Schnur R E, Gao M, Wick P A, Keller M, Benke P J, Edwards M J, Grix A W, Hockey A, Jung J H, Kidd K K, Kistenmacher M, Levin A V, Lewis R A, Musarella M A, Nowakowski R W, Orlow S J, Pagon R S, Pillers D A, Punnett H H, Quinn G E, Tezcan K, Wagstaff J, Weleber R G
Division of Genetics, Children's Regional Hospital, Camden, NJ 08103, USA.
Am J Hum Genet. 1998 Apr;62(4):800-9. doi: 10.1086/301776.
X-linked ocular albinism (OA1), Nettleship-Falls type, is characterized by decreased ocular pigmentation, foveal hypoplasia, nystagmus, photodysphoria, and reduced visual acuity. Affected males usually demonstrate melanin macroglobules on skin biopsy. We now report results of deletion and mutation screening of the full-length OA1 gene in 29 unrelated North American and Australian X-linked ocular albinism (OA) probands, including five with additional, nonocular phenotypic abnormalities (Schnur et al. 1994). We detected 13 intragenic gene deletions, including 3 of exon 1, 2 of exon 2, 2 of exon 4, and 6 others, which span exons 2-8. Eight new missense mutations were identified, which cluster within exons 1, 2, 3, and 6 in conserved and/or putative transmembrane domains of the protein. There was also a splice acceptor-site mutation, a nonsense mutation, a single base deletion, and a previously reported 17-bp exon 1 deletion. All patients with nonocular phenotypic abnormalities had detectable mutations. In summary, 26 (approximately 90%) of 29 probands had detectable alterations of OA1, thus confirming that OA1 is the major locus for X-linked OA.
X连锁眼白化病(OA1),内特尔希普-福尔斯型,其特征为眼部色素沉着减少、黄斑发育不全、眼球震颤、畏光和视力下降。受影响的男性在皮肤活检时通常会显示黑色素大球。我们现在报告对29名北美和澳大利亚无关的X连锁眼白化病(OA)先证者进行全长OA1基因缺失和突变筛查的结果,其中包括5名伴有其他非眼部表型异常的患者(施努尔等人,1994年)。我们检测到13个基因内缺失,包括外显子1的3个、外显子2的2个、外显子4的2个以及其他6个,这些缺失跨越外显子2至8。鉴定出8个新的错义突变,它们聚集在外显子1、2、3和6中该蛋白的保守和/或假定跨膜结构域内。还存在一个剪接受体位点突变、一个无义突变、一个单碱基缺失以及一个先前报道的17碱基对外显子1缺失。所有伴有非眼部表型异常的患者都有可检测到的突变。总之,29名先证者中有26名(约90%)有可检测到的OA1改变,从而证实OA1是X连锁OA的主要基因座。