• Proceedings of the Korean Society of Applied Entomolohy Conference
• /
• 2001.11a
• /
• pp.127-127
• /
• 2001

• Proceedings of the Zoological Society Korea Conference
• /
• 2001.10a
• /
• pp.188.1-188
• /
• 2001

No Abstract, See Full Text

• Proceedings of the Zoological Society Korea Conference
• /
• 2003.08a
• /
• pp.164.4-164
• /
• 2003

No Abstract, See Full Text

• Proceedings of the Zoological Society Korea Conference
• /
• 2000.04a
• /
• pp.89.1-89
• /
• 2000

No Abstract, See Full Text

• Proceedings of the Korean Society of Applied Entomolohy Conference
• /
• 2000.05a
• /
• pp.39-39
• /
• 2000

• Korean journal of applied entomology
• /
• v.61 no.1
• /
• pp.109-115
• /
• 2022

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.