Didona Biagio, Codispoti Andrea, Bertini Enrico, Rizzo Wiliam B, Carney Gael, Zambruno Giovanna, Dionisi-Vici Carlo, Paradisi Mauro, Pedicelli Cristina, Melino Gerry, Terrinoni Alessandro
I Dermatology Division, IDI-IRCCS, Via Monti di Creta, 104, Rome, Italy.
Department of Experimental Medicine, IDI-IRCCS Biochemistry Laboratory, c/o University of Tor Vergata, Via Montpellier 1, 00133, Rome, Italy.
J Hum Genet. 2007;52(10):865-870. doi: 10.1007/s10038-007-0180-z.
Sjögren-Larsson syndrome (SLS; MIM#270200) is an autosomal recessive neurocutaneous disease caused by mutations in the ALDH3A2 gene for fatty aldehyde dehydrogenase (FALDH), a microsomal enzyme that catalyzes the oxidation of medium- and long- chain aliphatic aldehydes fatty acids. We studied two unrelated Italian SLS patients with ichthyosis, developmental delay, spastic diplegia and brain white matter disease. One patient was homozygous for a novel ALDH3A2 insertion mutation (c.767insA) in exon 5. The other SLS patient was a compound heterozygote for two previously reported mutations: a slice site mutation (c.1094C > T; S365L) in exon 7. Analysis of fibroblast RNA by RT-PCR indicated that the spice-site mutation caused skipping of exons 2 and 3. The c.1094C > T mutation, previously associated with two ALDH3A2 haplotypes, was found on a third distinct haplotype in our patient, which indicates that arose independently in this kindred. These results add to understanding of the genetic basis of SLS and will be useful for DNA diagnosis of this disease.
舍格伦-拉松综合征(SLS;医学遗传学国际疾病分类编号#270200)是一种常染色体隐性神经皮肤疾病,由脂肪酸醛脱氢酶(FALDH)的ALDH3A2基因突变引起,FALDH是一种微粒体酶,可催化中链和长链脂肪醛脂肪酸的氧化。我们研究了两名患有鱼鳞病、发育迟缓、痉挛性双侧瘫痪和脑白质病的意大利无关SLS患者。一名患者在第5外显子中存在一种新的ALDH3A2插入突变(c.767insA)的纯合子。另一名SLS患者是两个先前报道的突变的复合杂合子:第7外显子中的一个剪接位点突变(c.1094C>T;S365L)。通过逆转录聚合酶链反应(RT-PCR)对成纤维细胞RNA进行分析表明,该剪接位点突变导致第2和第3外显子缺失。先前与两种ALDH3A2单倍型相关的c.1094C>T突变,在我们的患者中发现于第三种不同的单倍型上,这表明它在这个家系中是独立出现的。这些结果有助于加深对SLS遗传基础的理解,并将对该疾病的DNA诊断有用。