonad development (Sox9, Amh, Dmrt1) and those that act later in foetal and adult gonads (Inha, Star, CYP11A1, CYP19A1, and much more). Our recent results indicate that GATA4 is a master regulator of steroidogenesis where its action are comparable to those of the nuclear receptor SF-1/NR5A1. It is known that functional deficiencies in certain GATA factors are associated to human diseases and we believe the same applies to the reproductive system. Our recent work has already highlighted the potential involvement of these factors in various pathologies such as breast cancer, endometriosis, polycystic ovarian syndrome and cases of sexual reversion associated to AMH production deficiency. Thus we hope to apply the results of our work to the development of new therapies for the treatment and prevention of these pathologies as well as of other diseases affecting reproductive health. 

 

 Continuing along this path, we are now very interested in defining: 1) the sub-group of genes directly targeted by GATA factors (i.e. those requiring a direct GATA bond) and 2) how GATA genes are regulated (at the transcriptional and post-translational levels). The classic molecular biology techniques we have used in the past impose severe restrictions for the study of our new questions. My laboratory has thus recently turned to the genome editing system CRISPR/Cas9 to directly generate in a mouse model a series of point mutations which target either post-translational modification sites or GATA binding motifs in the promoter region of certain target genes. The use of genome editing technologies such as the CRISPR/Cas9 system has made possible new studies that can now go beyond in vitro gene regulation by enabling the direct analysis of target genes and more importantly, establish more precise genetic regulation network in vivo.