The development of skeletal muscle requires progression of a highly ordered cascade of events comprising myogenic lineage commitment, myoblast proliferation, and terminal differentiation. The process of myogenesis is controlled by several myogenic transcription factors that act as terminal effectors of signaling cascades and produce appropriate developmental stage-specific transcripts. PHD finger protein 20 (PHF20) is a multidomain protein and subunit of a lysine acetyltransferase complex that acetylates histone H4 and p53, but its function is unclear. Notably, it has been reported that PHF20 knockout mice die shortly after birth and display a wide variety of phenotypes within the skeletal and hematopoietic systems. Therefore, the putative role of PHF20 in myogenic differentiation was further investigated. In the present study, we found that protein and mRNA expression levels of PHF20 were decreased during myogenic differentiation in C₂C₁₂ cells. At the same time, Yin Yang 1 (YY1) was also decreased during myogenic differentiation. PHF20 overexpression increased YY1 expression during myogenic differentiation, together with a delay in MyoD expression. PHF20 expression enhanced the transcriptional activity of YY1 while shRNA-mediated depletion of PHF20 resulted in the reduction of YY1 promoter activity in C₂C₁₂ cells. In addition, PHF20 directly bounds to the YY1 promoter in C₂C₁₂ cells. In a similar manner, YY1 expression was elevated while myosin heavy chain expression was decreased in PHF20 transgenic (TG) mice. Histological analysis revealed abnormalities in the shape and length of muscles in PHF20-TG mice. Furthermore, PHF20-TG muscles slowly regenerated after cardiotoxin injection, indicating that PHF20 affected muscle differentiation and regeneration after injury in vivo. Taken together, these results suggested that PHF20 plays an important role in myogenic differentiation by regulating YY1.

骨骼肌的发育需要高度有序的级联事件的进展，包括生肌谱系承诺、成肌细胞增殖和终末分化。肌生成过程由几个肌源性转录因子控制，这些转录因子充当信号级联的末端效应器并产生适当的发育阶段特异性转录物。PHD 指状蛋白 20 (PHF20) 是一种多结构域蛋白和赖氨酸乙酰转移酶复合物的亚基，可将组蛋白 H4 和 p53 乙酰化，但其功能尚不清楚。值得注意的是，据报道，PHF20 基因敲除小鼠在出生后不久就会死亡，并在骨骼和造血系统中显示出多种表型。因此，进一步研究了 PHF20 在肌原性分化中的假定作用。在目前的研究中，₂ C ₁₂细胞。同时，在生肌分化过程中，阴阳 1 (YY1) 也降低。PHF20 过表达增加了肌源性分化过程中 YY1 的表达，同时延迟了 MyoD 的表达。PHF20 表达增强了 YY1 的转录活性，而 shRNA 介导的 PHF20 消耗导致 C ₂ C ₁₂细胞中 YY1 启动子活性的降低。此外，PHF20 直接与 C ₂ C _{12 中}的 YY1 启动子结合细胞。以类似的方式，在 PHF20 转基因 (TG) 小鼠中，YY1 表达升高而肌球蛋白重链表达降低。组织学分析揭示了 PHF20-TG 小鼠肌肉形状和长度的异常。此外，PHF20-TG 肌肉在注射心脏毒素后缓慢再生，表明 PHF20 影响体内损伤后的肌肉分化和再生。总之，这些结果表明 PHF20 通过调节 YY1 在肌原性分化中发挥重要作用。