PUBLICATION
The characterization of zebrafish antimorphic mib alleles reveals that Mib and Mind bomb-2 (Mib2) function redundantly
- Authors
- Zhang, C., Li, Q., Lim, C.H., Qiu, X., and Jiang, Y.J.
- ID
- ZDB-PUB-070303-40
- Date
- 2007
- Source
- Developmental Biology 305(1): 14-27 (Journal)
- Registered Authors
- Jiang, Yun-Jin, Lim, Chiaw Hwee, Qiu, Xuehui, Zhang, Chengjin
- Keywords
- Mib homologs, mib alleles, Delta, Notch, E3 ligase, Endocytosis
- MeSH Terms
-
- Alleles*
- Animals
- Cloning, Molecular
- Embryo, Nonmammalian/metabolism
- Gene Expression Regulation/physiology
- Immunohistochemistry
- In Situ Hybridization
- Mutation/genetics
- Oligonucleotides, Antisense
- Receptors, Notch/metabolism
- Signal Transduction/genetics
- Ubiquitin-Protein Ligases/genetics*
- Ubiquitin-Protein Ligases/metabolism
- Zebrafish/genetics*
- Zebrafish Proteins/genetics*
- Zebrafish Proteins/metabolism
- PubMed
- 17331493 Full text @ Dev. Biol.
Citation
Zhang, C., Li, Q., Lim, C.H., Qiu, X., and Jiang, Y.J. (2007) The characterization of zebrafish antimorphic mib alleles reveals that Mib and Mind bomb-2 (Mib2) function redundantly. Developmental Biology. 305(1):14-27.
Abstract
Both mind bomb (mib) and mind bomb-2 (mib2) encode RING E3 ubiquitin ligases that promote Delta ubiquitylation and endocytosis in Notch activation. Detailed morphological and molecular examinations revealed that zebrafish mib(ta52b) (missense mutation in the C-terminal RING Finger (RF), M1013R) and mib(m132) (nonsense mutation resulting in a truncated protein that loses all three RFs, C785stop) are strong and weak antimorphic alleles, respectively, compared to the null allele, mib(tfi91) (nonsense mutation resulting in a truncated protein of only 60 amino acids, Y60stop). Zebrafish mib2 ortholog was identified in this study. Zebrafish Mib and Mib2 are colocalized in transfected cells and function redundantly in regulating Notch signaling in embryos. Mib(ta52b) and Mib(m132) have a dosage-dependent dominant-negative effect, at least, on Mib2, which is a molecular basis for the antimorphic phenotypes. It was also shown that Notch signaling negatively regulates mib expression in a Su(H)-dependent manner, forming a negative feedback loop in modulating Notch activation.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping