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Female infertility in mice lacking connexin 37

机译:缺乏连接蛋白的小鼠的女性不育37

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The signals regulating ovarian follicle development and the mechanisms by which they are communicated are largely undefined. At birth, the ovary contains primordial follicles consisting of meiotically arrested oocytes surrounded by a single layer of supporting (granulosa) cells. Periodically, subsets of primordial follicles undergo further development during which the oocyte increases in size and the granulosa cells proliferate, stratify and develop a fluid-filled antrum. After ovulation, oocytes resume meiosis and granulosa cells retained in the follicle differentiate into steroidogenic cells, forming the corpus luteum. It has been proposed that intercellular signalling through gap junction channels may influence aspects of follicular development. Gap junctions are aggregations of intercellular channels composed of connexins, a family of at least 13 related proteins that directly connect adjacent cells allowing the diffusional movement of ions, metabolites, and other potential signalling molecules. Here we show that connexin 37 is present in gap junctions between oocyte and granulosa cells and that connexin 37-deficient mice lack mature (Graafian) follicles, fail to ovulate and develop numerous inappropriate corpora lutea. In addition, oocyte development arrests before meiotic competence is achieved. Thus, cell-cell signalling through intercellular channels critically regulates the highly coordinated set of cellular interactions required for successful oogenesis and ovulation.
机译:调节卵巢卵泡发育的信号及其传递机制在很大程度上尚不清楚。出生时,卵巢中含有原始卵泡,该卵泡由减数分裂停滞的卵母细胞组成,卵母细胞被单层支持(颗粒)细胞包围。原始卵泡的子集会定期进行进一步发育,在此期间卵母细胞会增大,颗粒细胞会增殖,分层并形成充满液体的胃窦。排卵后,卵母细胞恢复减数分裂,保留在卵泡中的颗粒细胞分化为类固醇生成细胞,形成黄体。已经提出通过间隙连接通道的细胞间信号传导可能影响卵泡发育的各个方面。间隙连接是由连接蛋白组成的细胞间通道的聚集体,连接蛋白是至少13个相关蛋白质的家族,直接连接相邻细胞,允许离子,代谢物和其他潜在信号分子的扩散运动。在这里,我们显示连接蛋白37存在于卵母细胞和颗粒细胞之间的间隙连接中,连接蛋白37缺乏的小鼠缺乏成熟的(Graafian)卵泡,无法排卵并发育出许多不合适的黄体。另外,卵母细胞发育在减数分裂能力获得之前就停止了。因此,通过细胞间通道的细胞信号传导关键性调节成功发生卵子和排卵所需的高度协调的细胞相互作用。

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