PUBLICATION

The RNA-binding protein Celf1 post-transcriptionally regulates p27Kip1 and Dnase2b to control fiber cell nuclear degradation in lens development

Authors
Siddam, A.D., Gautier-Courteille, C., Perez-Campos, L., Anand, D., Kakrana, A., Dang, C.A., Legagneux, V., Méreau, A., Viet, J., Gross, J.M., Paillard, L., Lachke, S.A.
ID
ZDB-PUB-180323-1
Date
2018
Source
PLoS Genetics   14: e1007278 (Journal)
Registered Authors
Gross, Jeffrey
Keywords
none
MeSH Terms
  • Animals
  • CELF1 Protein/physiology*
  • Cell Line
  • Cell Nucleus/metabolism*
  • Cyclin-Dependent Kinase Inhibitor p27/genetics*
  • Endodeoxyribonucleases/genetics*
  • Gene Expression Regulation
  • Lens, Crystalline/cytology
  • Lens, Crystalline/growth & development*
  • Lens, Crystalline/metabolism
  • Mice
  • RNA-Binding Proteins/physiology*
  • Xenopus Proteins/physiology*
  • Xenopus laevis
  • Zebrafish
  • Zebrafish Proteins/physiology*
PubMed
29565969 Full text @ PLoS Genet.
Abstract
Opacification of the ocular lens, termed cataract, is a common cause of blindness. To become transparent, lens fiber cells undergo degradation of their organelles, including their nuclei, presenting a fundamental question: does signaling/transcription sufficiently explain differentiation of cells progressing toward compromised transcriptional potential? We report that a conserved RNA-binding protein Celf1 post-transcriptionally controls key genes to regulate lens fiber cell differentiation. Celf1-targeted knockout mice and celf1-knockdown zebrafish and Xenopus morphants have severe eye defects/cataract. Celf1 spatiotemporally down-regulates the cyclin-dependent kinase (Cdk) inhibitor p27Kip1 by interacting with its 5' UTR and mediating translation inhibition. Celf1 deficiency causes ectopic up-regulation of p21Cip1. Further, Celf1 directly binds to the mRNA of the nuclease Dnase2b to maintain its high levels. Together these events are necessary for Cdk1-mediated lamin A/C phosphorylation to initiate nuclear envelope breakdown and DNA degradation in fiber cells. Moreover, Celf1 controls alternative splicing of the membrane-organization factor beta-spectrin and regulates F-actin-crosslinking factor Actn2 mRNA levels, thereby controlling fiber cell morphology. Thus, we illustrate new Celf1-regulated molecular mechanisms in lens development, suggesting that post-transcriptional regulatory RNA-binding proteins have evolved conserved functions to control vertebrate oculogenesis.
Genes / Markers
Figures
Show all Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping