The Role of Mtss1 in Cortical Development

The role of the membrane-shaping and actin-scaffolding protein Mtss1 in the central nervous system (CNS) is being unravelled more and more. Previous publications investigating malformations that arise under deficiency of Mtss1 put great emphasison the cerebellum and hippocampus. However, a salient consequence of Mtss1 knock-out (KO), namely reduced thickness of the cerebral cortex, has to mynknowledge gone unexplained so far. As a novel feature of the Mtss1-KO phenotype, I report alterations to the pools of neural progenitor cells, which give rise to thencerebral cortex: Numbers of Tbr2-expressing neurogenic intermediate progenitor cells are increased in the brains of mice in late embryonic and perinatal development. At the same time, expression of glial markers and genes associated with apoptosis are reduced, and in the neurogenic germinal zones, more cells are in a proliferative state. Furthermore, expression of Egfr, which is a player in neuro- and gliogenesis, and is known to be controlled by Mtss1 in other contexts, is also affected. In adult Mtss1 KO mice, reduced cortical thickness goes along with reduced cell numbers and increased expression of glial marker Gfap, which both are features of Egfr deficiency. Taken together, these findings seem to suggest an Egfr-related disruption of neocortical development as a result of Mtss1 deficiency.