PUBLICATION

The Dynamics of Epidermal Stratification During Post-larval Development in Zebrafish

Authors
Rangel-Huerta, E., Guzman, A., Maldonado, E.
ID
ZDB-PUB-200904-10
Date
2020
Source
Developmental Dynamics : an official publication of the American Association of Anatomists   250(2): 175-190 (Journal)
Registered Authors
Maldonado, Ernesto
Keywords
Asymmetric cell division, Epidermal stratification, Progenitors, Stem cells, Zebrafish
MeSH Terms
  • Animals
  • Cell Differentiation
  • Epidermal Cells/cytology
  • Epidermis/growth & development*
  • Epidermis/metabolism
  • Phosphoproteins/metabolism
  • Trans-Activators/metabolism
  • Zebrafish/growth & development*
  • Zebrafish/metabolism
  • Zebrafish Proteins/metabolism
PubMed
32877571 Full text @ Dev. Dyn.
Abstract
The epidermis, as a defensive barrier, is a consistent trait throughout animal evolution. During post-larval development, the zebrafish epidermis thickens by stratification or addition of new cell layers. Epidermal basal stem cells, expressing the transcription factor p63, are known to be involved in this process. Zebrafish post-larval epidermal stratification is a tractable system to study how stem cells participate in organ growth.
We used immunohistochemistry, in combination with EdU cell proliferation detection, to study zebrafish epidermal stratification. For this procedure, we selected a window of post-larval stages (5 - 8 mm of standard length or SL, which normalizes age by size). Simultaneously, we used markers for asymmetric cell division and the Notch signaling pathway.
We found that epidermal stratification is the consequence of two events, changes in cell shape and active cell proliferation. We identified a subset of highly proliferative epidermal cells with reduced levels of p63, which differed from the basal stem cells with high levels of p63. Additionally, we described different mechanisms that participate in the stratification process, including the phosphorylation of p63, asymmetric cell division regulated by the Par3 and LGN proteins, and expression of Notch genes. This article is protected by copyright. All rights reserved.
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Human Disease / Model
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