Nutritional status affects 20-hydroxyecdysone concentration and progression of oogenesis in Drosophila melanogaster.
Drosophila egg production depends upon the nutritional available to females. When food is in short supply, oogenesis is arrested and apoptosis of the nurse cells is induced at mid-oogenesis via a mechanism that is probably controlled by ecdysteroid hormone. We have shown that expression of some ecdysone-response genes is correlated with apoptosis of egg chambers. Moreover, ecdysteroid injection and application of juvenile hormone induces and suppresses the apoptosis, respectively. In this study, we investigated which tissues show increases in the concentration of ecdysteroids under nutritional shortage to begin to link together nutrient intake, hormone regulation and the choice between egg development or apoptosis made within egg chambers. We measured ecdysteroid levels in the whole body, ovaries and haemolymph samples by RIA and found that the concentration of ecdysteroid increased in all samples. This contributes to the idea that nutritional shortage leads to a rapid high ecdysteroid concentration within the fly and that the high concentration induces apoptosis. Low concentrations of ecdysteroid are essential for normal oogenesis. We suggest there is threshold concentration in the egg chambers and that apoptosis at mid-oogenesis is induced when the ecdysteroid levels exceed the threshold. Starvation causes the ovary to retain the ecdysteroid it produces, thus enabling individual egg chambers to undergo apoptosis and thus control the number of eggs produced in relation to food intake.
Terashima
J
J
Institute of Cell and Molecular Biology, University of Edinburgh, Darwin Building, King's Buildings, Mayfield Road, Edinburgh EH9 3JR, UK. jterashi@mail.pharm.tohoku.ac.jp
Takaki
K
K
Sakurai
S
S
Bownes
M
M
D000824:Animal Nutritional Physiological Phenomena; D000818:Animals; D017209:Apoptosis; D004331:Drosophila melanogaster / Q000378:metabolism* / Q000502:physiology; D004441:Ecdysterone / Q000032:analysis / Q000378:metabolism*; D005260:Female; D006066:Gonads / Q000166:cytology; D006458:Hemolymph / Q000737:chemistry; D009866:Oogenesis / Q000502:physiology*; D010053:Ovary / Q000737:chemistry
D004441:Ecdysterone