Functional analysis of sperm from c-mos(-/-) mice.
Functional analysis of sperm from c-mos(-/-) mice.
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c-mos(-/-) 小鼠精子的功能分析。
DOI：
10.1002/mrd.10140
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发表时间：
2002
期刊：
影响因子：
--
通讯作者：
Cooper,GeoffreyM
中科院分区：
文献类型：
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作者：
Gross,VeraS;Cooper,GeoffreyM
c-mos原癌基因主要在雄性和雌性生殖细胞中表达，对小鼠的正常卵母细胞减数分裂和雌性生育力至关重要。c-mos的失活导致卵母细胞发育异常，并导致体内卵巢囊肿和肿瘤。与c-mos消融对雌性小鼠的严重影响相反，c-mos靶向灭活未报告会影响雄性小鼠的精子发生。然而，先前报道的雄性c-mos −/−小鼠的研究仅限于睾丸和体内交配的组织学分析，这两者都是精子产生和功能的相对不敏感的指标。因此，我们在体外条件下测定了c-mos −/−男性的精子功能，以确定发育过程中Mos的缺乏是否会影响精子的产生或可交配性。我们发现从c-mos −/−和野生型小鼠收集的精子数量之间没有显着差异。此外，来自c-mos −/−和c-mos +/+男性的精子在体外受精（IVF）和受精相关事件（包括透明带（ZP）穿透、精子/卵子质膜融合和精子染色质重塑）试验中表现同样良好。因此，我们认为，Mos在精子发生中的功能要么与精子的最终受精潜能无关，要么Mos的缺乏被多余的激酶所掩盖。摩尔Reprod. Dev. 62：519-524，2002.© 2002 Wiley利斯公司
The c‐mosprotooncogene, which is expressed predominantly in male and female germ cells, is crucial for normal oocyte meiosis and female fertility in mice. Inactivation of c‐mosresults in abnormal oocyte development and leads to ovarian cysts and tumors in vivo. In contrast to the severe effects of c‐mosablation in females, targeted inactivation of c‐moshas not been reported to affect spermatogenesis in male mice. However, previously reported studies of male c‐mos−/−mice have been limited to histological analyses of testes and in vivo matings, both of which are relatively insensitive indicators of sperm production and function. Therefore, we assayed sperm function of c‐mos−/−males under in vitro conditions to determine whether the absence of Mos during development affected sperm production or fertilizing ability. We found no significant differences between the number of sperm collected from c‐mos−/−and wild type mice. Additionally, sperm from c‐mos−/−and c‐mos+/+males performed equally well in assays of in vitro fertilization (IVF) and fertilization‐associated events including zona pellucida (ZP) penetration, sperm/egg plasma membrane fusion, and sperm chromatin remodeling. Therefore, we suggest that the function of Mos in spermatogenesis is either not related to the ultimate fertilizing potential of the sperm, or else the absence of Mos is masked by a redundant kinase. Mol. Reprod. Dev. 62:519–524, 2002. © 2002 Wiley‐Liss, Inc.