Japanese
 NBRP Rat No: 0104 Strain NameWIC-Tgrdw/Kts Commmon Name: WIC-<i>rdw</i>, rdw
 Principal Investigator  Sen-ichi Furudate
 Organization   School of Medicine, Kitasato University Department of Laboratory Animal Sciences
 Address  1-15-1, Kitasato, Sagamihara

228-8555 Kanagawa

 Japan
 Telephone  042-778-9319  Fax:  042-778-7555  furudate@med.kitasato-u.ac.jp
 Inbred Generations   F15+13 (08.5.30) 
   
 Coat Color
 Deposition Status
 
 albino (c)
  Embryo      Sperm      Live Animals
 Usage Restrictions  In publishing, an acknowledgment to the DEPOSITOR is requested 
 Genetic Status   Inbred   Segregating   Congenic   Consomic    Recombinant 
  Coisogenic   Spont. Mutant    Transgene   Ind. Mutant    Others 
 Comercial Availability   
 Research Category   Diabetes Obesity    Neurobiology    Ophthalmology    Dentistry    Cardio- Hypertension 
  Oncology   Metabolism   Otorhinology    Immunology    Infectious Disease
  Osteology    Internal Medicine   Dermatology   Reproduction    Development
  Behavior    Hematology    Urology   Pharmacology   Others 
  Control Strains   Reporter gene Strains  
 Gene Tg: thyroglobulin
 Origin The WIC-<i>rdw</i> rat, established from a closed colony of Wistar-Imamichi (WIC) rats as a spontaneous mutant exhibiting congenital dwarfism (<i>rdw</i>), is inherited as an autosomal recessive.  
 Strain Characteristics A convincing line of evidence is being developed that the congenital nongoitrous hypothyroidism and dwarfism observed in the WIC-<i>rdw</i> rat may indeed be caused by a primary defect in thyroid hormonogenesis. In support of this hypothesis, several recent reports have shown the presence of elevated molecular chaperone levels in the WIC-<i>rdw</i> thyrocytes, the endoplasmic reticulum of which was markedly dilated, suggesting a defect in intracellular protein transport. It was reported that A missense mutation, G2320R, in the Tg gene is responsible for the rdw mutation in the WIC-<i>rdw</i> rat. 
 Breeding Conditions Homozygous <i>rdw</i> rats are infertile in both sexes. So, the mutant rats are maintained as a segregating inbred strain. 
 Genotyping <a href="http://www.anim.med.kyoto-u.ac.jp/nbr/documents/PCR_Gene/Tg_en.pdf">Genotyping protocol for Tg</a> 
 References  Shibayama K, Ohyama Y, Ono M, Furudate S
Expression of mRNA coding for pituitary hormones and pituitary-specific transcription factor in the pituitary gland of the rdw rat with hereditary dwarfism. J Endocrinol. 138: 307-313, 1993.

Ono M, Harigai T, Furudate S.
Pituitary-specific transcription factor Pit-1 in rdw rat with GH- and PRL- deficient dwarfism.
J. Endocrinol. 143, 479-487, 1994.

Oh-Ishi M, Omori A, Kwon JY, Agui T, Maeda T, Furudate S.
Detecion and identication of proteins related to the hereditary dwarfism of the rdw rat.
Endocrinology 139(3): 1288-1299, 1998.

Hishinuma A, Furudate S, Oh-ishi M, Nagakubo N, Namatame T, Ieiri T
A novel missense mutation (G2320R) of the thyroglobulin gene causes hereditary hypothyroidism of the rdw rat.
Endocrinology 141 (11): 4050-4055, 2000.

Sakai Y, Yamashina S, Furudate S
Missing Secretory Granules, dilated Endoplasmic reticulum, and nuclear dislocation in
the thyroid gland of rdw rats with hereditary dwarfism.
Anat Rec 259: 60-66, 2000.

Kim PS, Ding M, Menon S, Jung C-G, Cheng J-M, Miyamoto T, Li B, Furudate S, Agui T
A missence mutation G2320R in the thyroglobulin gene causes non-goitrous congenital primary hypothyroidism in the WIC-rdw rat.
Mol Endocrinol 14 (12): 1944-1953, 2000.