Department of Biology, University of Rome Tor Vergata, Rome, Italy.
Department of Biology, University of Bari, Bari, Italy.
Oxid Med Cell Longev. 2018 May 7;2018:7640272. doi: 10.1155/2018/7640272. eCollection 2018.
The presence of tetraplex structures in the promoter region of the myogenic differentiation 1 gene (MyoD1) was investigated with a specific tetraplex-binding porphyrin (TMPyP4), to test its influence on the expression of MyoD1 itself and downstream-regulated genes during myogenic differentiation. TMPyP4-exposed C2C12 myoblasts, blocking MyoD1 transcription, proliferated reaching confluence and fused forming elongated structures, resembling myotubes, devoid of myosin heavy chain 3 (MHC) expression. Besides lack of MHC, upon MyoD1 inhibition, other myogenic gene expressions were also affected in treated cells, while untreated control cell culture showed normal myotube formation expressing MyoD1, Myog, MRF4, Myf5, and MHC. Unexpectedly, the myomaker (Mymk) gene expression was not affected upon TMPyP4 exposure during C2C12 myogenic differentiation. At the genomic level, the bioinformatic comparison of putative tetraplex sites found that three tetraplexes in MyoD1 and Myog are highly conserved in mammals, while Mymk and MHC did not show any conserved tetraplexes in the analysed regions. Thus, here, we report for the first time that the inhibition of the MyoD1 promoter function, stabilizing the tetraplex region, affects downstream myogenic genes by blocking their expression, while leaving the expression of Mymk unaltered. These results reveal the existence of two distinct pathways: one leading to cell fusion and one guaranteeing correct myotube differentiation.
研究了肌生成分化 1 基因(MyoD1)启动子区域中四链体结构的存在情况,使用特定的四链体结合卟啉(TMPyP4)来测试其对肌生成分化过程中 MyoD1 自身及其下游调节基因表达的影响。TMPyP4 暴露的 C2C12 成肌细胞阻断了 MyoD1 的转录,细胞增殖达到汇合并融合形成伸长结构,类似于缺乏肌球蛋白重链 3(MHC)表达的肌管。除了缺乏 MHC 之外,在 MyoD1 抑制后,处理细胞中的其他肌生成基因表达也受到影响,而未经处理的对照细胞培养则显示出正常的肌管形成,表达 MyoD1、Myog、MRF4、Myf5 和 MHC。出乎意料的是,在 C2C12 成肌分化过程中,TMPyP4 暴露并不会影响肌生成因子(Mymk)基因的表达。在基因组水平上,对假定四链体位点的生物信息学比较发现,MyoD1 和 Myog 中的三个四链体在哺乳动物中高度保守,而 Mymk 和 MHC 在分析区域中没有显示任何保守的四链体。因此,我们首次报道了 MyoD1 启动子功能的抑制,通过稳定四链体区域,影响下游肌生成基因的表达,同时使 Mymk 的表达保持不变。这些结果揭示了存在两种不同的途径:一种途径导致细胞融合,另一种途径保证正确的肌管分化。