PUBLICATION
A Notch-mediated, temporal asymmetry in BMP pathway activation promotes photoreceptor subtype diversification
- Authors
- Cau, E., Ronsin, B., Bessière, L., Blader, P.
- ID
- ZDB-PUB-190201-8
- Date
- 2019
- Source
- PLoS Biology 17: e2006250 (Journal)
- Registered Authors
- Blader, Patrick, Cau, Elise
- Keywords
- none
- MeSH Terms
-
- Gene Expression Regulation, Developmental/genetics
- Photoreceptor Cells, Vertebrate/physiology*
- Animals
- Zebrafish/genetics
- Zebrafish/metabolism
- Cell Lineage
- Embryo, Nonmammalian/metabolism
- Pineal Gland/embryology*
- Pineal Gland/metabolism
- Pineal Gland/physiology
- Time Factors
- Bone Morphogenetic Proteins/metabolism
- Signal Transduction
- Receptors, Notch/metabolism*
- Neurons/metabolism
- Zebrafish Proteins/metabolism
- Cell Differentiation/genetics
- PubMed
- 30703098 Full text @ PLoS Biol.
Citation
Cau, E., Ronsin, B., Bessière, L., Blader, P. (2019) A Notch-mediated, temporal asymmetry in BMP pathway activation promotes photoreceptor subtype diversification. PLoS Biology. 17:e2006250.
Abstract
Neural progenitors produce neurons whose identities can vary as a function of the time that specification occurs. Here, we describe the heterochronic specification of two photoreceptor (PhR) subtypes in the zebrafish pineal gland. We find that accelerating PhR specification by impairing Notch signaling favors the early fate at the expense of the later fate. Using in vivo lineage tracing, we show that most pineal PhRs are born from a fate-restricted progenitor. Furthermore, sister cells derived from the division of PhR-restricted progenitors activate the bone morphogenetic protein (BMP) signaling pathway at different times after division, and this heterochrony requires Notch activity. Finally, we demonstrate that PhR identity is established as a function of when the BMP pathway is activated. We propose a novel model in which division of a progenitor with restricted potential generates sister cells with distinct identities via a temporal asymmetry in the activation of a signaling pathway.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping