PUBLICATION
Myosin1G promotes Nodal signaling to control zebrafish left-right asymmetry
- Authors
- Kurup, A.J., Bailet, F., Fürthauer, M.
- ID
- ZDB-PUB-240804-1
- Date
- 2024
- Source
- Nature communications 15: 65476547 (Journal)
- Registered Authors
- Fürthauer, Maximilian, Kurup, Akshai Janardhana
- Keywords
- none
- MeSH Terms
-
- Animals
- Body Patterning*/genetics
- Embryo, Nonmammalian/metabolism
- Endosomes/metabolism
- Gene Expression Regulation, Developmental
- Mutation
- Myosin Type I/genetics
- Myosin Type I/metabolism
- Myosins/genetics
- Myosins/metabolism
- Nodal Protein/genetics
- Nodal Protein/metabolism
- Signal Transduction*
- Zebrafish*/embryology
- Zebrafish*/genetics
- Zebrafish*/metabolism
- Zebrafish Proteins*/genetics
- Zebrafish Proteins*/metabolism
- PubMed
- 39095343 Full text @ Nat. Commun.
Citation
Kurup, A.J., Bailet, F., Fürthauer, M. (2024) Myosin1G promotes Nodal signaling to control zebrafish left-right asymmetry. Nature communications. 15:65476547.
Abstract
Myosin1D (Myo1D) has recently emerged as a conserved regulator of animal Left-Right (LR) asymmetry that governs the morphogenesis of the vertebrate central LR Organizer (LRO). In addition to Myo1D, the zebrafish genome encodes the closely related Myo1G. Here we show that while Myo1G also controls LR asymmetry, it does so through an entirely different mechanism. Myo1G promotes the Nodal-mediated transfer of laterality information from the LRO to target tissues. At the cellular level, Myo1G is associated with endosomes positive for the TGFβ signaling adapter SARA. myo1g mutants have fewer SARA-positive Activin receptor endosomes and a reduced responsiveness to Nodal ligands that results in a delay of left-sided Nodal propagation and tissue-specific laterality defects in organs that are most distant from the LRO. Additionally, Myo1G promotes signaling by different Nodal ligands in specific biological contexts. Our findings therefore identify Myo1G as a context-dependent regulator of the Nodal signaling pathway.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping