Norsworthy Michael W, Bei Fengfeng, Kawaguchi Riki, Wang Qing, Tran Nicholas M, Li Yi, Brommer Benedikt, Zhang Yiming, Wang Chen, Sanes Joshua R, Coppola Giovanni, He Zhigang
F.M. Kirby Neurobiology Center, Children's Hospital, and Department of Neurology, Harvard Medical School, 300 Longwood Avenue, Boston, MA 02115, USA; PhD Program in Biological and Biomedical Sciences, Harvard Medical School, Boston, MA 02115, USA.
F.M. Kirby Neurobiology Center, Children's Hospital, and Department of Neurology, Harvard Medical School, 300 Longwood Avenue, Boston, MA 02115, USA; Department of Neurosurgery, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Neuron. 2017 Jun 21;94(6):1112-1120.e4. doi: 10.1016/j.neuron.2017.05.035.
At least 30 types of retinal ganglion cells (RGCs) send distinct messages through the optic nerve to the brain. Available strategies of promoting axon regeneration act on only some of these types. Here we tested the hypothesis that overexpressing developmentally important transcription factors in adult RGCs could reprogram them to a "youthful" growth-competent state and promote regeneration of other types. From a screen of transcription factors, we identified Sox11 as one that could induce substantial axon regeneration. Transcriptome profiling indicated that Sox11 activates genes involved in cytoskeletal remodeling and axon growth. Remarkably, α-RGCs, which preferentially regenerate following treatments such as Pten deletion, were killed by Sox11 overexpression. Thus, Sox11 promotes regeneration of non-α-RGCs, which are refractory to Pten deletion-induced regeneration. We conclude that Sox11 can reprogram adult RGCs to a growth-competent state, suggesting that different growth-promoting interventions promote regeneration in distinct neuronal types.
至少30种视网膜神经节细胞(RGC)通过视神经向大脑发送不同的信息。现有的促进轴突再生的策略仅作用于其中一些类型的细胞。在此,我们测试了一个假设,即在成年RGC中过表达对发育重要的转录因子可以将它们重编程为具有“年轻”生长能力的状态,并促进其他类型细胞的再生。通过对转录因子的筛选,我们确定Sox11是一种能够诱导大量轴突再生的因子。转录组分析表明,Sox11激活参与细胞骨架重塑和轴突生长的基因。值得注意的是,在诸如PTEN缺失等处理后优先再生的α-RGC,会因Sox11的过表达而死亡。因此,Sox11促进非α-RGC的再生,而非α-RGC对PTEN缺失诱导的再生具有抗性。我们得出结论,Sox11可以将成年RGC重编程为具有生长能力的状态,这表明不同的促进生长的干预措施在不同的神经元类型中促进再生。