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首页> 外文期刊>Molecular and Cellular Biology >Purα and Purβ Collaborate with Sp3 To Negatively Regulate β-Myosin Heavy Chain Gene Expression during Skeletal Muscle Inactivity
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Purα and Purβ Collaborate with Sp3 To Negatively Regulate β-Myosin Heavy Chain Gene Expression during Skeletal Muscle Inactivity

机译：Purα和Purβ与Sp3协同负向调节骨骼肌无活动时β-肌球蛋白重链基因的表达

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Adult skeletal muscle retains the capability of transcriptional reprogramming. This attribute is readily observable in the non-weight-bearing (NWB) soleus muscle, which undergoes a slow-to-fast fiber type transition concurrent with decreased β-myosin heavy chain (βMyHC) gene expression. Our previous work showed that Sp3 contributes to decreased βMyHC gene expression under NWB conditions. In this study, we demonstrate that physical and functional interactions between Sp3, Purα, and Purβ proteins mediate repression of βMyHC expression under NWB conditions. Binding of Purα or Purβ to the single-stranded βMyHC distal negative regulatory element-sense strand (dβNRE-S) element is markedly increased under NWB conditions. Ectopic expression of Purα and Purβ decreasedβ MyHC reporter gene expression, while mutation of the dβNRE-S element increased expression in C2C12 myotubes. The dβNRE-S element conferred Pur-dependent decreased expression on a minimal thymidine kinase promoter. Short interfering RNA sequences specific for Sp3 or for Purα and Purβ decreased endogenous Sp3 and Pur protein levels and increased βMyHC reporter gene expression in C2C12 myotubes. Immunoprecipitation assays revealed an association between endogenous Purα, Purβ, and Sp3, while chromatin immunoprecipitation assays demonstrated Purα, Purβ, and Sp3 binding to the βMyHC proximal promoter region harboring the dβNRE-S and C-rich elements in vivo. These data demonstrate that Pur proteins collaborate with Sp3 to regulate a transcriptional program that enables muscle cells to remodel their phenotype.
机译：成年骨骼肌保留转录重编程的能力。该属性在非负重比目鱼肌中很容易观察到，该比目鱼肌经历了从慢到快的纤维类型过渡，同时β-肌球蛋白重链（βMyHC）基因表达降低。我们以前的工作表明Sp3有助于在NWB条件下降低βMyHC基因的表达。在这项研究中，我们证明了在NWB条件下，Sp3，Purα和Purβ蛋白之间的物理和功能相互作用介导了βMyHC表达的抑制。 Purα或Purβ与单链β MyHC d istal n 阴性 r 调节性 e的结合在NWB条件下， -em链（dβNRE-S）元素明显增加。 Purα和Purβ的异位表达降低了βMyHC报告基因的表达，而dβNRE-S元件的突变增加了C2C12肌管的表达。 dβNRE-S元件在最小的胸苷激酶启动子上使Pur依赖性表达降低。特异于Sp3或Purα和Purβ的短干扰RNA序列可降低C2C12肌管中内源性Sp3和Pur蛋白的水平，并增加βMyHC报告基因的表达。免疫沉淀测定法揭示了内源性Purα，Purβ和Sp3之间的关联，而染色质免疫沉淀测定法则表明Purα，Purβ和Sp3与体内含有dβNRE-S和富含C元素的βMyHC近端启动子区域结合。这些数据表明，Pur蛋白与Sp3协同调节转录程序，使肌肉细胞能够重塑其表型。

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