PUBLICATION
A cluster of non-redundant Ngn1 binding sites is required for regulation of deltaA expression in zebrafish
- Authors
- Madelaine, R., and Blader, P.
- ID
- ZDB-PUB-101108-2
- Date
- 2011
- Source
- Developmental Biology 350(1): 198-207 (Journal)
- Registered Authors
- Blader, Patrick, Madelaine, Romain
- Keywords
- Ngn1, Ascl1, deltaA, Transcriptional regulation, Cis-regulatory module (CRM), E-box
- MeSH Terms
-
- Animals
- Base Sequence
- Basic Helix-Loop-Helix Transcription Factors/genetics
- Basic Helix-Loop-Helix Transcription Factors/metabolism*
- Binding Sites
- Gene Expression Regulation, Developmental*
- Intracellular Signaling Peptides and Proteins
- Membrane Proteins/genetics*
- Molecular Sequence Data
- Nerve Tissue Proteins/genetics
- Nerve Tissue Proteins/metabolism*
- Transcription, Genetic
- Zebrafish/embryology*
- Zebrafish/genetics
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism*
- PubMed
- 21034732 Full text @ Dev. Biol.
Citation
Madelaine, R., and Blader, P. (2011) A cluster of non-redundant Ngn1 binding sites is required for regulation of deltaA expression in zebrafish. Developmental Biology. 350(1):198-207.
Abstract
Proneural genes encode bHLH transcription factors that are key regulator of neurogenesis in both vertebrates and invertebrates. How these transcription factors regulate targets required for neural determination and/or specification is beginning to be understood. In this study, we show that zebrafish deltaA is a transcriptional target of proneural factors. Using a combination of transient and stable transgenic reporters, we show that regulation of deltaA by one such proneural factor, Ngn1, requires three clustered E-box binding sites that act in a non-redundant manner. Furthermore, we show that as for other proneural targets, members of the different proneural families regulate deltaA expression via distinct cis-regulatory modules (CRMs). Interestingly, however, while the deltaA CRM regulated by a second proneural factor, Ascl1, has been conserved between delta genes of different species, we show that the Ngn1 CRM has not. These results suggest that evolutionary constraints on the mechanism by which Ngn1 regulates gene expression appear less strict than for Ascl1.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping