Nakashima Mitsuko, Takano Kyoko, Osaka Hitoshi, Aida Noriko, Tsurusaki Yoshinori, Miyake Noriko, Saitsu Hirotomo, Matsumoto Naomichi
Department of Human Genetics, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
1] Division of Neurology, Kanagawa Children's Medical Center, Yokohama, Japan [2] Department of Medical Genetics, Shinshu University School of Medicine, Matsumoto, Japan.
J Hum Genet. 2014 Aug;59(8):471-4. doi: 10.1038/jhg.2014.51. Epub 2014 Jun 26.
We report on a 1-year-old boy with microcephaly with a simplified gyral pattern, early-onset seizures, congenital hearing loss and a severe developmental delay. Trio-based whole-exome sequencing identified candidate compound heterozygous mutations in two genes: c.163G>T (p.Ala55Ser) and c.874G>A (p.Gly292Arg) in polynucleotide kinase 3'-phosphatase gene (PNKP), and c.195G>A (p.Met65Ile) and c.1210A>C (p.Ser404Arg) in PCDH15. PNKP and PCDH15 mutations have been reported in autosomal recessive microcephaly with early-onset seizures and developmental delay syndrome, and Usher syndrome type 1F, respectively. Our patient showed neurological features similar to reported cases of both syndromes that could be explained by the observed mutations in both PNKP and PCDH15, which therefore appear to be pathogenic in this case.
我们报告了一名1岁男童,患有小头畸形,脑回模式简化,早发性癫痫,先天性听力损失和严重发育迟缓。基于三联体的全外显子组测序在两个基因中鉴定出候选复合杂合突变:多核苷酸激酶3'-磷酸酶基因(PNKP)中的c.163G>T(p.Ala55Ser)和c.874G>A(p.Gly292Arg),以及PCDH15中的c.195G>A(p.Met65Ile)和c.1210A>C(p.Ser404Arg)。PNKP和PCDH15突变分别在伴有早发性癫痫和发育迟缓综合征的常染色体隐性小头畸形以及1F型Usher综合征中被报道。我们的患者表现出与这两种综合征的报道病例相似的神经学特征,这可以通过在PNKP和PCDH15中观察到的突变来解释,因此在这种情况下这些突变似乎具有致病性。