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<p>This study aims to investigate the role and molecular mechanism of the circular RNA circDCAF6, which is specifically highly expressed in the muscle tissue of Qinchuan cattle, during myoblast differentiation. Through cell experiments, it was found that the expression level of circDCAF6 first increased and then decreased during myoblast differentiation. Overexpression of circDCAF6 significantly promoted myotube formation and the expression of myogenic differentiation marker genes, while knockdown of circDCAF6 inhibited differentiation. RNA pull-down and mass spectrometry analysis identified ACTC1 as an interacting protein of circDCAF6. circDCAF6 promotes myogenic differentiation by inhibiting the ubiquitination modification of ACTC1, thereby maintaining its stability. Further research revealed that the ubiquitin ligase TRIM28 is a target protein of ACTC1 and participates in the regulation of ACTC1 ubiquitination by circDCAF6. This study elucidates the regulatory mechanism of the “circDCAF6-ACTC1-TRIM28” signaling axis in myogenic differentiation, provides new insights into the role of circRNA in muscle development regulation, Provide new insights into the regulation of muscle development and offer potential clues for future breeding research.</p>

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CircDCAF6 promotes myoblast differentiation by inhibiting the ubiquitination of ACTC1

  • 期刊论文

  • 发表日期：

    2026年2月17日

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  • Liang Chengcheng,
  • Yu Shengchen,
  • Hina Sultana,
  • Zhao Chunping,
  • Cheng Gong,
  • Sameerh Alsahafi,
  • Safa H. Qahl,
  • Fatimah A. Alqahtani,
  • Dalal Alenizi,
  • Dalal Alardan,
  • Linsen Zan

摘要

This study aims to investigate the role and molecular mechanism of the circular RNA circDCAF6, which is specifically highly expressed in the muscle tissue of Qinchuan cattle, during myoblast differentiation. Through cell experiments, it was found that the expression level of circDCAF6 first increased and then decreased during myoblast differentiation. Overexpression of circDCAF6 significantly promoted myotube formation and the expression of myogenic differentiation marker genes, while knockdown of circDCAF6 inhibited differentiation. RNA pull-down and mass spectrometry analysis identified ACTC1 as an interacting protein of circDCAF6. circDCAF6 promotes myogenic differentiation by inhibiting the ubiquitination modification of ACTC1, thereby maintaining its stability. Further research revealed that the ubiquitin ligase TRIM28 is a target protein of ACTC1 and participates in the regulation of ACTC1 ubiquitination by circDCAF6. This study elucidates the regulatory mechanism of the “circDCAF6-ACTC1-TRIM28” signaling axis in myogenic differentiation, provides new insights into the role of circRNA in muscle development regulation, Provide new insights into the regulation of muscle development and offer potential clues for future breeding research.