Lawriston Wilson

Publications (2)13.61 Total impact

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

  Gareth Howell, Richard Libby, Jeffrey Marchant, Lawriston Wilson, Ioan Cosma, Richard Smith, Michael Anderson, Simon John
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  ABSTRACT: Abstract Background 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. Results 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. Conclusion 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.
  BMC Genetics. 01/2007;
• Article: Random mutagenesis of proximal mouse chromosome 5 uncovers predominantly embryonic lethal mutations.

  Lawriston Wilson, Yung-Hao Ching, Michael Farias, Suzanne A Hartford, Gareth Howell, Hongguang Shao, Maja Bucan, John C Schimenti
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  ABSTRACT: A region-specific ENU mutagenesis screen was conducted to elucidate the functional content of proximal mouse Chr 5. We used the visibly marked, recessive, lethal inversion Rump White (Rw) as a balancer in a three-generation breeding scheme to identify recessive mutations within the approximately 50 megabases spanned by Rw. A total of 1003 pedigrees were produced, representing the largest inversion screen performed in mice. Test-class animals, homozygous for the ENU-mutagenized proximal Chr 5 and visibly distinguishable from nonhomozygous littermates, were screened for fertility, hearing, vestibular function, DNA repair, behavior, and dysmorphology. Lethals were identifiable by failure to derive test-class animals within a pedigree. Embryonic lethal mutations (total of 34) were overwhelmingly the largest class of mutants recovered. We characterized them with respect to the time of embryonic death, revealing that most act at midgestation (8.5-10.5) or sooner. To position the mutations within the Rw region and to guide allelism tests, we performed complementation analyses with a set of new and existing chromosomal deletions, as well as standard recombinational mapping on a subset of the mutations. By pooling the data from this and other region-specific mutagenesis projects, we calculate that the mouse genome contains approximately 3479-4825 embryonic lethal genes, or about 13.7%-19% of all genes.
  Genome Research 09/2005; 15(8):1095-105. · 13.61 Impact Factor