PUBLICATION

Dachsous1b cadherin regulates actin and microtubule cytoskeleton during early zebrafish embryogenesis

Authors
Li-Villarreal, N., Forbes, M.M., Loza, A.J., Chen, J., Ma, T., Helde, K., Moens, C.B., Shin, J., Sawada, A., Hindes, A.E., Dubrulle, J., Schier, A.F., Longmore, G.D., Marlow, F.L., Solnica-Krezel, L.
ID
ZDB-PUB-150711-1
Date
2015
Source
Development (Cambridge, England)   142(15): 2704-18 (Journal)
Registered Authors
Chen, Jiakun, Dubrulle, Julien, Forbes, Meredyth, Helde, Kathryn, Hindes, Anna, Marlow, Florence, Ma, Taylur, Moens, Cecilia, Sawada, Atsushi, Schier, Alexander, Shin, Jimann, Solnica-Krezel, Lilianna
Keywords
Actin, Cell fate, dchs1b, Egg activation, Microtubule, Morphogenesis
MeSH Terms
  • Actins/metabolism*
  • Animals
  • Cadherins/genetics
  • Cadherins/metabolism*
  • Cytoskeleton/physiology*
  • DNA Primers/genetics
  • Exocytosis/physiology
  • Female
  • Immunohistochemistry
  • In Situ Hybridization
  • Microscopy, Confocal
  • Microtubules/metabolism*
  • Optical Imaging
  • Ovary/anatomy & histology
  • RNA, Messenger/metabolism
  • Real-Time Polymerase Chain Reaction
  • Zebrafish/embryology*
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
PubMed
26160902 Full text @ Development
Abstract
Dachsous (Dchs), an atypical cadherin, is an evolutionarily conserved regulator of planar cell polarity, tissue size, and cell adhesion. In humans, DCHS1 mutations cause pleiotropic Van Maldergem syndrome. Here, we report that mutations in zebrafish dchs1b and dchs2 disrupt several aspects of embryogenesis, including gastrulation. Unexpectedly, maternal zygotic (MZ) dchs1b mutants show defects in the earliest developmental stage, egg activation, including abnormal cortical granule exocytosis (CGE), cytoplasmic segregation, cleavages, and maternal mRNA translocation, in transcriptionally quiescent embryos. Later, MZdchs1b mutants exhibit altered dorsal organizer and mesendodermal gene expression, due to impaired dorsal determinant transport and Nodal signaling. Mechanistically, MZdchs1b phenotypes can be explained in part by defective actin or microtubule networks, which appear bundled in mutants. Accordingly, disruption of actin cytoskeleton in wild-type embryos phenocopied MZdchs1b mutant defects in cytoplasmic segregation and CGE. Whereas, interfering with microtubules in wild-type embryos impaired dorsal organizer and mesodermal gene expression without perceptible earlier phenotypes. Moreover, the bundled microtubule phenotype was partially rescued by expressing either full-length Dchs1b or its intracellular domain, suggesting Dchs1b affects microtubules and some developmental processes independent of its known ligand Fat. Our results indicate novel roles for vertebrate Dchs in actin and microtubule cytoskeleton regulation in the unanticipated context of the single-celled embryo.
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
Erratum.