Localized Gurken translation specifies the anterior/posterior and dorsal/ventral axes of the developing Drosophila oocyte. spindle-class females lay ventralized eggs resulting from inefficient grk translation. This phenotype is thought to result from inhibition of the Vasa RNA helicase. In a screen for modifiers of the eggshell phenotype in spn-B flies, we identified a mutation in the lnk gene. We show that lnk mutations restore Grk expression, but do not suppress the persistence of double strand breaks nor other spn-B phenotypes. This suppression does not affect Egfr directly, but rather overcomes the translational block of grk messages seen in spindle mutants. Lnk was recently identified as a component of the insulin/insulin-like growth factor signaling (IIS) / TOR pathway. Interestingly, direct inhibition of TOR with rapamycin can also suppress the ventralized eggshell phenotype in spn-B or vasa mutant mothers. When dietary protein is inadequate, reduced IIS/TOR activity inhibits cap-dependent translation by promoting the activity of the translation inhibitor eIF4E binding protein. We hypothesize that reduced TOR activity promotes grk translation independent of the canonical Vasa/cap-dependent mechanism. This model suggests a means by which flies can maintain the translation of developmentally important transcripts during periods of nutrient limitation when bulk cap-dependent translation is repressed.