| Drosophila females deprived of sufficient protein in their food (starved) have low fecundity due to slowed stem cell divisions, slowed egg chamber development and apoptosis of egg chambers just prior to the onset of vitellogenesis (stage 8). Previously, I found that previtellogenic egg chambers (stage 7 and younger) from starved females contained large cytoplasmic foci in nurse cells that contain processing body (P body) components and the oskar mRNP. Starved chambers also had cortical enrichment of microtubules, which may interfere with polarized transport of maternal components to the oocyte. Importantly, both P body aggregation and microtubule cortical condensation were rapidly reversed upon re-feeding or culturing egg chambers with insulin. To determine the functional significance of these responses to starvation, I manipulated systemic insulin secretion from the brain. Activation of insulin secretion prevented the previtellogenic starvation response egg chambers, while blocking secretion induced a constitutive starvation response. Importantly, blocking the ability of egg chambers to respond to starvation reduced progeny survival, suggesting the starvation response contributes to the production of healthy eggs. Using cell type-specific modulation of gene expression in egg chambers, I found that Insulin/TOR pathway activity in the follicle cells regulates the starvation response of the germline. In the germline, Kinesin and Dynein activity regulate nutrient-responsive microtubule distribution, which is upstream of P body aggregation. These data reveal a mechanism that allows female to maximize fecundity even during periods of poor nutrient availability by mounting a protective response in immature egg chambers. |
