PUBLICATION

A small change with a twist ending - a single residue in EGF-CFC drives Bilaterian asymmetry

Authors
Truchado-García, M., Perry, K.J., Cavodeassi, F., Kenny, N.J., Henry, J.Q., Grande, C.
ID
ZDB-PUB-221221-1
Date
2022
Source
Molecular Biology and Evolution   40(2): (Journal)
Registered Authors
Cavodeassi, Florencia
Keywords
Crepidula fornicata, Cripto, EGF-CFC, Evo-Devo, Nodal, Spiralia, Zebrafish, gene expression pattern, left-right asymmetry
MeSH Terms
  • Animals
  • Body Patterning/genetics
  • Chordata*/genetics
  • Epidermal Growth Factor*/chemistry
  • Epidermal Growth Factor*/genetics
  • Gene Expression Regulation, Developmental
  • Mutation
  • Zebrafish/genetics
PubMed
36537201 Full text @ Mol Bio Evol
Abstract
Asymmetries are essential for proper organization and function of organ systems. Genetic studies in bilaterians have shown signaling through the Nodal/Smad2 pathway plays a key, conserved role in the establishment of body asymmetries. However, while the main molecular players in the network for the establishment of left-right asymmetry (LRA) have been deeply described in deuterostomes, little is known about the regulation of Nodal signaling in spiralians. Here, we identified orthologs of the egf-cfc gene, a master regulator of the Nodal pathway in vertebrates, in several invertebrate species, which includes the first evidence of its presence in non-deuterostomes. Our functional experiments indicate that despite being present, egf-cfc does not play a role in the establishment of LRA in gastropods. However, experiments in zebrafish suggest that a single amino acid mutation in the egf-cfc gene in at least the common ancestor of chordates was the necessary step to induce a gain-of-function in LRA regulation. This study shows that the egf-cfc gene likely appeared in the ancestors of deuterostomes and protostomes, before being adopted as a master mechanism to regulate the Nodal pathway and the establishment of LRA in some lineages of deuterostomes.
Genes / Markers
Figures
Show all Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping