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The AP-1 transcription factor JunB functions in Xenopus tail regeneration by positively regulating cell proliferation.

Authors
  • Nakamura, Makoto1
  • Yoshida, Hitoshi2
  • Takahashi, Eri1
  • Wlizla, Marcin2
  • Takebayashi-Suzuki, Kimiko1
  • Horb, Marko E2
  • Suzuki, Atsushi3
  • 1 Amphibian Research Center, Graduate School of Integrated Sciences for Life, Hiroshima University, 1-3-1 Kagamiyama, Higashi-Hiroshima, Hiroshima, 739-8526, Japan. , (Japan)
  • 2 National Xenopus Resource and Eugene Bell Center for Regenerative Biology and Tissue Engineering, Marine Biological Laboratory, Woods Hole, MA, 02543, United States. , (United States)
  • 3 Amphibian Research Center, Graduate School of Integrated Sciences for Life, Hiroshima University, 1-3-1 Kagamiyama, Higashi-Hiroshima, Hiroshima, 739-8526, Japan. Electronic address: [email protected] , (Japan)
Type
Published Article
Journal
Biochemical and Biophysical Research Communications
Publisher
Elsevier
Publication Date
Dec 04, 2019
Identifiers
DOI: 10.1016/j.bbrc.2019.11.060
PMID: 31812242
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Xenopus tropicalis tadpoles can regenerate an amputated tail, including spinal cord, muscle and notochord, through cell proliferation and differentiation. However, the molecular mechanisms that regulate cell proliferation during tail regeneration are largely unknown. Here we show that JunB plays an important role in tail regeneration by regulating cell proliferation. The expression of junb is rapidly activated and sustained during tail regeneration. Knockout (KO) of junb causes a delay in tail regeneration and tissue differentiation. In junb KO tadpoles, cell proliferation is prevented before tissue differentiation. Furthermore, TGF-β signaling, which is activated just after tail amputation, regulates the induction and maintenance of junb expression. These findings demonstrate that JunB, a downstream component of TGF-β signaling, works as a positive regulator of cell proliferation during Xenopus tail regeneration. Copyright © 2019 Elsevier Inc. All rights reserved.

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