PUBLICATION

Apoptosis in Zebrafish Embryos: Removing Cells from Inappropriate Locations

Authors
Rojo, C., and González, E.
ID
ZDB-PUB-080327-18
Date
2008
Source
Zebrafish   5(1): 25-37 (Journal)
Registered Authors
Keywords
none
MeSH Terms
  • Animals
  • Apoptosis*
  • Embryo, Nonmammalian/metabolism
  • Embryo, Nonmammalian/ultrastructure
  • Fetal Proteins
  • Gene Expression Regulation, Developmental
  • Heparan Sulfate Proteoglycans/genetics
  • Microscopy, Electron, Transmission
  • Morphogenesis
  • Mutation
  • T-Box Domain Proteins/genetics
  • Tail/embryology*
  • Tail/ultrastructure
  • Zebrafish/embryology*
  • Zebrafish/genetics
  • Zebrafish/metabolism
  • Zebrafish Proteins/genetics
PubMed
18361682 Full text @ Zebrafish
Abstract
The purpose of this study was to analyze by transmission electron microscopy the morphology and dynamics of the excess cells remaining in the truncated tail of the zebrafish compound mutant, knypek;no tail (kny;ntl). We mainly focused on two periods during tail extension: first, the stage when the primordia of both notochord and spinal cord should be already formed; second, the stage when morphogenesis of the tail is almost complete. Not only double mutants but also wild-type (wt) embryos were examined to compare with. A massive wave of morphologically normal apoptotic cellular death was detected by 22 h of development in the kny;ntl compound mutants. However, apoptosis was a rare event in the tail of wt embryos. We described the ultrastructural features and possible evolution of the apoptotic cells in the tail region, and also assayed the distribution of apoptotic cells in the different tissues conforming the tail: the covering epithelium or epidermis, the bulk of mesenchymal tissue, and the primordia of the spinal cord and the notochord. Huge amounts of apoptotic bodies were found in the mesenchymal tissue of the double-mutant embryos, just the location where excess cells are erroneously accumulated inside the truncated tail. This fact, together with striking findings regarding both some morphological aspects and the distribution of apoptosis, is discussed and suggested to be an indirect consequence of the genetic defects in kny;ntl mutants.
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