May 2005
Volume 46, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2005
Large–Scale Sequencing of the Optineurin Gene in Familial and Sporadic Cases With Primary Open–Angle Glaucoma
Author Affiliations & Notes
  • T. Rezaie
    Molecular Ophthalmic Genetics Laboratory, University of Connecticut Health Center, Farmington, CT
  • A. Child
    Department of Cardiological Sciences, St. Georges Medical School, London, United Kingdom
  • S. Popinchalk
    Molecular Ophthalmic Genetics Laboratory, University of Connecticut Health Center, Farmington, CT
  • T. Krupin
    University Eye Specialists, Chicago, IL
  • R. Ritch
    New York Eye and Ear Infirmary, New York, NY
  • J. Liebmann
    New York Eye and Ear Infirmary, New York, NY
  • E. Ilitchev
    New York Eye and Ear Infirmary, New York, NY
  • R. Crick
    International Glaucoma Association, London, United Kingdom
  • M. Sarfarazi
    Molecular Ophthalmic Genetics Laboratory, University of Connecticut Health Center, Farmington, CT
  • Footnotes
    Commercial Relationships  T. Rezaie, None; A. Child, None; S. Popinchalk, None; T. Krupin, None; R. Ritch, None; J. Liebmann, None; E. Ilitchev, None; R. Crick, None; M. Sarfarazi, None.
  • Footnotes
    Support  NIH Grants EY–09947, EY–014959 and M01RR–06192.
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 1306. doi:
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      T. Rezaie, A. Child, S. Popinchalk, T. Krupin, R. Ritch, J. Liebmann, E. Ilitchev, R. Crick, M. Sarfarazi; Large–Scale Sequencing of the Optineurin Gene in Familial and Sporadic Cases With Primary Open–Angle Glaucoma . Invest. Ophthalmol. Vis. Sci. 2005;46(13):1306.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Abstract: : Purpose: Previously, we showed that mutations in the Optineurin (OPTN) gene are involved in the etiology of adult–onset primary open–angle glaucoma (POAG) linked to the GLC1E locus on 10p14 (Science 295:1077–1079; 2002). The purpose of this study was to screen the entire coding regions of OPTN in a cohort of familial and sporadic patients with high– or low–pressure glaucoma by direct DNA sequencing. Methods: Genomic DNA from 650 unrelated POAG subjects were used to screen for OPTN mutations. Clinical diagnosis of all the affected subjects was confirmed prior to this study. All the 13 coding exons of OPTN gene and their intron–exon boundaries were PCR amplified and screened for potential sequence alteration by direct DNA sequencing. Results: So far, a total of 36 sequence alterations have been observed in the Optineurin gene. Of these, 11 DNA variations are considered disease–causing mutations (i.e., P16A, Q42H, E50K, K66R, E92V, c.691_692insAG, H228Y, E293A, E322K, A466S, R545Q); another 10 were amino acid polymorphisms (i.e., T34T, L41L, R83R, M98K, A134A, E163E, Q245Q, P292P, S297S, S321S) and the remaining 15 were intronic single nucleotide polymorphisms (i.e., IVS5+38T>G, IVS6–5T>C, IVS7–10T>C, IVS7+24G>A, IVS8–53T>C, IVS8–21C>T, IVS8+20G>A, IVS9+3G>A, IVS10–5C>T, IVS11–86G>T, IVS11–44G>T, IVS14–49T>C, IVS15–3C>T, IVS15+9C>G, IVS15+10G>A). The exact role of observed sequence alterations in the etiology of POAG is currently being investigated further. Conclusions: Our findings provide additional evidences for involvement of Optineurin mutations in both low– and high–pressure glaucoma. Supported by EY–09947, EY–014959 and M01RR–06192.

Keywords: genetics • gene screening • mutations 
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