Open Access Research article

Absence of glaucoma in DBA/2J mice homozygous for wild-type versions of Gpnmb and Tyrp1

Gareth R Howell1, Richard T Libby16, Jeffrey K Marchant2, Lawriston A Wilson13, Ioan M Cosma1, Richard S Smith13, Michael G Anderson4 and Simon WM John135*

Author Affiliations

1 The Jackson Laboratory, 600 Main Street, Bar Harbor, Maine, USA

2 Department of Anatomy and Cell Biology, Tufts University of Medicine, Boston, MA, USA

3 The Howard Hughes Medical Institute, Bar Harbor, Maine, USA

4 Department of Physiology and Biophysics, The University of Iowa, Iowa City, IA, USA

5 Department of Ophthalmology, Tufts University of Medicine, Boston, MA, USA

6 University of Rochester Eye Institute, University of Rochester Medical Center, Rochester, NY, USA

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BMC Genetics 2007, 8:45  doi:10.1186/1471-2156-8-45

Published: 3 July 2007



The glaucomas are a common but incompletely understood group of diseases. DBA/2J mice develop a pigment liberating iris disease that ultimately causes elevated intraocular pressure (IOP) and glaucoma. We have shown previously that mutations in two genes, Gpnmb and Tyrp1, initiate the iris disease. However, mechanisms involved in the subsequent IOP elevation and optic nerve degeneration remain unclear.


Here we present new mouse strains with Gpnmb and/or Tyrp1 genes of normal function and with a DBA/2J genetic background. These strains do not develop elevated IOP or glaucoma with age.


These strains provide much needed controls for studying pathogenic mechanisms of glaucoma using DBA/2J mice. Given the involvement of Gpnmb and/or Tyrp1 in areas such as immunology and tumor development and progression, these strains are also important in other research fields.