Université Libre de Bruxelles (Brussels, BELGIUM)
Professor J. SOUOPGUI was born in Cameroon and studied biology, ending with his first PhD in Molecular Parasitology in 1999 at the University of Yaoundé 1, Cameroon. Motivated to improve his background training and research skills, he moved to the University of Göttingen in Germany in 1999 where he achieved his second PhD in Molecular genetics of Development in 2002. After his first postdoc training in Germany, he moved to Belgium in 2006 where he did a second postdoc and was granted a chair in Developmental Biology in 2009 at the Université Libre de Bruxelles (ULB).
Jacob SOUOPGUI is a Professor of Molecular Genetics and Biotechnology at the ULB-BioPARK. Since 2012 he created and is the Chair of the Laboratory of Embryology and Biotechnology. His main research interest focuses on understanding the origin of some human malformation and genetic diseases, using laboratory animal models.
Besides his fundamental research goals, Professor SOUOPGUI is very active in the field of R&D aiming at strengthening capacity building in African countries. He is presently one of the team leaders of the Belgian institutional support to the University of Rwanda and is in charge of technology platform implementation to support research and teaching in the field of biotechnology and life sciences. Jacob is a coordinator and partner in several big health-related research grants in Cameroon and in Rwanda.
Title of the talk: Adressing the Holoprosencephaly etiology at the functional genomic levels using laboratory animal models
In Africa congenital malformations at birth are subjected to serious socio-cultural tabous, which lead, in absence of genetic counseling, to destruction of relations between couples and/or entire families. Holoprosencencephaly (HPE) is one of such malformation. HPE is a structural anomaly of the brain in which there is failed or incomplete separation of the forebrain early in gestation. HPE is accompanied by a spectrum of characteristic craniofacial anomalies. The spectrum of facial anomalies begins with cyclopia, the most severe presentation, and extends in an unbroken continuum to the normal face as seen in individuals who have, but are not expressing, a pathogenic variant in HPE inherited in an autosomal dominant manner. Common clinical features in individuals without obvious findings such as cyclopia, synophthalmia, or a proboscis include microcephaly, closely spaced eyes, depressed nasal bridge, single maxillary central incisor and cleft lip and/or palate. HPE is a multi factorial genetic malformation whose etiology is not yet fully elucidated at the molecular levels. Evidence from laboratory animal models indicates that signaling pathways emanating from the Spemann Organizer known as node in mammals during early development drive the patterning of the embryo. Perturbed regulation or mutation of genes of these signaling networks reproduces HPE in animal models. This communication aims at sharing our results and provide evidence that fundamental research in the field of molecular genetics of development is required and could be successfully done in African institutions.