조은영 (University of Connecticut) | 한빛사논문 > 한빛사

한빛사논문

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University of Connecticut

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Proc. Natl. Acad. Sci. USA, Sep 24 2024, 121 (39) | https://doi.org/10.1073/pnas.2407083121 Actomyosin contraction in the follicular epithelium provides the major mechanical force for follicle rupture during Drosophila ovulation

Stella E. Cho^a, Wei Li^a,1, Andrew M. Beard^a, Jonathan A. Jackson^b,c,2, Risa Kiernan^a, Kazunori Hoshino^d, Adam C. Martin^b, and Jianjun Sun^a,e,3

^aDepartment of Physiology and Neurobiology, University of Connecticut, Storrs, CT 06269

^bDepartment of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139

^cGraduate Program in Biophysics, Harvard University, Boston, MA 02115

^dDepartment of Biomedical Engineering, University of Connecticut, Storrs, CT 06269

^eInstitute for Systems Genomics, University of Connecticut, Storrs, CT 06269

¹Present address: Diagnostic Development & Validation, Foundation Medicine Inc., Cambridge, MA 02141.

²Present address: Max Planck Institute of Molecular Cell Biology and Genetics, Dresden 01307, Germany.

³To whom correspondence may be addressed. : Jianjun Sun

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 Drosophila 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 Drosophila 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 Drosophila 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.

논문정보

형식Research article
게재일2024년 09월 (BRIC 등록일 2024-09-25)
연구진국외 연구진
분야 생명과학 > 세포생물학

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