Apfelstedt-Sylla E, Kunisch M, Horn M, Rüther K, Gerding H, Gal A, Zrenner E
Department of Pathophysiology of Vision and Neuroophthalmology, University Eye Hospital, Tübingen, Germany.
Br J Ophthalmol. 1993 Aug;77(8):495-501. doi: 10.1136/bjo.77.8.495.
A family is described in which an 8 base pair deletion (nucleotides 5252-5259, codons 341-343) of the rhodopsin gene cosegregates with autosomal dominant retinitis pigmentosa (adRP). The deletion results in a shift in the reading frame, causing a rhodopsin molecule extended by one residue and substantially altered at the carboxyl terminus. Phenotypic expression is relatively mild. In affected members, night blindness did not occur before the age of 16, and late onset of visual field loss was consistently reported. Even older individuals (59 and 76 years) had preserved central islands in the visual field; a younger female patient had normal visual fields until the age of 34. ERG and psychophysical tests showed well preserved cone function at stages of virtually abolished rod function. Phenotypic differences and similarities between this form of adRP and others associated with mutations at the carboxyl terminus of the rhodopsin molecule are discussed. The cause of RP by mutations in this region remains to be clarified.
本文描述了一个家系,其中视紫红质基因的一个8碱基对缺失(核苷酸5252 - 5259,密码子341 - 343)与常染色体显性视网膜色素变性(adRP)共分离。该缺失导致阅读框移位,使得视紫红质分子延长了一个残基,并在羧基末端发生了显著改变。表型表达相对较轻。在受影响的成员中,16岁之前未出现夜盲症,且一致报告有视野丧失的迟发性。甚至年龄较大的个体(59岁和76岁)视野中仍保留中心岛;一名年轻女性患者在34岁之前视野正常。视网膜电图(ERG)和心理物理学测试显示,在视杆功能几乎完全丧失的阶段,视锥功能仍保存良好。本文讨论了这种形式的adRP与视紫红质分子羧基末端突变相关的其他形式之间的表型差异和相似性。该区域突变导致视网膜色素变性的原因仍有待阐明。