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Infertility associated with meiotic failure in the tremor rat (tm/tm) is caused by the deletion of spermatogenesis associated 22.

Authors: Ishishita, Satoshi  Inui, Toshihide  Matsuda, Yoichi  Serikawa, Tadao  Kitada, Kazuhiro 
Citation: Ishishita S, etal., Exp Anim. 2013;62(3):219-27. doi: 10.1538/expanim.62.219.
Pubmed: (View Article at PubMed) PMID:23903057
DOI: Full-text: DOI:10.1538/expanim.62.219

The tremor rat is an autosomal recessive mutant exhibiting sterility with gonadal hypoplasia in both sexes. The causative mutation tremor (tm) is known as a genomic deletion spanning >200 kb in Chr 10q24. Spermatogenesis associated 22 (Spata22) has been shown to be a vertebrate-specific gene essential for the progression of meiosis through prophase I and completion of chromosome synapsis and meiotic recombination using a mouse repro42 mutant carrying an N-ethyl-N-nitrosourea (ENU)-induced nonsense mutation in Spata22. In this study, we show that Spata22 was identified as the gene responsible for the failure of gametogenesis to progress beyond meiosis I in tm homozygous rats by a transgenic rescue experiment. Meiosis was arrested during prophase I in the mutant testis. Precise mapping of the breakage point revealed that the deleted genomic region spanned approximately 240 kb and comprised at least 13 genes, including Spata22. Rat Spata22 was predominantly expressed in the testis, and its transcription increased with the first wave of spermatogenesis, as seen in the mouse ortholog. These results suggest that Spata22 may play an important role in meiotic prophase I in rats, as seen in mice, and that the tm homozygous rat may be useful for investigating the physiological function of Spata22, as an experimental system for clarifying the effect of a null mutation, and may be an animal model for studying the pathogenesis and treatment of infertility caused by impaired meiosis.


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CRRD Object Information
CRRD ID: 38549346
Created: 2020-08-27
Species: All species
Last Modified: 2020-08-27
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.