ssp411基因敲除小鼠生育表型的初步研究

Preliminary exploration of reproductive phenotype in ssp411 gene knockout mice

目的对ssp411基因的生育功能进行初步研究。方法利用PB转座子插入建立小鼠模型ssp411基因敲除小鼠各基因型之间交配后,检查雌鼠生殖道是否见栓。记录出生小鼠的窝仔数,性别,出生20 d仔鼠体质量、基因型等数据;记录出生后90 d雄仔鼠的睾丸重量,进行组织形态学研究,并对附睾尾精子进行活力分析。结果 ssp411缺陷型雌鼠可以正常生育,而雄鼠无自然生育能力。ssp411基因敲除雄鼠能够与母鼠自然交配形成阴道栓,但是没有子代出生,且在交配后母鼠输卵管壶腹部未见精子。睾丸的组织形态学研究和睾丸称量结果表明,ssp411蛋白缺失可以影响精子的生成。ssp411基因敲除雄鼠的附睾精子活力也明显差于对照组。结论 ssp411基因缺陷不影响雌性生殖,但影响雄鼠的精子生成功能,造成少弱精子症,并引起雄性不育。

Objective To study reproductive phenotype of ssp411 gene deficiency. Methods By using mouse model with inserted PB transposon after natural mating between different genotypes, females were examined for the presence of vaginal plugs. The data such as litter size, genders, genotypes and body weights of pups were recorded. Testicular weights of adult mice were also recorded. Histomorphological analysis of testes and activity analysis of cauda epididymal sperms were performed. Results Male ssp411 knockout mice showed infertile, while female mice showed same degree of fertility as that of wild types. Although male mice could normally perform mating, their sperms were not capable to reach to ampulla of fallopian tube. Their testis weights, cauda epididymal sperm concentration and activity were significantly low. Histomorpgological analysis suggested that spermatogenesis was injured in ssp411 deficient males. Conclusion Females with ssp411 deficiency are fertile. ssp411 deficiency could negatively affect spermatogenesis, which will lead to oligoasthenospermia and male stertility.