Gene Expression and Muscular Dystrophy Unit, Division of Genetics and Cell Biology, IRCCS San Raffaele Scientific Institute, 20132 Milan, Italy.
Gene Expression and Muscular Dystrophy Unit, Division of Genetics and Cell Biology, IRCCS San Raffaele Scientific Institute, 20132 Milan, Italy; Center for Genomic Science of IIT@SEMM, Fondazione Istituto Italiano di Tecnologia, Milan, Italy.
Cell Rep. 2023 Sep 26;42(9):113120. doi: 10.1016/j.celrep.2023.113120. Epub 2023 Sep 12.
Facioscapulohumeral muscular dystrophy (FSHD) is one of the most common neuromuscular disorders and has no cure. Due to an unknown molecular mechanism, FSHD displays overlapping manifestations with the neurodegenerative disease amyotrophic lateral sclerosis (ALS). FSHD is caused by aberrant gain of expression of the transcription factor double homeobox 4 (DUX4), which triggers a pro-apoptotic transcriptional program resulting in inhibition of myogenic differentiation and muscle wasting. Regulation of DUX4 activity is poorly known. We identify Matrin 3 (MATR3), whose mutation causes ALS and dominant distal myopathy, as a cellular factor controlling DUX4 expression and activity. MATR3 binds to the DUX4 DNA-binding domain and blocks DUX4-mediated gene expression, rescuing cell viability and myogenic differentiation of FSHD muscle cells, without affecting healthy muscle cells. Finally, we characterize a shorter MATR3 fragment that is necessary and sufficient to directly block DUX4-induced toxicity to the same extent as the full-length protein. Collectively, our data suggest MATR3 as a candidate for developing a treatment for FSHD.
面肩肱型肌营养不良症(FSHD)是最常见的神经肌肉疾病之一,目前尚无治愈方法。由于未知的分子机制,FSHD 与神经退行性疾病肌萎缩侧索硬化症(ALS)表现出重叠的症状。FSHD 是由转录因子双同源盒 4(DUX4)的异常表达引起的,这触发了促凋亡的转录程序,导致肌肉生成分化抑制和肌肉消耗。DUX4 活性的调节知之甚少。我们确定了 Matrin 3(MATR3),其突变会导致 ALS 和显性远端肌病,是一种控制 DUX4 表达和活性的细胞因子。MATR3 与 DUX4 的 DNA 结合域结合并阻断 DUX4 介导的基因表达,从而挽救 FSHD 肌肉细胞的细胞活力和肌生成分化,而不影响健康的肌肉细胞。最后,我们鉴定了一个较短的 MATR3 片段,该片段对于直接阻断 DUX4 诱导的毒性是必需和充分的,与全长蛋白的效果相同。总的来说,我们的数据表明 MATR3 是开发 FSHD 治疗方法的候选者。