[논문]노랑초파리 난황형성과정 제어 신경 메커니즘

김영준; 장진

doi:10.5656/ksae.2022.02.0.009

노랑초파리 난황형성과정 제어 신경 메커니즘
Neuronal Mechanisms that Regulate Vitellogenesis in the Fruit Fly 원문보기

한국응용곤충학회지 = Korean journal of applied entomology, v.61 no.1, 2022년, pp.109 - 115

김영준 (광주과학기술원 생명과학부) , 장진 (광주과학기술원 생명과학부)

초록
AI-Helper

난황형성과정(Vitellogenesis)은 발달하는 난모세포에 난황이 축적되는 과정으로, 이 과정의 개시는 알형성과정(oogenesis)을 제어하는 주요 메커니즘이다. 곤충생리학 모델인 노랑초파리(Drosophila melanogaster)에서 난황형성과정은 성충으로 우화한 직후 시작하여 성적 성숙이 일어나는 2-3일간 지속된다. 성숙한 난모세포가 충분히 만들어지고 성적 성숙이 종료되면, 짝짓기 후 알형성과정이 다시 시작될 때까지 난황형성과정은 멈춘다. 수컷 초파리의 정액 단백질인 성 펩타이드(Sex peptide, SP)는 짝짓기의 신호로서 알라타체(corpora allata)를 자극해 유약호르몬(Juvenile hormone, JH) 생합성 및 분비를 유도하며, 혈림프(hemolymph) JH 농도의 증가는 난황형성과정을 자극한다. 최근 연구 결과에 따르면, SP수용체 뉴런은 자궁 내막의 수상돌기를 통해 교미 중 정액과 함께 자궁으로 전달된 SP를 감지함으로써, 축삭돌기를 통해 중추신경계인 복부 신경절에 짝짓기 신호를 보내는데, 이러한 중추신경계 SP 신호가 JH 생합성 및 분비, 그리고 난황형성과정을 유도하는 것으로 밝혀졌다. 짝짓기 후 암컷에서의 난황형성과정은 일주기 리듬을 보이는데, 노랑초파리의 일주기 리듬은 중추 신경계 뉴런들에 의해 제어된다. 본 종설은 성적 성숙, 짝짓기 신호, 그리고 일주기 리듬에 따라 난황형성과정을 제어하는 신경 메커니즘에 관한 최근 연구 성과를 다룬다.

Abstract ▼ AI-Helper

Vitellogenesis is the process by which yolk accumulates in developing oocytes. The initiation of vitellogenesis represents an important control point in oogenesis. When females of the model insect Drosophila melanogaster molt to become adults, their ovaries lack mature vitellogenic oocytes, only producing them after reproductive maturation. After maturation, vitellogenesis stops until a mating signal re-activates it. Juvenile hormone (JH) from the endocrine organ known as the corpora allata (CA) is the major insect gonadotropin that stimulates vitellogenesis, and the seminal protein sex peptide (SP) has long been implicated as a mating signal that stimulates JH biosynthesis. In this review, we discuss our new findings that explain how the nervous system gates JH biosynthesis and vitellogenesis associated with reproductive maturation and the SP-induced post-mating response. Mated females exhibit diurnal rhythmicity in oogenesis. A subset of brain circadian pacemaker neurons produce Allatostatin C (AstC) to generate a circadian oogenesis rhythm by indirectly regulating JH and vitellogenesis through the brain insulin-producing cells. We also discuss genetic evidence that supports this model and future research directions.

주제어

표/그림 (1)

그림 Fig. 1. A schematic that explains the neuronal and endocrine regulation of vitellogenesis before and after mating. In virgin females (left), SPSNs activate Mip-vAL/vAM and SAG neurons in sequence. The SAG neurons stimulate AstC-mTh neurons indirectly (dotted arrow) to secrete AstC into circulation. Circulating AstC then sets up a vitellogenesis blockade by inhibiting JH biosynthesis in the CA. In their activated state, SAG neurons also activate brain pC1 neurons. This activation inhibits oviposition via the oviIN/oviEN-oviDN network and promotes mating receptivity in virgin females. In mated females (right), SP silences SPSNs via SPR, consequently inhibiting Mip-vAL/vAM and SAG neurons in sequence. This inhibition relieves the AstC-induced vitellogenesis blockade by silencing AstC-mTh neurons. SP also elevates 20E levels by silencing SPSNs via an unknown pathway (dotted line). This 20E stimulates the endocrine Inka cells to secrete ETH. The resulting ETH induces JH biosynthesis in the CA. AstC-DN1p neurons, a subset of the brain circadian pacemaker neurons that express AstC, inhibit IPCs rhythmically, generating a circadian oogenesis rhythm. Black and gray lines indicate active and inactive signaling states, respectively. Filled boxes indicate cells or neurons in an activated state, whereas empty boxes indicate those in an inactivated state.

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