Retinoid-independent motor neurogenesis from human embryonic stem cells reveals a medial columnar ground state

R. Patani, A. J. Hollins, T. M. Wishart, C. A. Puddifoot, S. Álvarez, A. R. de Lera, D. J. A. Wyllie, D. A. S. Compston, R. A. Pedersen, T. H. Gillingwater, G. E. Hardingham, N. D. Allen () and S. Chandran ()
Additional contact information
R. Patani: Anne Mclaren Laboratory for Regenerative Medicine, University of Cambridge
A. J. Hollins: School of Biosciences, Cardiff University
T. M. Wishart: Centre for Integrative Physiology, University of Edinburgh
C. A. Puddifoot: Centre for Integrative Physiology, University of Edinburgh
S. Álvarez: Facultade de Química, Universidade de Vigo
A. R. de Lera: Facultade de Química, Universidade de Vigo
D. J. A. Wyllie: Centre for Integrative Physiology, University of Edinburgh
D. A. S. Compston: Cambridge Centre for Brain Repair, University of Cambridge
R. A. Pedersen: Anne Mclaren Laboratory for Regenerative Medicine, University of Cambridge
T. H. Gillingwater: Centre for Integrative Physiology, University of Edinburgh
G. E. Hardingham: Centre for Integrative Physiology, University of Edinburgh
N. D. Allen: School of Biosciences, Cardiff University
S. Chandran: Anne Mclaren Laboratory for Regenerative Medicine, University of Cambridge

Nature Communications, 2011, vol. 2, issue 1, 1-10

Abstract: Abstract A major challenge in neurobiology is to understand mechanisms underlying human neuronal diversification. Motor neurons (MNs) represent a diverse collection of neuronal subtypes, displaying differential vulnerability in different human neurodegenerative diseases. The ability to manipulate cell subtype diversification is critical to establish accurate, clinically relevant in vitro disease models. Retinoid signalling contributes to caudal precursor specification and subsequent MN subtype diversification. Here we investigate the necessity for retinoic acid in motor neurogenesis from human embryonic stem cells. We show that activin/nodal signalling inhibition, followed by sonic hedgehog agonist treatment, is sufficient for MN precursor specification, which occurs even in the presence of retinoid pathway antagonists. Importantly, precursors mature into HB9/ChAT-expressing functional MNs. Furthermore, retinoid-independent motor neurogenesis results in a ground state biased to caudal, medial motor columnar identities from which a greater retinoid-dependent diversity of MNs, including those of lateral motor columns, can be selectively derived in vitro.

Date: 2011
References: Add references at CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/ncomms1216 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:2:y:2011:i:1:d:10.1038_ncomms1216

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/ncomms1216

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().