[1] Howard Hughes Medical Institute, Department of Neurology, Beth Israel Deaconess Medical Center and Program in Neuroscience, Harvard Medical School, Boston, Massachusetts, USA. [2] These authors contributed equally to the work.
Nat Genet. 2010 Mar;42(3):245-9. doi: 10.1038/ng.526. Epub 2010 Jan 31.
Maintenance of DNA integrity is crucial for all cell types, but neurons are particularly sensitive to mutations in DNA repair genes, which lead to both abnormal development and neurodegeneration. We describe a previously unknown autosomal recessive disease characterized by microcephaly, early-onset, intractable seizures and developmental delay (denoted MCSZ). Using genome-wide linkage analysis in consanguineous families, we mapped the disease locus to chromosome 19q13.33 and identified multiple mutations in PNKP (polynucleotide kinase 3'-phosphatase) that result in severe neurological disease; in contrast, a splicing mutation is associated with more moderate symptoms. Unexpectedly, although the cells of individuals carrying this mutation are sensitive to radiation and other DNA-damaging agents, no such individual has yet developed cancer or immunodeficiency. Unlike other DNA repair defects that affect humans, PNKP mutations universally cause severe seizures. The neurological abnormalities in individuals with MCSZ may reflect a role for PNKP in several DNA repair pathways.
DNA 完整性的维持对所有细胞类型都至关重要,但神经元对 DNA 修复基因的突变特别敏感,这会导致发育异常和神经退行性变。我们描述了一种以前未知的常染色体隐性疾病,其特征为小头畸形、早发性、难治性癫痫发作和发育迟缓(表示为 MCSZ)。我们在近亲家庭中使用全基因组连锁分析,将疾病定位到 19q13.33 染色体上,并鉴定出 PNKP(多核苷酸激酶 3'-磷酸酶)中的多个突变,这些突变导致严重的神经疾病;相比之下,剪接突变与更中度的症状相关。出乎意料的是,尽管携带该突变的个体的细胞对辐射和其他 DNA 损伤剂敏感,但没有个体因此患上癌症或免疫缺陷。与影响人类的其他 DNA 修复缺陷不同,PNKP 突变普遍导致严重的癫痫发作。MCSZ 个体的神经异常可能反映了 PNKP 在几种 DNA 修复途径中的作用。