Nkx2.1-derived astrocytes and neurons together with Slit2 are indispensable for anterior commissure formation

Shilpi Minocha, Delphine Valloton, Athena R. Ypsilanti, Hubert Fiumelli, Elizabeth A. Allen, Yuchio Yanagawa, Oscar Marin, Alain Chédotal, Jean-Pierre Hornung and Cécile Lebrand ()
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Shilpi Minocha: University of Lausanne
Delphine Valloton: University of Lausanne
Athena R. Ypsilanti: INSERM UMR-S968, Institut de la Vision
Hubert Fiumelli: King Abdullah University of Science and Technology
Elizabeth A. Allen: EPFL, Station 19, Batiment-SV
Yuchio Yanagawa: Gunma University Graduate School of Medicine and Japan Science and Technology Agency, CREST
Oscar Marin: Instituto de Neurociencias, Consejo Superior de Investigaciones Científicas and Universidad Miguel Hernández
Alain Chédotal: INSERM UMR-S968, Institut de la Vision
Jean-Pierre Hornung: University of Lausanne
Cécile Lebrand: University of Lausanne

Nature Communications, 2015, vol. 6, issue 1, 1-15

Abstract: Abstract Guidepost cells present at and surrounding the midline provide guidance cues that orient the growing axons through commissures. Here we show that the transcription factor Nkx2.1 known to control the specification of GABAergic interneurons also regulates the differentiation of astroglia and polydendrocytes within the mouse anterior commissure (AC). Nkx2.1-positive glia were found to originate from three germinal regions of the ventral telencephalon. Nkx2.1-derived glia were observed in and around the AC region by E14.5. Thereafter, a selective cell ablation strategy showed a synergistic role of Nkx2.1-derived cells, both GABAergic interneurons and astroglia, towards the proper formation of the AC. Finally, our results reveal that the Nkx2.1-regulated cells mediate AC axon guidance through the expression of the repellent cue, Slit2. These results bring forth interesting insights about the spatial and temporal origin of midline telencephalic glia, and highlight the importance of neurons and astroglia towards the formation of midline commissures.

Date: 2015
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DOI: 10.1038/ncomms7887

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