Xavier Jaglin, PhD
Education and Training:
- 2011-present: Postdoctoral Fellow, Gordon Fishell Lab. Human Frontier Science Program (HFSP) and European Molecular Biology Organization (EMBO) fellow.
- 2007-2010: Ph.D. in molecular genetics. Université Paris - Diderot, France.
- "Pathophysiological mechanisms of malformations of cortical development associated with mutations in the Tubulin genes TUBA1A and TUBB2B". Supervised by Prof. J. Chelly and Dr. F. Francis.
- 2005-2007: M.Sc. in molecular and cellular biology. Université Paris - Diderot, France and Université Laval, Quebec, Canada. Training in EW. Khandjian's lab (Quebec): Characterization of novel proteins interacting with the Fragile X Mental Retardation Protein FMRP.
Current or Past Study:
Over the past years, my research has focused on the comprehension of molecular and cellular basis of types of human cognitive defects. My postdoctoral training will allow me to proceed with my research in the field of neurodevelopment and to further explore and understand how the interneuron diversity in the cortex is build and how they acquire their organization. I expect to further gain into insight in the understanding of inhibition in the forebrain and its pathological alterations.
I am particularly interested in the period of synaptogenesis and interneuron integration into the nascent cortical network. These processes are of major importance and interest. Indeed, the alteration of synapse development and cell-type specific subcellular targeting might impair brain connectivity and lead to autism spectrum disorder (ASD). The goal of my postdoctoral work is to gain insight into the developmental processes establishing cortical neural networks and underlying the development of cell-type specific interneuron connectivity. Activity-dependent alternative splicing (AS) of transmembrane proteins or ion channels has recently emerged as a potent post-transcriptional contributor to the dynamic regulation of cell-cell recognition or synaptic plasticity, respectively. Therefore, I propose that AS may tailor the transcriptome to promote the integration of specific interneuron subtypes into developing cortical circuits.