Doulazmi Mohamed, Capone Francesca, Frederic Florence, Bakouche Joëlle, Lemaigre-Dubreuil Yolande, Mariani Jean
Université Pierre et Marie Curie-Paris 6, Unité Mixte de Recherche, Neurobiologie des Processus Adaptatifs, Centre National de la Recherche Scientifique, Paris, France.
J Neurogenet. 2006 Jan-Jun;20(1-2):1-17. doi: 10.1080/01677060600685832.
The staggerer (sg) mutation is a spontaneous deletion in the Rora gene that prevents the translation of the ligand-binding domain (LBD), leading to the loss of RORalpha activity. The homozygous Rorasg/sg mutant mouse, whose most obvious phenotype is ataxia associated with cerebellar degeneration, also displays a variety of other phenotypes. The heterozygous Rora+/sg is able to develop a cerebellum that is qualitatively normal but which suffers a significant loss of cerebellar neuronal cells with advancing age. A truncated protein synthesized by the mutated allele may play a role both in Rorasg/sg and Rora+/sg. To determine the effects during life span of true haplo-insufficiency of the RORalpha protein, derived from the invalidation of the gene, we compared the evolution of Purkinje cell numbers in heterozygous Rora knock-out males (Rora+/-) and in their wild-type counterparts from 1 to 24 months of age. We also compared the evolution of Purkinje cell (PC) numbers in Rora+/- and Rora+/sg males from 1 to 9 months. The main finding is that in Rora+/- mice, for which only one-half the normal amount of protein is produced, the deficit was established as early as 1 month and did not change during the animals' adult lifespans. Thus, the effects of aging on PC number were apparent much earlier in Rora+/- than in Rora+/sg, although at 24 months of age the degrees of deficit were similar.
蹒跚者(sg)突变是Rora基因中的一个自发缺失,它阻止了配体结合域(LBD)的翻译,导致RORα活性丧失。纯合Rorasg/sg突变小鼠最明显的表型是与小脑变性相关的共济失调,它还表现出多种其他表型。杂合Rora+/sg能够发育出一个在质量上正常的小脑,但随着年龄的增长,小脑神经元细胞会大量减少。由突变等位基因合成的截短蛋白可能在Rorasg/sg和Rora+/sg中都起作用。为了确定由于基因无效导致的RORα蛋白真正单倍体不足在寿命期间的影响,我们比较了杂合Rora基因敲除雄性小鼠(Rora+/-)及其野生型对应小鼠从1到24个月大时浦肯野细胞数量的变化。我们还比较了Rora+/-和Rora+/sg雄性小鼠从1到9个月大时浦肯野细胞(PC)数量的变化。主要发现是,在Rora+/-小鼠中,其仅产生正常量一半的蛋白质,这种缺陷早在1个月时就已确立,并且在动物成年寿命期间没有变化。因此,衰老对PC数量的影响在Rora+/-小鼠中比在Rora+/sg小鼠中出现得更早,尽管在24个月大时缺陷程度相似。