Japanese
 NBRP Rat No: 0597 Strain NameTT/Sgn Commmon Name: TTラット
 Principal Investigator  Tomoyuki Tokunaga
 Organization   National Institute of Agrobiological Sciences Reproductive Biology Research Unit
 Address  2-1-2 Kannondai, Tsukuba

305-8602 Ibaraki

 Japan
 Telephone  029-838-7447  Fax:  029-838-7408  jgucci@nias.affrc.go.jp
 Inbred Generations   F20 (Nov 2009) 
   
 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 Fkbp6: FK506 binding protein 6
 Origin Rats with bilateral small testes were found in a Wistar-Imamichi derived inbred strain in 1986 at the Institute for Animal Reproduction (Ikadai, 1992). TT was established from these mutant rats as known as aspermia rats. (May 31, 2010) 
 Strain Characteristics Their phenotype is caused by autosomal recessive mutation, <i>as</i> (aspermia). Homozygous mutant males show arrest of spermatogenesis, mainly at the pachytene stage (Ikadai, 1992). Testis weight of mutants was about one-third of that of normal males. A large basophilic inclusion-like body existed in the cytoplasm of late pachytene spermatocytes. The result of spermatogonial transplantation suggested that defective spermatogenesis is caused by defects of both germ cell itself and somatic cell component such as blood-testis barrier (Noguchi, 2002). Heterozygous males and homozygous females are fertile.
<i>as</i>was revealed to be caused by a genomic deletion including exon 8 of Fkbp6 gene on rat chromosome 12 (Crackower, 2003). (May 31, 2010) 
 Breeding Conditions Maintained by crossing between heterozygous males and homozygous or heterozygous females. (May 31, 2010) 
 Genotyping Genotyping by PCR analysis. (May 31, 2010) 
 References  Ikadai H, Noguchi J, Yoshida M, Imamichi T.
An aspermia rat mutant (as/as) with spermatogenic failure at meiosis.
J Vet Med Sci. 1992 Aug;54(4):745-9.

Noguchi J, Toyama Y, Yuasa S, Kikuchi K, Kaneko H.
Hereditary defects in both germ cells and the blood-testis barrier system in as-mutant rats: evidence from spermatogonial transplantation and tracer-permeability analysis.
Biol Reprod. 2002 Sep;67(3):880-8.

Crackower MA, Kolas NK, Noguchi J, Sarao R, Kikuchi K, Kaneko H, Kobayashi E, Kawai Y, Kozieradzki I, Landers R, Mo R, Hui CC, Nieves E, Cohen PE, Osborne LR, Wada T, Kunieda T, Moens PB, Penninger JM.
Essential role of Fkbp6 in male fertility and homologous chromosome pairing in meiosis.
Science. 2003 May 23;300(5623):1291-5.