LncRNA-FKBP1C regulates muscle fiber type switching by affecting the stability of MYH1B.
Jia-Ao YuZhijun WangXin YangManting MaZhenhui LiQinghua NiePublished in: Cell death discovery (2021)
Long non-coding RNAs (lncRNAs) are well-known to participate in a variety of important regulatory processes in myogenesis. In our previous RNA-seq study (accession number GSE58755), we found that lncRNA-FKBP1C was differentially expressed between White Recessive Rock (WRR) and Xinghua (XH) chicken. Here, we have further demonstrated that lncRNA-FKBP1C interacted directly with MYH1B by biotinylated RNA pull-down assay and RNA immunoprecipitation (RIP). Protein stability and degradation experiments identified that lncRNA-FKBP1C enhanced the protein stability of MYH1B. Overexpression of lncRNA-FKBP1C inhibited myoblasts proliferation, promoted myoblasts differentiation, and participated in the formation of skeletal muscle fibers. LncRNA-FKBP1C could downregulate the fast muscle genes and upregulate slow muscle genes. Conversely, its interference promoted cell proliferation, repressed cell differentiation, and drove the transformation of slow-twitch muscle fibers to fast-twitch muscle fibers. Similar results were observed after knockdown of the MYH1B gene, but the difference was that the MYH1B gene had no effects on fast muscle fibers. In short, these data demonstrate that lncRNA-FKBP1C could bound with MYH1B and enhance its protein stability, thus affecting proliferation, differentiation of myoblasts and conversion of skeletal muscle fiber types.
Keyphrases
- skeletal muscle
- long non coding rna
- hypertrophic cardiomyopathy
- cell proliferation
- rna seq
- insulin resistance
- long noncoding rna
- genome wide
- poor prognosis
- genome wide identification
- signaling pathway
- single cell
- transcription factor
- copy number
- amino acid
- binding protein
- type diabetes
- metabolic syndrome
- cell cycle
- gene expression
- dna methylation
- high throughput
- machine learning
- small molecule
- atrial fibrillation