Fendri-Kriaa Nourhene, Rouissi Aida, Ghorbel Rania, Mkaouar-Rebai Emna, Belguith Neila, Gouider-Khouja Naziha, Fakhfakh Faiza
Laboratoire de Génétique Moléculaire Humaine, Faculté de Médecine de Sfax, Université de Sfax, Tunisia.
J Child Neurol. 2012 May;27(5):564-8. doi: 10.1177/0883073811420496. Epub 2011 Sep 22.
Rett syndrome (RTT), an X-linked dominant neurodevelopmental disorder in females, is caused mainly by de novo mutations in the methyl-CpG-binding protein 2 gene (MECP2). Rett patients present an apparently normal psychomotor development during the first 6 to 18 months of life. Thereafter, they show a short period of developmental stagnation followed by a rapid regression in language and motor development. In the present study, we performed a mutational analysis of the MECP2 gene in 2 typical Rett syndrome patients and in 1 atypical Rett syndrome girl. The results showed the presence of 3 de novo point mutations in the C-terminal region: 2 novel mutations: c.1065C>A (p.S355R) and c.1030C>G (p.R344G) in the 2 typical Rett syndrome girls, but also the c.996C>T (p.S332S) mutation first described in the atypical Rett syndrome patient.
雷特综合征(RTT)是一种女性X连锁显性神经发育障碍,主要由甲基CpG结合蛋白2基因(MECP2)的新发突变引起。雷特综合征患者在生命的最初6至18个月表现出明显正常的精神运动发育。此后,他们会出现一段短暂的发育停滞期,随后语言和运动发育迅速倒退。在本研究中,我们对2例典型雷特综合征患者和1例非典型雷特综合征女孩的MECP2基因进行了突变分析。结果显示在C末端区域存在3个新发点突变:2个新突变,分别在2例典型雷特综合征女孩中发现的c.1065C>A(p.S355R)和c.1030C>G(p.R344G),但也有在非典型雷特综合征患者中首次描述的c.996C>T(p.S332S)突变。