Strain information
 NBRP Rat No: 0217  Strain name: UPL/Cas  Commmon Name: UPL Rat Genome Database
Principal Investigator:  Toshinori Furukawa  Hiroshima University           734-8551 Hiroshima     Japan
Tel: 082-257-5108    Fax: 082-257-5109 Email: toshi@fumi.mayu.hiroshima-u.ac.jp
Preservation Status:   Embryo        Sperm       Living Animals
Coat Color  albino (c)
Inbred Generations  F14+9 (Mar 2004)
Usage Restrictions  In publishing, a citation of the following literature(s) designated by the DEPOSITOR is requested.
In publishing, an acknowledgment to the DEPOSITOR is requested.
Genetic Status
 Inbred  Segregating  Congenic  Consomic  Recombinant
 Coisogenic  Spont. Mutant  Transgene  Ind. Mutant  Category Other 
Comercial Availability
Research Category
 Diabetes Obesity  Neurobiology  Ophthalmology  Dentistry  Cardio Hypertension
 Cancer  Metabolism  Otorhinology  Immunology  Infectious
 Osteosis  Internal Organ  Dermatology  Reproduction  Development
 Behavior  Hematology  Urology  Pharmacology  Research Area Others 
 Control Strain  Marker Strain
Gene Affected Gja8: gap junction membrane channel protein alpha 8
Origin Genetic analysis of the mutant showed that a single gene was semidominantly involved in the development of cataract. Homozygotes of UPL rats displayed early-onset cataract, which manifested as lens opacification before eye opening at 14 days of age and was often accompanied by microphthalmos and/or buphthalmos. Heterozygotes of UPL rats displayed late-onset cataract that started to appear at 2 to 4 weeks of age and developed into complete opacity of the lenses in both eyes (mature cataract) at 7 to 8 weeks of age. A candidate gene for formation of cataracts in UPL rats was mapped to rat chr 2, and a missense mutation (R340W) of the Cx50 (Gja8) gene was a strong candidate (Yamashita, 2002). In UPL lenses, decreases in ATP content, increases in Ca2+ATPase mRNA and Ca2+ATPase activity, increase in the expression levels of interleukin-18 and interferon-γexistence of calpain-dependent proteolysis are recognized (Nabekura, 2004; Tomohiro, 1997; Nagai, 2007). Disulfiram, a powerful antioxidant, and aminoguanidine, an inhibitor of inducible NO synthase, can prevent lens opacification in UPL rats (Nabekuma, 2003; Nabekuma, 2004). The etiology of cataract in UPL rat is different from that in ICR rat (NBRP No.0290), and that in diabetic models (Nagai, 2008). The biological characteristics of UPL rats are considered to be normal except for the cataract. (Oct 7, 2010)
Strain characteristics Genetic analysis of the mutant showed that a single gene was semidominantly involved in the development of cataract. Homozygotes of UPL rats displayed early-onset cataract, which manifested as lens opacification before eye opening at 14 days of age and was often accompanied by microphthalmos and/or buphthalmos. Heterozygotes of UPL rats displayed late-onset cataract that started to appear at 2 to 4 weeks of age and developed into complete opacity of the lenses in both eyes (mature cataract) at 7 to 8 weeks of age. A candidate gene for formation of cataracts in UPL rats was mapped to rat chr 2, and a missense mutation (R340W) of the Cx50 (Gja8) gene was a strong candidate (Yamashita, 2002). (Mar 3, 2009)
Breeding Conditions Maintained by rotation breeding of 3 groups (group A, B and C). Resulting heterozygoutes are used for breeding. Offspring born from group A×B are defined as group C, group B×C are defined as group A, group C×A are defined as group B. (Mar 3, 2009)
Genotyping
References Tomohiro M, Maruyama Y, Yazawa K, Shinzawa S, Mizuno A.
The UPL rat: a new model for hereditary cataracts with two cataract formation types.
Exp Eye Res. 1993 Oct;57(4):507-10.

Tomohiro M, Aida Y, Inomata M, Ito Y, Mizuno A, Sakuma S.
Immunohistochemical study of calpain-mediated alpha-crystallin proteolysis in the UPL rat hereditary cataract.
Jpn J Ophthalmol. 1997 May-Jun;41(3):121-9.

Nabekura T, Koizumi Y, Nakao M, Tomohiro M, Inomata M, Ito Y.
Delay of cataract development in hereditary cataract UPL rats by disulfiram and aminoguanidine.
Exp Eye Res. 2003 Feb;76(2):169-74.

Nabekura T, Tomohiro M, Ito Y, Kitagawa S.
Changes in plasma membrane Ca2+ -ATPase expression and ATP content in lenses of hereditary cataract UPL rats.
Toxicology. 2004 Apr 15;197(2):177-83.

Nagai N, Ito Y.
Adverse effects of excessive nitric oxide on cytochrome c oxidase in lenses of hereditary cataract UPL rats.
Toxicology. 2007 Dec 5;242(1-3):7-15. Epub 2007 Sep 8.

Nagai N, Ito Y, Okamura H.
Involvement of interleukin 18 in cataract development in hereditary cataract UPL rats.
J Biochem. 2007 Nov;142(5):597-603.

Nagai N, Ito Y, Takeuchi N, Usui S, Hirano K.
Comparison of the mechanisms of cataract development involving differences in Ca2+ regulation in lenses among three hereditary cataract model rats.
Biol Pharm Bull. 2008 Nov;31(11):1990-5.
Additional strain information UPL