A Cdh1-FoxM1-Apc axis controls muscle development and regeneration.

Cell Death & Disease
Zhe ChenYu Hou

Abstract

Forkhead box M1 (FoxM1) transcriptional factor has a principal role in regulating cell proliferation, self-renewal, and tumorigenesis. However, whether FoxM1 regulates endogenous muscle development and regeneration remains unclear. Here we found that loss of FoxM1 in muscle satellite cells (SCs) resulted in muscle atrophy and defective muscle regeneration. FoxM1 functioned as a direct transcription activator of adenomatous polyposis coli (Apc), preventing hyperactivation of wnt/β-catenin signaling during muscle regeneration. FoxM1 overexpression in SCs promoted myogenesis but impaired muscle regeneration as a result of spontaneous activation and exhaustion of SCs by transcriptional regulation of Cyclin B1 (Ccnb1). The E3 ubiquitin ligase Cdh1 (also termed Fzr1) was required for FoxM1 ubiquitylation and subsequent degradation. Loss of Cdh1 promoted quiescent SCs to enter into the cell cycle and the SC pool was depleted by serial muscle injuries. Haploinsufficiency of FoxM1 ameliorated muscle regeneration of Cdh1 knock-out mice. These data demonstrate that the Cdh1-FoxM1-Apc axis functions as a key regulator of muscle development and regeneration.

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Citations

Dec 18, 2020·Laboratory Investigation; a Journal of Technical Methods and Pathology·Wenjie LaiXingqiao Wen

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Datasets Mentioned

BETA
135486

Methods Mentioned

BETA
flow cytometry
immunoprecipitation
co-immunoprecipitation
nuclear translocation
transgenic
genotyping
fluorescence-activated cell sorter
confocal microscopy
PCR
transfection

Software Mentioned

AxioVision
DESeq2
Cufflinks

Related Concepts

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