Edvardson Simon, Shaag Avraham, Kolesnikova Olga, Gomori John Moshe, Tarassov Ivan, Einbinder Tom, Saada Ann, Elpeleg Orly
Pediatric Neurology Unit, Hadassah-Hebrew University Medical Center, Jerusalem, 91120, Israel.
Am J Hum Genet. 2007 Oct;81(4):857-62. doi: 10.1086/521227. Epub 2007 Aug 24.
Homozygosity mapping was performed in a consanguineous Sephardic Jewish family with three patients who presented with severe infantile encephalopathy associated with pontocerebellar hypoplasia and multiple mitochondrial respiratory-chain defects. This resulted in the identification of an intronic mutation in RARS2, the gene encoding mitochondrial arginine-transfer RNA (tRNA) synthetase. The mutation was associated with the production of an abnormally short RARS2 transcript and a marked reduction of the mitochondrial tRNA(Arg) transcript in the patients' fibroblasts. We speculate that missplicing mutations in mitochondrial aminoacyl-tRNA synthethase genes preferentially affect the brain because of a tissue-specific vulnerability of the splicing machinery.
对一个近亲婚配的西班牙裔犹太家庭进行了纯合子定位分析,该家庭中有三名患者,表现为严重的婴儿期脑病,伴有脑桥小脑发育不全和多种线粒体呼吸链缺陷。这导致在RARS2基因中鉴定出一个内含子突变,该基因编码线粒体精氨酸转移RNA(tRNA)合成酶。该突变与患者成纤维细胞中异常短的RARS2转录本的产生以及线粒体tRNA(Arg)转录本的显著减少有关。我们推测,线粒体氨酰tRNA合成酶基因中的剪接突变优先影响大脑,这是由于剪接机制存在组织特异性易损性。