Fas-associated protein with death domain regulates notch signaling during muscle regeneration

Rong Zhang, Lu Wang, Liangqiang He, Bingya Yang, Chun Yao, Pan Du, Qiang Xu, Wei Cheng*, Zi Chun Hua

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

6 Scopus citations

Abstract

Notch signaling plays critical roles during myogenesis by promoting the proliferation and inhibiting the differentiation of myogenic progenitors. However, the mechanism of the temporal regulation of Notch signaling during the myogenic lineage progression remains elusive. In the present study, we show that a constitutively phosphoryl-mimicking mutation of Fas-associated death domain (FADD-D) enhances Notch-1 signaling and compromises Wnt signaling in both cultured myoblasts and regenerating muscles, which results in inhibited myogenic differentiation and muscle regeneration. Inhibition of Notch signaling recovers the regeneration ability in injured FADD-D muscles through rescuing Wnt signaling. Furthermore, we found that protein kinase Cα mediates FADD-D-induced Notch-1 signaling by stabilizing Notch-1. Collectively, these data identify a novel mechanism for the temporal regulation of Notch signaling during myogenic lineage progression and muscle regeneration.

Original languageEnglish (US)
Pages (from-to)253-264
Number of pages12
JournalCells Tissues Organs
Volume200
DOIs
StatePublished - Sep 24 2015

Keywords

  • Fas-associated death domain
  • Mouse
  • Muscle regeneration
  • Notch
  • Protein kinase C
  • Wnt

ASJC Scopus subject areas

  • Anatomy
  • Histology

Fingerprint

Dive into the research topics of 'Fas-associated protein with death domain regulates notch signaling during muscle regeneration'. Together they form a unique fingerprint.

Cite this