PUBLICATION

Zebrafish maternal-effect mutations causing cytokinesis defect without affecting mitosis or equatorial vasa deposition

Authors
Kishimoto, Y., Koshida, S., Furutani-Seiki, M., and Kondoh, H.
ID
ZDB-PUB-040109-12
Date
2004
Source
Mechanisms of Development   121(1): 79-89 (Journal)
Registered Authors
Furutani-Seiki, Makoto, Kishimoto, Yasuyuki, Kondoh, Hisato, Koshida, Sumito
Keywords
none
MeSH Terms
  • Animals
  • Crosses, Genetic
  • Mitosis/physiology*
  • Mutation*
  • Phenotype
  • Zebrafish/embryology
  • Zebrafish/genetics*
PubMed
14706702 Full text @ Mech. Dev.
Abstract
Maternal-effect genes play essential roles in early embryogenesis particularly before activation of the zygotic genes. A genetic screen for mutations affecting such maternal-effect genes was carried out employing an F3 screen strategy, identifying six recessive mutations out of 60 mutagenized genomes. Three of the mutations (acytokinesis mutations: ack(kt5), ack(kt62) and ack(kt119)) caused absence of cell cleavage in the embryos derived from homozygous females regardless of the paternal genotype, without affecting nuclear divisions. These embryos are defective in generating contractile rings, ack(kt62) mutation abolishing reactions to organize cortical F-actin, while other mutations causing abortive contractile ring-like structures at ectopic sites. Defect of contractile ring formation in the affected embryos leads to the absence of microtubule arrays at the prospective cleavage plane. Thus, these mutations reveal the sequence of events associated with cytokinesis, in particular, the cortical actin dynamics. It is remarkable that in all acytokinetic embryos, daughter nuclei after mitosis are arranged in spatially normal positions, and maternal vasa mRNAs accumulate in the prospective planes of the first and second cell cleavages in the total absence of cytokinesis. This indicates that the basic cell architectures of early embryos are largely established by the autonomous activities of the mitotic apparatus, without much dependence on the cell cleavage machinery.
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Human Disease / Model
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