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通过FOXL2除来对成年卵巢进行体质性重编程,使其变成丸
N Henriette Uhlenhaut1, Susanne Jakob, Katrin Anlag
1Developmental Biology Unit, European Molecular Biology Laboratory, D-69117 Heidelberg, Germany.
Cell
|December 17, 2009
概括
叉转录调节器FOXL2在小鼠中积极维持成年卵巢表型. 它的去除触发了卵巢到丸的转差,突出了卵巢维护的积极性.
科学领域:
- 遗传学和发育生物学
- 哺乳动物繁殖 哺乳动物繁殖
- 分子内分泌学分子内分泌学
背景情况:
- 在Y染色体上的SRY基因通常从哺乳动物中无关的前体中启动男性性腺发育 (丸).
- 卵巢的发育和维护对女性生殖功能至关重要,但确保卵巢稳定的分子机制尚未完全理解.
- 即使没有SRY,丸分化也可能发生,这表明涉及其他途径或调节因素.
研究的目的:
- 调查沟转录调节器FOXL2在维持成年卵巢表型中的作用.
- 确定FOXL2是否对于防止成年卵巢转化为丸至关重要.
- 探索成年卵巢毛囊中FOXL2损失的分子后果.
主要方法:
- 在成年小鼠卵巢毛囊中利用了Foxl2基因的诱导性删除.
- 在Foxl2删除后分析了丸特异性基因的表达,包括SRY目标基因Sox9.
- 评估了卵巢细胞系 (粒素和theca) 的重编程,使其成为类似塞尔托利和类似莱迪格的细胞.
- 在诱导Foxl2删除的小鼠中测量丸激素水平.
主要成果:
- 成人卵巢毛囊中Foxl2的诱导性缺失导致丸特异性基因的立即上调,包括Sox9.9.
- 颗粒素和甲基细胞系被重新编程成分别类似于塞尔托利的和类似于莱迪格的细胞系.
- 这些小鼠的丸激素水平与正常XY雄性 littermates的水平相当.
结论:
- 对于小鼠来说,FOXL2 是一个关键因素,需要积极防止成年卵巢转化为丸.
- 维持卵巢表型是一个活跃的,持续的过程,整个成年生活,不仅仅是一个默认状态.
- 这些发现对理解和治疗性发育障碍和过早更年期的潜在影响.
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