Major transcriptome re-organisation and abrupt changes in signalling, cell cycle and chromatin regulation at neural differentiation<i>in vivo</i>

Olivera-Martínez, Isabel; Schurch, Nicholas J.; Li, Roman A.; Song, Junfang; Halley, Pamela A.; Das, Raman M; Burt, David W.; Barton, Geoffrey J.; Storey, Kate G.

doi:10.1242/dev.112623

Cited by 56 publications

(68 citation statements)

References 58 publications

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“…Androgen receptor nuclear signalling is the most CNH-enriched pathway revealed by pathway enrichment analysis of our differentially expressed genes ( Fig. 1C; Table S4; Supplementary Information), and enriched Greb1 expression has been found in previous studies of axial and neuromesodermal progenitors (Table S3; Gouti et al, 2017;Olivera-Martinez et al, 2014;Wymeersch et al, 2019).…”

Section: Greb1 Expression Coincides With Axial Elongation In Vertebrasupporting

confidence: 69%

“…We also compared our list of CNH-enriched genes with those previously identified in previous studies of the CNH or NMPs (Table S3; Gouti et al, 2017;Olivera-Martinez et al, 2014;Wymeersch et al, 2019). Expression of seven of the ten most-enriched genes (Fgf8, Cdx2, T, Wnt3a, Sp5, Evx1, and Fgf17) was previously reported in the CNH and TBM, and to be functionally important for axial development (Cambray and Wilson, 2007;Dunty et al, 2014;Maruoka et al, 1998;Takada et al, 1994).…”

Section: Greb1 Expression Coincides With Axial Elongation In Vertebramentioning

confidence: 99%

“…Briefly, a positive feedback loop between Brachyury/T and Wnt3a maintains axial progenitors in the tail bud (Martin and Kimelman, 2010;Wilson et al, 2009). In parallel, Fgf signalling protects axial progenitors from differentiation induced by Retinoic acid (RA) that is secreted by differentiating and young somites and diffuses into the PSM (Diez del Corral et al, 2003;Olivera-Martinez et al, 2012;Ribes et al, 2009). However, Fgf8, Wnt3, and T are all expressed in much larger domains than the CNH and so do not specifically distinguish axial progenitors from more specialised cells such as the TBM.…”

Section: Introductionmentioning

confidence: 99%

“…However, Fgf8, Wnt3, and T are all expressed in much larger domains than the CNH and so do not specifically distinguish axial progenitors from more specialised cells such as the TBM. Transcriptome analysis of dissected axial progenitor tissue during the period of axial elongation and of in vitro-derived NMPs has identified genes that are differentially expressed between progenitors and presomitic mesoderm cells (Gouti et al, 2017;Olivera-Martinez et al, 2014;Wymeersch et al, 2019). However, the functional significance of many of these genes has yet to be defined.…”

Section: Introductionmentioning

confidence: 99%

“…helps maintain axial progenitors by protecting them from premature differentiation induced by retinoic acid secreted by the anterior PSM and somites(Diez del Corral et al, 2003;Martin and Kimelman, 2010;Olivera- Martinez et al, 2012;Ribes et al, 2009). …”

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confidence: 99%

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Greb1is required for axial elongation and segmentation in vertebrate embryos

Prajapati

Mitter

Vezzaro

et al. 2019

Preprint

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During vertebrate embryonic development, the formation of axial structures is driven by a population of stem-like cells that reside in a region of the tailbud called the chordoneural hinge (CNH). We have compared the CNH transcriptome with those of surrounding tissues and shown that the CNH and tailbud mesoderm are transcriptionally similar, and distinct from the presomitic mesoderm. Amongst CNH-enriched genes are several that are required for axial elongation, including Wnt3a, Cdx2, Brachyury/T and Fgf8, and androgen/estrogen receptor nuclear signalling components such as Greb1.We show that the pattern and duration of tailbud Greb1 expression is conserved in mouse, zebrafish, and chicken embryos, and that Greb1 is required for axial elongation and somitogenesis in zebrafish embryos. The axial truncation phenotype of Greb1 morphant embryos is explained by much reduced expression of No tail (Ntl/Brachyury) which is required for axial progenitor maintenance. Posterior segmentation defects in the morphants (including misexpression of genes such as mespb, myoD and papC) appear to result, in part, from lost expression of the segmentation clock gene, her7. Brown, J. M. and Storey, K. G. (2000). A region of the vertebrate neural plate in which neighbouring cells can adopt neural or epidermal fates. Current biology : CB 10, 869-872. Cambray, N. and Wilson, V. (2002). Axial progenitors with extensive potency are localised to the mouse chordoneural hinge. Development 129, 4855-4866. Cambray, N. and Wilson, V. (2007). Two distinct sources for a population of maturing axial progenitors. Development 134, 2829-2840. Catala, M., Teillet, M. A., De Robertis, E. M. and Le Douarin, M. L. (1996). A spinal cord fate map in the avian embryo: while regressing, Hensen's node lays down the notochord and floor plate thus joining the spinal cord lateral walls. Development 122, 2599-2610. Choorapoikayil, S., Willems, B., Strohle, P. and Gajewski, M. (2012). Analysis of her1 and her7 mutants reveals a spatio temporal separation of the somite clock module. PloS one 7, e39073. Deniziak, M., Thisse, C., Rederstorff, M., Hindelang, C., Thisse, B. and Lescure, A. (2007). Loss of selenoprotein N function causes disruption of muscle architecture in the zebrafish embryo. Exp Cell Res 313, 156-167.

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Section: Greb1 Expression Coincides With Axial Elongation In Vertebrasupporting

confidence: 69%

Section: Greb1 Expression Coincides With Axial Elongation In Vertebramentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

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Greb1is required for axial elongation and segmentation in vertebrate embryos

Prajapati

Mitter

Vezzaro

et al. 2019

Preprint

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Cell transplantation and secretome based approaches in spinal cord injury regenerative medicine

Silva

Pinto

Salgado

2021

Medicinal Research Reviews

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The axonal growth‐restrictive character of traumatic spinal cord injury (SCI) makes finding a therapeutic strategy a very demanding task, due to the postinjury events impeditive to spontaneous axonal outgrowth and regeneration. Considering SCI pathophysiology complexity, it has been suggested that an effective therapy should tackle all the SCI‐related aspects and provide sensory and motor improvement to SCI patients. Thus, the current aim of any therapeutic approach for SCI relies in providing neuroprotection and support neuroregeneration. Acknowledging the current SCI treatment paradigm, cell transplantation is one of the most explored approaches for SCI with mesenchymal stem cells (MSCs) being in the forefront of many of these. Studies showing the beneficial effects of MSC transplantation after SCI have been proposing a paracrine action of these cells on the injured tissues, through the secretion of protective and trophic factors, rather than attributing it to the action of cells itself. This manuscript provides detailed information on the most recent data regarding the neuroregenerative effect of the secretome of MSCs as a cell‐free based therapy for SCI. The main challenge of any strategy proposed for SCI treatment relies in obtaining robust preclinical evidence from in vitro and in vivo models, before moving to the clinics, so we have specifically focused on the available vertebrate and mammal models of SCI currently used in research and how can SCI field benefit from them.

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Regulation of size and scale in vertebrate spinal cord development

Kuzmicz-Kowalska

Kicheva

2020

WIREs Developmental Biology

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All vertebrates have a spinal cord with dimensions and shape specific to their species. Yet how species‐specific organ size and shape are achieved is a fundamental unresolved question in biology. The formation and sculpting of organs begins during embryonic development. As it develops, the spinal cord extends in anterior–posterior direction in synchrony with the overall growth of the body. The dorsoventral (DV) and apicobasal lengths of the spinal cord neuroepithelium also change, while at the same time a characteristic pattern of neural progenitor subtypes along the DV axis is established and elaborated. At the basis of these changes in tissue size and shape are biophysical determinants, such as the change in cell number, cell size and shape, and anisotropic tissue growth. These processes are controlled by global tissue‐scale regulators, such as morphogen signaling gradients as well as mechanical forces. Current challenges in the field are to uncover how these tissue‐scale regulatory mechanisms are translated to the cellular and molecular level, and how regulation of distinct cellular processes gives rise to an overall defined size. Addressing these questions will help not only to achieve a better understanding of how size is controlled, but also of how tissue size is coordinated with the specification of pattern. This article is categorized under: Establishment of Spatial and Temporal Patterns > Regulation of Size, Proportion, and Timing Signaling Pathways > Global Signaling Mechanisms Nervous System Development > Vertebrates: General Principles

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Major transcriptome re-organisation and abrupt changes in signalling, cell cycle and chromatin regulation at neural differentiationin vivo

Cited by 56 publications

References 58 publications

Greb1is required for axial elongation and segmentation in vertebrate embryos

Greb1is required for axial elongation and segmentation in vertebrate embryos

Cell transplantation and secretome based approaches in spinal cord injury regenerative medicine

Regulation of size and scale in vertebrate spinal cord development

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