Norton Christine R, Chen Ying, Han Xiang Hua, Bradley Cara K, Krebs Luke T, Yoon Jeong Kyo, Gridley Thomas
Center for Molecular Medicine, Maine Medical Center Research Institute, Scarborough, Maine, USA.
PLoS Curr. 2013 Nov 8;5:ecurrents.md.e495b27ee347fd3870a8316d4786fc17. doi: 10.1371/currents.md.e495b27ee347fd3870a8316d4786fc17.
The Snail gene family encodes DNA-binding zinc finger proteins that function as transcriptional repressors. While the Snai1 and Snai2 genes are required for normal development in mice, Snai3 mutant mice exhibit no obvious abnormalities. The Snai3 gene is expressed at high levels in skeletal muscle. However, we demonstrate by histological analysis that Snai3 null mutant mice exhibit normal skeletal muscle. During hindlimb muscle regeneration after cardiotoxin-mediated injury, the Snai3 null mice exhibited efficient regeneration. To determine whether the Snai3 gene functions redundantly with the Snai1 gene during skeletal muscle regeneration, we performed hindlimb muscle regeneration in mice with skeletal muscle-specific deletion of the Snai1 gene on a Snai3 null genetic background. These mice also exhibited efficient regeneration, demonstrating that there is no major role for the Snai1 and Snai3 genes in regulating skeletal muscle regeneration in mice.
蜗牛基因家族编码作为转录抑制因子发挥作用的DNA结合锌指蛋白。虽然Snai1和Snai2基因是小鼠正常发育所必需的，但Snai3突变小鼠未表现出明显异常。Snai3基因在骨骼肌中高水平表达。然而，我们通过组织学分析表明，Snai3基因敲除突变小鼠的骨骼肌正常。在心脏毒素介导的损伤后后肢肌肉再生过程中，Snai3基因敲除小鼠表现出高效的再生能力。为了确定在骨骼肌再生过程中Snai3基因是否与Snai1基因功能冗余，我们在Snai3基因敲除的遗传背景下，对骨骼肌特异性缺失Snai1基因的小鼠进行了后肢肌肉再生实验。这些小鼠也表现出高效的再生能力，表明Snai1和Snai3基因在调节小鼠骨骼肌再生中没有主要作用。
