Ikadai H, Noguchi J, Yoshida M, Imamichi T
Imamichi Institute for Animal Reproduction, Ibaraki, Japan.
J Vet Med Sci. 1992 Aug;54(4):745-9. doi: 10.1292/jvms.54.745.
A newly identified aspermia rat mutant was investigated on testicular histology and mode of inheritance of the defect. Average testis weight of mutants was about one-third of that of phenotypically normal males. Spermatogenesis was interrupted at meiosis. Pachytene spermatocytes significantly decreased in number. Secondary spermatocytes and few round spermatids were seen, but no elongated spermatids and sperms were observed. A large basophilic inclusion-like body existed in the cytoplasm of late pachytene spermatocytes. Genetic analysis revealed an autosomal recessive transmission of the defect. Aspermia (As) was designated for the locus.
对新发现的无精子症大鼠突变体进行了睾丸组织学及该缺陷遗传模式的研究。突变体的平均睾丸重量约为表型正常雄性大鼠的三分之一。精子发生在减数分裂阶段中断。粗线期精母细胞数量显著减少。可见次级精母细胞和少量圆形精子细胞，但未观察到延长型精子细胞和精子。在粗线期晚期精母细胞的细胞质中存在一个大的嗜碱性包涵体样结构。遗传分析显示该缺陷为常染色体隐性遗传。将该基因座命名为无精子症（As）。
