Department of Genetic and Metabolic Diseases, Hadassah-Hebrew University Medical Center, 9112001, Jerusalem, Israel.
Pediatric Intensive Unit, Department of Pediatrics, Mount Scopus Hadassah-Hebrew University Medical Center, Jerusalem, Israel.
Eur J Hum Genet. 2019 Sep;27(9):1419-1426. doi: 10.1038/s41431-019-0400-y. Epub 2019 Apr 11.
The ATP/GTP-Binding Protein 1 (AGTPBP1) gene (OMIM *606830) catalyzes deglutamylation of polyglutamylated proteins, and its deficiency manifests by cerebellar ataxia and peripheral neuropathy in mice and lower motor neuron-like disease in sheep. In the mutant mice, cerebellar atrophy due to Purkinje cell degeneration is observed, likely due to increased tubulin polyglutamylation in affected brain areas. We report two unrelated individuals who presented with early onset cerebellar atrophy, developmental arrest with progressive muscle weakness, and feeding and respiratory difficulties, accompanied by severe motor neuronopathy. Whole exome sequencing followed by segregation analysis in the families and cDNA studies revealed deleterious biallelic variants in the AGTPBP1 gene. We conclude that complete loss-of-function of AGTPBP1 in humans, just like in mice and sheep, is associated with cerebellar and motor neuron disease, reminiscent of Pontocerebellar Hypoplasia Type 1 (PCH1).
ATP/GTP-结合蛋白 1(AGTPBP1)基因(OMIM *606830)催化多聚谷氨酰胺化蛋白的脱谷氨酰化,其缺陷在小鼠中表现为小脑性共济失调和周围神经病,在绵羊中表现为下运动神经元样疾病。在突变小鼠中,观察到由于浦肯野细胞退化引起的小脑萎缩,这可能是由于受影响脑区的微管蛋白多聚谷氨酰化增加所致。我们报告了两名无关联的个体,他们表现为小脑萎缩、发育停滞伴进行性肌无力、进食和呼吸困难,伴有严重的运动神经元病。对两个家系进行全外显子组测序,然后进行遗传分析,以及 cDNA 研究,结果显示 AGTPBP1 基因存在有害的纯合双等位基因突变。我们得出结论,AGTPBP1 在人类中的完全功能丧失,就像在小鼠和绵羊中一样,与小脑和运动神经元疾病相关,使人联想到桥脑小脑发育不良 1 型(PCH1)。