April 2011
Volume 52, Issue 14
Free
ARVO Annual Meeting Abstract  |   April 2011
Blue-cone Monochromacy In A Patient With Compound Heterozygosity For Mutations In Thyroid Hormone Receptor Beta 2 Gene
Author Affiliations & Notes
  • Avery H. Weiss
    Ophthalmology, Roger Johnson Vision Lab., Seattle Children's Hospital / W-7729, Seattle, Washington
    University of Washington, Seattle, Washington
  • John P. Kelly
    Ophthalmology, Roger Johnson Vision Lab., Seattle Children's Hospital / W-7729, Seattle, Washington
    University of Washington, Seattle, Washington
  • Samir Deeb
    Department of Medicine, Division of Medical Genetics,
    University of Washington, Seattle, Washington
  • Footnotes
    Commercial Relationships  Avery H. Weiss, None; John P. Kelly, None; Samir Deeb, None
  • Footnotes
    Support  NEI grant EY08295, W.O. Rogers, Le Haye, and Anderson research funds.
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 4894. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      Avery H. Weiss, John P. Kelly, Samir Deeb; Blue-cone Monochromacy In A Patient With Compound Heterozygosity For Mutations In Thyroid Hormone Receptor Beta 2 Gene. Invest. Ophthalmol. Vis. Sci. 2011;52(14):4894.

      Download citation file:


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

      ×
  • Supplements
Abstract

Purpose: : To describe the first case of blue-cone monochromatism (BCM) in an infant with severe thyroid hormone resistance due to mutations in the gene (THRβ2) encoding thyroid hormone receptor beta 2 (Trβ2).

Methods: : We PCR-amplified and directly sequenced exons 8-10 of the THRβ2 gene in a child with blue cone monochromacy documented by electroretinogram (ERG) testing including spectral stimuli.

Results: : Molecular analysis revealed that the child is a compound heterozygote for p.R338W and p.R429W mutations in the THRβ2 gene. These two mutations lie within the ligand-binding domain but are known to selectively inhibit Trβ2 binding as homodimers to the thyroid hormone receptor response elements (TREs). ERG testing showed a reduced photopic response. Spectral testing on a white background showed a small amplitude b-wave (11 µV) to the red flash and a larger amplitude b-wave (31 µV) to the blue flash.

Conclusions: : This report is the first to document BCM caused by deleterious mutations in the THRβ2 gene. Therefore, thyroid hormone, via TRβ2, is critical for middle-wave-sensitive (MWS) and long-wave-sensitive (LWS) cone development in the fovea and peripheral retina in humans.

Keywords: color pigments and opsins • retinal development • electroretinography: clinical 
×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×