PUBLICATION

The E3 Ubiquitin Ligase Mindbomb1 controls planar cell polarity-dependent convergent extension movements during zebrafish gastrulation

Authors
Saraswathy, V.M., Kurup, A.J., Sharma, P., Polès, S., Poulain, M., Fürthauer, M.
ID
ZDB-PUB-220211-8
Date
2022
Source
eLIFE   11: (Journal)
Registered Authors
Fürthauer, Maximilian, Kurup, Akshai Janardhana, Polès, Sophie, Poulain, Morgane
Keywords
developmental biology, zebrafish
MeSH Terms
  • Animals
  • Cell Movement/genetics
  • Cell Polarity/physiology
  • Gastrulation*/physiology
  • Ubiquitin-Protein Ligases/genetics
  • Wnt Proteins/metabolism
  • Zebrafish*/metabolism
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism
PubMed
35142609 Full text @ Elife
Abstract
Vertebrate Delta/Notch signaling involves multiple ligands, receptors and transcription factors. Delta endocytosis - a critical event for Notch activation - is however essentially controlled by the E3 Ubiquitin ligase Mindbomb1 (Mib1). Mib1 inactivation is therefore often used to inhibit Notch signaling. However, recent findings indicate that Mib1 function extends beyond the Notch pathway. We report a novel Notch-independent role of Mib1 in zebrafish gastrulation. mib1 null mutants and morphants display impaired Convergence Extension (CE) movements. Comparison of different mib1 mutants and functional rescue experiments indicate that Mib1 controls CE independently of Notch. Mib1-dependent CE defects can be rescued using the Planar Cell Polarity (PCP) downstream mediator RhoA, or enhanced through knock-down of the PCP ligand Wnt5b. Mib1 regulates CE through its RING Finger domains that have been implicated in substrate ubiquitination, suggesting that Mib1 may control PCP protein trafficking. Accordingly, we show that Mib1 controls the endocytosis of the PCP component Ryk and that Ryk internalization is required for CE. Numerous morphogenetic processes involve both Notch and PCP signaling. Our observation that during zebrafish gastrulation Mib1 exerts a Notch-independent control of PCP-dependent CE movements suggest that Mib1 loss of function phenotypes should be cautiously interpreted depending on the biological context.
Genes / Markers
Figures
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Expression
Phenotype
Mutation and Transgenics
Human Disease / Model Data
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping
Errata and Notes