PUBLICATION
Greb1 is required for axial elongation and segmentation in vertebrate embryos
- Authors
- Prajapati, R.S., Mitter, R., Vezzaro, A., Ish-Horowicz, D.
- ID
- ZDB-PUB-200129-6
- Date
- 2020
- Source
- Biology Open 9(2): (Journal)
- Registered Authors
- Keywords
- Axial stem cells, Clock, Neural tube, Progenitors, Somites, Tailbud, Transcriptome
- MeSH Terms
-
- Animals
- Computational Biology/methods
- Embryonic Development/genetics*
- Gene Expression Profiling
- Gene Expression Regulation, Developmental
- Gene Knockdown Techniques
- Membrane Proteins/genetics*
- Mice
- Morphogenesis/genetics*
- Neoplasm Proteins/genetics*
- Phenotype
- Stem Cells/cytology
- Stem Cells/metabolism
- Transcriptome
- Zebrafish Proteins/genetics*
- PubMed
- 31988092 Full text @ Biol. Open
Citation
Prajapati, R.S., Mitter, R., Vezzaro, A., Ish-Horowicz, D. (2020) Greb1 is required for axial elongation and segmentation in vertebrate embryos. Biology Open. 9(2):.
Abstract
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 mouse 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 can be 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.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping