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A sensor mechanism involving the lipophorin receptors couples the metabolic status of the female fly with oogenesis progression

AutorCuli, Joaquim
Fecha de publicación2012
Citación1st Spanish Conference on the Molecular, Cellular and Developmental Biology of Drosophila (2012)
ResumenIt has been known for a long time that females adjust the number of eggs laid to nutrient availability. Work mostly from Drummond-Barbosa's lab indicated that this regulation was mediated in part by two systemic signals, insulin-like peptides and ecdyson. Both signals impact on germ-line stem cells proliferation and maintenance in the germarium. In addition, under poor nutrition there is a strong increase in the loss of egg chambers at stage 8 by apoptosis. How this cell death is triggered is not currently known. We have observed that disruption of lipid metabolism causes a similar effect, the abrupt death of most egg chambers by apoptosis at stage 9-10a. In particular, knockdown of lipophorin, of LTP or a mutation in the lipophorin receptors all cause this phenotype. Expression of the lipophorin receptors exclusively in the somatic follicle cells that surround the oocyte and nurse cells rescues egg chambers death under these conditions. This suggests that follicle cells sense the availability of lipids and trigger the death of the egg chamber when they are low. We have identified the TOR pathway as a central component of this sensor mechanism. Our data suggests that in the absence of lipid uptake in the follicular epithelia, the energysensing kinase AMPK represses the TOR pathway, triggering the destruction of the egg chamber. In contrast, the insulin pathway is not involved. We are currently analyzing the link between the lipophorin receptors and AMPK.
DescripciónResumen del trabajo presentado al 1st Spanish Conference on the Molecular, Cellular and Developmental Biology of Drosophila, celebrado en Girona (España) del 25 al 28 de septiembre de 2012.
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