Cortex folding by combined progenitor expansion and adhesion-controlled neuronal migration

Seung Hee Chun, Da Eun Yoon, D. Santiago Diaz Almeida, Mihail Ivilinov Todorov, Tobias Straub, Tobias Ruff, Wei Shao, Jianjun Yang, Gönül Seyit-Bremer, Yi-Ru Shen, Ali Ertürk, Daniel del Toro, Songhai Shi and Rüdiger Klein ()
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Seung Hee Chun: Department of Molecules – Signaling – Development, Max Planck Institute for Biological Intelligence
Da Eun Yoon: Max Plank Institute of Biochemistry
D. Santiago Diaz Almeida: Department of Molecules – Signaling – Development, Max Planck Institute for Biological Intelligence
Mihail Ivilinov Todorov: Ludwig-Maximilians-University Munich (LMU)
Tobias Straub: Ludwig-Maximilians University (LMU)
Tobias Ruff: Eidgenössische Technische Hochschule (ETH) Zürich
Wei Shao: Weill Cornell Medical College
Jianjun Yang: Tsinghua University
Gönül Seyit-Bremer: Department of Molecules – Signaling – Development, Max Planck Institute for Biological Intelligence
Yi-Ru Shen: Department of Molecules – Signaling – Development, Max Planck Institute for Biological Intelligence
Ali Ertürk: Ludwig-Maximilians-University Munich (LMU)
Daniel del Toro: University of Barcelona
Songhai Shi: Tsinghua University
Rüdiger Klein: Department of Molecules – Signaling – Development, Max Planck Institute for Biological Intelligence

Nature Communications, 2025, vol. 16, issue 1, 1-18

Abstract: Abstract Folding of the mammalian cerebral cortex into sulcal fissures and gyral peaks is the result of complex processes that are incompletely understood. Previously we showed that genetic deletion of Flrt1/3 adhesion molecules causes folding of the smooth mouse cortex into sulci resulting from increased lateral dispersion and faster neuron migration, without progenitor expansion. Here, we show in mice that combining the Flrt1/3 double knockout with an additional genetic deletion that causes progenitor expansion, greatly enhances cortex folding. Expansion of intermediate progenitors by deletion of Cep83 leads to a relative increase in Flrt-mutant neurons resulting in enhanced formation of sulci. Expansion of apical progenitors by deletion of Fgf10 leads to a relative reduction in Flrt-mutant neurons resulting in enhanced formation of gyri. These results together with computational modeling identify key developmental mechanisms, such as adhesive properties, cell densities and migration of cortical neurons, that cooperate to promote cortical gyrification.

Date: 2025
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DOI: 10.1038/s41467-025-62858-9

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