PUBLICATION
Eaf1 and Eaf2 mediate zebrafish dorsal-ventral axis patterning via suppressing Wnt/β-Catenin activity.
- Authors
- Liu, J.X., Xu, Q.H., Yu, X., Zhang, T., Xie, X., Ouyang, G.
- ID
- ZDB-PUB-180622-2
- Date
- 2018
- Source
- International journal of biological sciences 14: 705-716 (Journal)
- Registered Authors
- Liu, Jing-xia, Ouyang, Gang, Xie, Xunwei
- Keywords
- eaf2, axin2, dorsal-ventral patterning, eaf1, ?-catenin
- MeSH Terms
-
- Zebrafish
- RNA, Messenger/genetics
- RNA, Messenger/metabolism*
- Animals
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism
- Axin Protein/genetics
- Axin Protein/metabolism*
- beta Catenin/genetics
- beta Catenin/metabolism*
- Wnt Proteins/genetics
- Wnt Proteins/metabolism*
- Immunoprecipitation
- In Situ Hybridization
- Clustered Regularly Interspaced Short Palindromic Repeats/genetics
- Body Patterning/genetics
- Body Patterning/physiology*
- Reverse Transcriptase Polymerase Chain Reaction
- PubMed
- 29910681 Full text @ Int. J. Biol. Sci.
Citation
Liu, J.X., Xu, Q.H., Yu, X., Zhang, T., Xie, X., Ouyang, G. (2018) Eaf1 and Eaf2 mediate zebrafish dorsal-ventral axis patterning via suppressing Wnt/β-Catenin activity.. International journal of biological sciences. 14:705-716.
Abstract
During early vertebrate embryogenesis, maternal Wnt/β-catenin signaling is thought to locally initiate expression of dorsal-specific genes. Here, eaf1 and eaf2 were identified as important maternal and zygotic modulators of Wnt signaling to initiate and specify ventral genes. Expression of ventral ved, vent, and vox was all obviously enhanced in either maternal or zygotic eaf1/2 morphants, and in both eaf1 heterozygous and homozygous mutants, but their expression was suppressed in embryos with over-expression of eaf1/2. Additionally, eaf1/2 were revealed to suppress ventral fates in embryos via Wnt/β-catenin1/Tcf signaling, complimentary to their roles in suppressing dorsal fates via Wnt/β-catenin2 signaling. Moreover, eaf1/2 were also revealed to obviously suppress the expression of axin2 induced by β-catenin2 rather than by β-catenin1, and the dorsal expression of axin2 in embryos was obviously suppressed by ectopic expression of eaf1/2. This study uncovers a novel dorsal-ventral patterning pathway, with eaf1 and eaf2 inhibiting ventral cells via suppressing Wnt/β-catenin1/Tcf signaling and inducing dorsal cells indirectly via suppressing β-catenin2-induced-axin2 on the dorsal side of embryos.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping