The role of larval fat cells in starvation resistance and reproduction in adult Drosophila melanogaster
- Publication Year:
- Repository URL:
- https://digitalscholarship.unlv.edu/thesesdissertations/1130; https://digitalscholarship.unlv.edu/cgi/viewcontent.cgi?article=2131&context=thesesdissertations
- Drosophila melanogaster--Larvae; Insects--Development; Insects--Metamorphosis; Insects--Reproduction; Larvae—Physiology; Entomology; Life Sciences; Physiology
thesis / dissertation description
The intricate life cycle of holometabolous insects includes well-defined larval and adult stages associated with feeding and non-feeding periods. The larval stage is distinguished by prevalent feeding and is necessary for supporting the animal as it quickly grows. The larval stage also serves as the period for the animal to obtain adequate energy stores, primarily in the larval fat body, to fuel the animal through the non-feeding pupal and immature adult stages. Acquiring sufficient energy stores is paramount for the success of the adult animal. In fact, certain insects, such as silkworms and mayflies, do not feed as adults and must obtain all their lifetime nutrients during the larval stage. In Drosophila melanogaster , the larval fat body is preserved during the pupal stage as individual dissociated cells, enabling the animal access to the energy stores. These larval fat cells do not undergo early pupal autophagic cell death that eliminates most of the larval cells during metamorphosis. Instead, these larval fat cells persist into the adult stage and have a nutritional role in the young adult. By utilizing cell markers, I show that the larval fat cells remain in the young adult and are ultimately removed in the adult by a caspase cascade leading to cell death. In addition, I demonstrate that the larval fat body plays a key role in enhancing starvation resistance and serving as a nutritional reservoir for the adult animal. I also report here that the rapid release of energy stores from larval fat cells by caspase-induced cell death promotes the rapid maturation of the ovaries and has an important role in establishing female fecundity. Furthermore, I suggest that the transfer of larval nutrients from the larval fat body to the adult gonadal tissues is necessary for the proper development of the ovaries. Finally, I demonstrate that in the absence of caspase-induced programmed cell death, the age of first reproduction is delayed and total fecundity is reduced in females. Overall these results reveal an important role for the larval fat reserves in the rapid development of the ovaries, which I propose in a model at the end of the dissertation.