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Evo-engineering and the cellular and molecular origins of the vertebrate spinal cord.

Accepted version
Peer-reviewed

Type

Article

Change log

Authors

Steventon, Benjamin  ORCID logo  https://orcid.org/0000-0001-7838-839X
Martinez Arias, Alfonso 

Abstract

The formation of the spinal cord during early embryonic development in vertebrate embryos is a continuous process that begins at gastrulation and continues through to the completion of somitogenesis. Despite the conserved usage of patterning mechanisms and gene regulatory networks that act to generate specific spinal cord progenitors, there now exists two seemingly disparate models to account for their action. In the first, a posteriorly localized signalling source transforms previously anterior-specified neural plate into the spinal cord. In the second, a population of bipotent stem cells undergo continuous self-renewal and differentiation to progressively lay down the spinal cord and axial mesoderm by posterior growth. Whether this represents fundamental differences between the experimental model organisms utilised in the generation of these models remains to be addressed. Here we review lineage studies across four key vertebrate models: mouse, chicken, Xenopus and zebrafish and relate them to the underlying gene regulatory networks that are known to be required for spinal cord formation. We propose that by applying a dynamical systems approach to understanding how distinct neural and mesodermal fates arise from a bipotent progenitor pool, it is possible to begin to understand how differences in the dynamical cell behaviours such as proliferation rates and cell movements can map onto conserved regulatory networks to generate diversity in the timing of tissue generation and patterning during development.

Description

Keywords

Animals, Cell Differentiation, Chickens, Developmental Biology, Mesoderm, Mice, Models, Animal, Morphogenesis, Neural Plate, Spinal Cord, Stem Cells, Xenopus, Zebrafish

Journal Title

Developmental Biology

Conference Name

Journal ISSN

0012-1606
1095-564X

Volume Title

432

Publisher

Elsevier
Sponsorship
Wellcome Trust (109408/Z/15/Z)
European Commission (330880)
The research of B.S. was supported by a Marie Curie IOF fellowship (PIOF-GA-2012-330880) and a Wellcome Trust Sir Henry Dale Fellowship (109408/Z/15/Z). This research of AMA was funded by an ERC advanced investigator grant.