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在排卵过程中,滤泡上皮细胞中的肌动球蛋白收缩为滤泡破裂提供了主要的机械力。

Actomyosin contraction in the follicular epithelium provides the major mechanical force for follicle rupture during ovulation.

机构信息

Department of Physiology and Neurobiology, University of Connecticut, Storrs, CT 06269.

Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139.

出版信息

Proc Natl Acad Sci U S A. 2024 Sep 24;121(39):e2407083121. doi: 10.1073/pnas.2407083121. Epub 2024 Sep 18.

Abstract

Ovulation is critical for sexual reproduction and consists of the process of liberating fertilizable oocytes from their somatic follicle capsules, also known as follicle rupture. The mechanical force for oocyte expulsion is largely unknown in many species. Our previous work demonstrated that ovulation, as in mammals, requires the proteolytic degradation of the posterior follicle wall and follicle rupture to release the mature oocyte from a layer of somatic follicle cells. Here, we identified actomyosin contraction in somatic follicle cells as the major mechanical force for follicle rupture. Filamentous actin (F-actin) and nonmuscle myosin II (NMII) are highly enriched in the cortex of follicle cells upon stimulation with octopamine (OA), a monoamine critical for ovulation. Pharmacological disruption of F-actin polymerization prevented follicle rupture without interfering with the follicle wall breakdown. In addition, we demonstrated that OA induces Rho1 guanosine triphosphate (GTP)ase activation in the follicle cell cortex, which activates Ras homolog (Rho) kinase to promote actomyosin contraction and follicle rupture. All these results led us to conclude that OA signaling induces actomyosin cortex enrichment and contractility, which generates the mechanical force for follicle rupture during ovulation. Due to the conserved nature of actomyosin contraction, this work could shed light on the mechanical force required for follicle rupture in other species including humans.

摘要

排卵对于有性生殖至关重要,它包括将可受精的卵母细胞从其体细胞滤泡囊中释放出来的过程,也称为滤泡破裂。在许多物种中,卵母细胞排出的机械力在很大程度上是未知的。我们之前的工作表明,与哺乳动物一样,排卵需要蛋白酶降解后滤泡壁和滤泡破裂,以将成熟的卵母细胞从一层体细胞滤泡细胞中释放出来。在这里,我们确定了体细胞滤泡细胞中的肌动球蛋白收缩是滤泡破裂的主要机械力。在受到单胺类物质章鱼胺(OA)刺激后,丝状肌动蛋白(F-actin)和非肌肉肌球蛋白 II(NMII)在滤泡细胞的皮质中高度富集,OA 对排卵至关重要。用药物破坏 F-actin 的聚合作用不会干扰滤泡壁的破裂,但可阻止滤泡破裂。此外,我们还证明 OA 诱导滤泡细胞皮质中 Rho1 鸟嘌呤三磷酸(GTP)酶的激活,从而激活 Ras 同源物(Rho)激酶,促进肌动球蛋白收缩和滤泡破裂。所有这些结果表明,OA 信号诱导肌动球蛋白皮质的富集和收缩,从而产生排卵过程中滤泡破裂所需的机械力。由于肌动球蛋白收缩的保守性质,这项工作可以为包括人类在内的其他物种的滤泡破裂所需的机械力提供线索。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/46c2/11441566/3ce20dd5bd8c/pnas.2407083121fig01.jpg

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