PUBLICATION
Reduced expression of the Nodal coreceptor Oep causes loss of mesendodermal competence in zebrafish
- Authors
- Vopalensky, P., Pralow, S., Vastenhouw, N.L.
- ID
- ZDB-PUB-180223-2
- Date
- 2018
- Source
- Development (Cambridge, England) 145(5): (Journal)
- Registered Authors
- Pralow, Sabrina, Vastenhouw, Nadine
- Keywords
- Activin, Competence, Development, Mesendoderm, Nodal, Oep
- MeSH Terms
-
- Animals
- Animals, Genetically Modified
- Ectoderm/embryology
- Ectoderm/metabolism
- Embryo, Nonmammalian
- Embryonic Development/genetics*
- Endoderm/embryology*
- Endoderm/metabolism
- Gene Expression Regulation, Developmental
- Homeodomain Proteins/genetics*
- Homeodomain Proteins/metabolism
- Mesoderm/embryology*
- Mesoderm/metabolism
- Nodal Protein/metabolism
- Signal Transduction/genetics
- Transcription Factors/genetics*
- Transcription Factors/metabolism
- Zebrafish*/embryology
- Zebrafish*/genetics
- Zebrafish Proteins/genetics*
- Zebrafish Proteins/metabolism
- PubMed
- 29440298 Full text @ Development
Citation
Vopalensky, P., Pralow, S., Vastenhouw, N.L. (2018) Reduced expression of the Nodal coreceptor Oep causes loss of mesendodermal competence in zebrafish. Development (Cambridge, England). 145(5).
Abstract
The activation of specific gene expression programs depends on the presence of the appropriate signals and the competence of cells to respond to these signals. Although it is well-established that cellular competence is regulated in space and time, the molecular mechanisms underlying the loss of competence remain largely unknown. Here we determine the time-window during which zebrafish prospective ectoderm loses its ability to respond to Nodal signals, and show that this coincides with a decrease in the levels of the Nodal co-receptor one-eyed pinhead (oep)Bypassing Oep using a photoactivatable receptor, or an Oep-independent ligand, allows activation of Nodal target genes for an extended period of time. These results suggest that the reduced expression of Oep causes the loss of responsiveness to Nodal signals in the prospective ectoderm. Indeed, extending the presence of Oep prolongs the window of competence to respond to Nodal signals. Our findings suggest a simple mechanism in which the decreasing level of one component of the Nodal signaling pathway regulates the loss of mesendodermal competence in the prospective ectoderm.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping