Regulation of Cerebral Cortex Folding by Controlling Neuronal Migration via FLRT Adhesion Molecules

Publication date: 4 May 2017
Source:Cell, Volume 169, Issue 4
Author(s): Daniel del Toro, Tobias Ruff, Erik Cederfjäll, Ana Villalba, Gönül Seyit-Bremer, Víctor Borrell, Rüdiger Klein
The folding of the mammalian cerebral cortex into sulci and gyri is thought to be favored by the amplification of basal progenitor cells and their tangential migration. Here, we provide a molecular mechanism for the role of migration in this process by showing that changes in intercellular adhesion of migrating cortical neurons result in cortical folding. Mice with deletions of FLRT1 and FLRT3 adhesion molecules develop macroscopic sulci with preserved layered organization and radial glial morphology. Cortex folding in these mutants does not require progenitor cell amplification but is dependent on changes in neuron migration. Analyses and simulations suggest that sulcus formation in the absence of FLRT1/3 results from reduced intercellular adhesion, increased neuron migration, and clustering in the cortical plate. Notably, FLRT1/3 expression is low in the human cortex and in future sulcus areas of ferrets, suggesting that intercellular adhesion is a key regulator of cortical folding across species.

Graphical abstract

Teaser

Physical migration of neurons can create the folded cortical surface characteristic of primate brains.


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