Gondré M, Burrola P, Weinstein D E
The Department of Neuroscience and the Department of Pathology, The Albert Einstein College of Medicine, Bronx, New York 10461, USA.
J Cell Biol. 1998 Apr 20;141(2):493-501. doi: 10.1083/jcb.141.2.493.
After injury, the peripheral nervous system (PNS) is capable of full regeneration and recovery of function. Many molecular events that are the hallmarks of the regenerating PNS are recapitulations of developmental processes. The expression of one such molecule, the POU transcription factor suppressed cAMP-inducible POU protein (SCIP), is required for the establishment of normal nerves and is reexpressed during regeneration. Here we describe markedly accelerated regeneration and hypertrophy of both myelin and axons in transgenic mice that express an amino-terminal deletion of the SCIP molecule. This mutant SCIP molecule retains the POU-specific and POU homeodomain moieties, which allow for both DNA binding and some protein-protein interaction. We demonstrate that the transgene indirectly effects dramatic axonal changes. This is the first demonstration of a genetically controlled acceleration of neural regeneration.
损伤后,外周神经系统(PNS)能够实现完全再生并恢复功能。许多作为再生性PNS标志的分子事件都是发育过程的重演。一种这样的分子,即POU转录因子抑制的cAMP诱导型POU蛋白(SCIP)的表达,是正常神经建立所必需的,并且在再生过程中会重新表达。在此我们描述了在表达SCIP分子氨基末端缺失的转基因小鼠中,髓鞘和轴突的再生和肥大均明显加速。这种突变的SCIP分子保留了POU特异性和POU同源结构域部分,这使得它既能与DNA结合,又能进行一些蛋白质-蛋白质相互作用。我们证明转基因间接影响了显著的轴突变化。这是首次证明通过基因控制加速神经再生。