Endocrine control of larval fat body histolysis in normal and mutant Drosophila melanogaster

Abstract

AbstractIn Drosophila melanogaster, about a thousand larval fat body cells survive metamorphosis, but histolyze and disappear in the first few days of adult life. We wondered what hormonal factors control larval fat cell disappearance in normal and mutant flies. In order to test the effect of anterior endocrine organs, we isolated abdomens from the head and thorax of newly eclosed flies. In isolated abdomens fat cells disappeared at a much slower rate, decreasing by only 30% instead of 100% by 72 hours. To find if the juvenile hormone was responsible for this result, we treated isolated abdomens with ZR‐515, a juvenile hormone analogue. In ZR‐515 treated isolated abdomens, the fat cell number decreased by 94% at 72 hours. This shows that juvenile hormone activity can replace the lytic factor missing from isolated abdomens. The mutation ap4 retards the rate of fat cell lysis: only 47% of the cells disappear by 48 hours compared to 99% in heterozygous controls. To find if JH activity could restore the normal phenotype, we treated these mutants with ZR‐515. The result was that hormonetreated mutants at 48 hours had destroyed 88% of their fat cells, thereby approaching the normal situation. To study the effect of an inhibitor of protein synthesis, we injected cycloheximide into freshly eclosed normal flies. A dose of 0.3 μl of 6 × 10−4 gm/ml cycloheximide inhibited both vitellogenesis and larval fat cell disappearance. This inhibition could not be overcome by administration of ZR‐515. From these studies we conclude that juvenile hormone activity is required for larval fat cell disappearance in both wild type and mutant flies. Since cycloheximide inhibits larval fat cell disappearance even in the presence of a juvenile hormone analogue, it is suggested that the lytic effect of juvenile hormone is mediated via protein synthesis.