PUBLICATION
miR-216a regulates snx5, a novel notch signaling pathway component, during zebrafish retinal development
- Authors
- Olena, A.F., Rao, M.B., Thatcher, E.J., Wu, S.Y., Patton, J.G.
- ID
- ZDB-PUB-150204-8
- Date
- 2015
- Source
- Developmental Biology 400(1): 72-81 (Journal)
- Registered Authors
- Patton, James G., Thatcher, Elizabeth, Wu, Shu-Yu (Simon)
- Keywords
- Microrna, Mir-216a, Notch signaling, Retina, Sorting nexin 5, Zebrafish
- MeSH Terms
-
- Analysis of Variance
- Animals
- Cloning, Molecular
- DNA Primers/genetics
- Gene Expression Profiling
- Gene Expression Regulation, Developmental/genetics
- Gene Expression Regulation, Developmental/physiology*
- Gene Knockdown Techniques
- Image Processing, Computer-Assisted
- Immunoblotting
- In Situ Hybridization
- Intracellular Signaling Peptides and Proteins/metabolism
- Membrane Proteins/metabolism
- MicroRNAs/genetics
- MicroRNAs/metabolism*
- Microarray Analysis
- Models, Biological
- Receptors, Notch/metabolism
- Retina/embryology*
- Retina/metabolism
- Signal Transduction/genetics
- Signal Transduction/physiology*
- Sorting Nexins/metabolism*
- Ubiquitin-Protein Ligases/metabolism*
- Zebrafish/embryology*
- Zebrafish Proteins/metabolism*
- PubMed
- 25645681 Full text @ Dev. Biol.
Citation
Olena, A.F., Rao, M.B., Thatcher, E.J., Wu, S.Y., Patton, J.G. (2015) miR-216a regulates snx5, a novel notch signaling pathway component, during zebrafish retinal development. Developmental Biology. 400(1):72-81.
Abstract
Precise regulation of Notch signaling is essential for normal vertebrate development. Mind bomb (Mib) is a ubiquitin ligase that is required for activation of Notch by Notch's ligand, Delta. Sorting Nexin 5 (SNX5) co-localizes with Mib and Delta complexes and has been shown to directly bind to Mib. We show that microRNA-216a (miR-216a) is expressed in the retina during early development and regulates snx5 to precisely regulate Notch signaling. miR-216a and snx5 have complementary expression patterns. Knocking down miR-216a and/or overexpression of snx5 resulted in increased Notch activation. Conversely, knocking down snx5 and/or miR-216a overexpression caused a decrease in Notch activation. We propose a model in which SNX5, precisely controlled by miR-216a, is a vital partner of Mib in promoting endocytosis of Delta and subsequent activation of Notch signaling.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping