RP2 and RPGR mutations and clinical correlations in patients with X-linked retinitis pigmentosa

被引:188
作者
Sharon, D
Sandberg, MA
Rabe, VW
Stillberger, M
Dryja, TP
Berson, EL
机构
[1] Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Berman Gund Lab Study Retinal Degenerat, Boston, MA 02114 USA
[2] Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Ocular Mol Genet Inst, Boston, MA 02114 USA
关键词
D O I
10.1086/379379
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
We determined the mutation spectrum of the RP2 and RPGR genes in patients with X-linked retinitis pigmentosa (XLRP) and searched for correlations between categories of mutation and severity of disease. We screened 187 unrelated male patients for mutations, including 135 with a prior clinical diagnosis of XLRP, 11 with probable XLRP, 30 isolate cases suspected of having XLRP, and 11 with cone-rod degeneration. Mutation screening was performed by single-strand conformation analysis and by sequencing of all RP2 exons and RPGR exons 1-14, ORF15, and 15a. The refractive error, visual acuity, final dark-adapted threshold, visual field area, and 30-Hz cone electroretinogram (ERG) amplitude were measured in each patient. Among the 187 patients, we found 10 mutations in RP2, 2 of which are novel, and 80 mutations in RPGR, 41 of which are novel; 66% of the RPGR mutations were within ORF15. Among the 135 with a prior clinical diagnosis of XLRP, mutations in the RP2 and RPGR genes were found in 9 of 135 (6.7%) and 98 of 135 (72.6%), respectively, for a total of 79% of patients. Patients with RP2 mutations had, on average, lower visual acuity but similar visual field area, final dark-adapted threshold, and 30-Hz ERG amplitude compared with those with RPGR mutations. Among patients with RPGR mutations, those with ORF15 mutations had, on average, a significantly larger visual field area and a borderline larger ERG amplitude than did patients with RPGR mutations in exons 1-14. Among patients with ORF15 mutations, regression analyses showed that the final dark-adapted threshold became lower (i.e., closer to normal) and that the 30-Hz ERG amplitude increased as the length of the wild-type ORF15 amino acid sequence increased. Furthermore, as the length of the abnormal amino acid sequence following ORF15 frameshift mutations increased, the severity of disease increased.
引用
收藏
页码:1131 / 1146
页数:16
相关论文
共 39 条
[31]   Mutational hot spot within a new RPGR exon in X-linked retinitis pigmentosa [J].
Vervoort, R ;
Lennon, A ;
Bird, AC ;
Tulloch, B ;
Axton, R ;
Miano, MG ;
Meindl, A ;
Meitinger, T ;
Ciccodicola, A ;
Wright, AF .
NATURE GENETICS, 2000, 25 (04) :462-466
[32]   Mutations of RPGR in X-linked retinitis pigmentosa (RP3) [J].
Vervoort, R ;
Wright, AF .
HUMAN MUTATION, 2002, 19 (05) :486-500
[33]   Values of electroretinogram responses according to axial length [J].
Westall C.A. ;
Dhaliwal H.S. ;
Panton C.M. ;
Sigesmund D. ;
Levin A.V. ;
Nischal K.K. ;
Héon E. .
Documenta Ophthalmologica, 2001, 102 (2) :115-130
[34]   Mutations in the RPGR gene cause X-linked cone dystrophy [J].
Yang, ZL ;
Peachey, NS ;
Moshfeghi, DM ;
Thirumalaichary, S ;
Chorich, L ;
Shugart, YY ;
Fan, K ;
Zhang, K .
HUMAN MOLECULAR GENETICS, 2002, 11 (05) :605-611
[35]   X-linked cone-rod dystrophy (locus COD1):: Identification of mutations in RPGR exon ORF15 [J].
Yesim, F ;
Demirci, K ;
Rigatti, BW ;
Wen, GP ;
Radak, AL ;
Mah, TS ;
Baic, CL ;
Traboulsi, EI ;
Alitalo, T ;
Ramser, J ;
Gorin, MB .
AMERICAN JOURNAL OF HUMAN GENETICS, 2002, 70 (04) :1049-1053
[36]   Different RPGR exon ORF15 mutations in Canids provide insights into photoreceptor cell degeneration [J].
Zhang, Q ;
Acland, GM ;
Wu, WX ;
Johnson, JL ;
Pearce-Kelling, S ;
Tulloch, B ;
Vervoort, R ;
Wright, AF ;
Aguirre, GD .
HUMAN MOLECULAR GENETICS, 2002, 11 (09) :993-1003
[37]   Identification of novel RPGR (retinitis pigmentosa GTPase regulator) mutations in a subset of X-linked retinitis pigmentosa families segregating with the RP3 locus [J].
Zito, I ;
Thiselton, DL ;
Gorin, MB ;
Stout, JT ;
Plant, C ;
Bird, AC ;
Bhattacharya, SS ;
Hardcastle, AJ .
HUMAN GENETICS, 1999, 105 (1-2) :57-62
[38]  
Zito I, 2000, HUM MUTAT, V16, DOI 10.1002/1098-1004(200009)16:3<273::AID-HUMU19>3.0.CO
[39]  
2-W