Service de Neurologie, Centre Hospitalier Universitaire du Point "G", Bamako, Mali; Neurogenetics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland.
Hum Mutat. 2013 Oct;34(10):1357-60. doi: 10.1002/humu.22378. Epub 2013 Aug 12.
We report here the genetic basis for a form of progressive hereditary spastic paraplegia (SPG43) previously described in two Malian sisters. Exome sequencing revealed a homozygous missense variant (c.187G>C; p.Ala63Pro) in C19orf12, a gene recently implicated in neurodegeneration with brain iron accumulation (NBIA). The same mutation was subsequently also found in a Brazilian family with features of NBIA, and we identified another NBIA patient with a three-nucleotide deletion (c.197_199del; p.Gly66del). Haplotype analysis revealed that the p.Ala63Pro mutations have a common origin, but MRI scans showed no brain iron deposition in the Malian SPG43 subjects. Heterologous expression of these SPG43 and NBIA variants resulted in similar alterations in the subcellular distribution of C19orf12. The SPG43 and NBIA variants reported here as well as the most common C19orf12 missense mutation reported in NBIA patients are found within a highly conserved, extended hydrophobic domain in C19orf12, underscoring the functional importance of this domain.
我们在此报告先前在两位马里姐妹中描述的一种进行性遗传性痉挛性截瘫(SPG43)的遗传基础。外显子组测序显示,C19orf12 中的纯合错义变异(c.187G>C;p.Ala63Pro),该基因最近与伴有脑铁蓄积的神经退行性疾病(NBIA)有关。随后在一个具有 NBIA 特征的巴西家族中也发现了相同的突变,我们还鉴定了另一位具有三个核苷酸缺失(c.197_199del;p.Gly66del)的 NBIA 患者。单倍型分析显示,p.Ala63Pro 突变具有共同的起源,但 MRI 扫描显示马里 SPG43 受试者没有脑铁沉积。这些 SPG43 和 NBIA 变体的异源表达导致 C19orf12 的亚细胞分布发生类似改变。在此报道的 SPG43 和 NBIA 变体以及在 NBIA 患者中报道的最常见的 C19orf12 错义突变位于 C19orf12 中高度保守的扩展疏水区内,突出了该区域的重要功能。