Award Date


Degree Type


Degree Name

Doctor of Philosophy (PhD)


Life Sciences

First Committee Member

Allen Gibbs

Second Committee Member

Laurel Raftery

Third Committee Member

Mo Weng

Fourth Committee Member

Kelly Tseng

Fifth Committee Member

Jefferson Kinney

Number of Pages



Brief periods of starvation are a common stressor that most animals encounter in the wild and must be able to survive in order to maximize their fitness. Starvation resistance of the adult fruit fly, Drosophila melanogaster, is thought to be primarily conferred by adult fat stores, body size, metabolic rate, behavior, and activity levels. Additionally, flies selected for starvation resistance also often show delayed pupariation, which is usually indicative of altered hormone signaling. How starvation selection extends development and if it contributes to adult starvation resistance remains incompletely studied. Identifying the targets of starvation selection that cause extended development and revealing how it might support adult starvation resistance will inform us on how organisms survive starvation stress and manifest the various phenotypes associated with starvation resistance, such as increased triglyceride stores.

My research aimed to reveal how starvation selection changes development time and how that contributes to adult starvation resistance. To address these questions, I first characterized the development of a strain of extremely starvation-resistant flies that have been under starvation selection for over 130 generations. Based on the pattern and distribution of the developmental delay, I then identified reduced ecdysone signaling as the likely effector of delayed development, which I corroborated by measuring ecdysteroid levels during larval development. I also verified that exogenous ecdysone could rescue development.

To measure the contribution of the extended larval development to adult starvation resistance, I used altered diets and dietary restriction to change development time and body composition, which exposed that the extra larval development time is not responsible for the majority of the adult starvation resistance in the starvation-selected flies. This may represent a biological spandrel, or exaptation, if larval development is later found to be a secondary consequence of selection on another adaptive trait. One hypothesis presented that is consistent with the results and evidence is that starvation selection has increased the prevalence in the population of alleles that globally reduce ecdysone production and signaling, and thus this drives processes that promote starvation resistance in the adult, but also happen to affect the larval development. Further, ecdysone signaling in the adult may not necessarily be the direct target of starvation selection either, with perhaps size or function of the steroidogenic organ being an upstream target. Lastly, I suggest a likely mechanism and present evidence that a nutritional sensing and signaling pathway sensitive to dietary yeast content (but not dietary cholesterol) regulates developmental time and triglyceride content differently in the starvation-selection population, and thereby promotes starvation survival in the adult. However, this mechanism (and extra development time or larval nutrition in general) is a small contributor to the overall starvation resistance of the SS population. These findings underscore the need to discover the primary targets of starvation selection and the limitations of interrogating evolutionary history without observing it directly.

Together, my results are of interest to developmental biologists, insect hormone biologists, nutritional biologists, and stress resistance physiologists and will support a broad range of health science that relies on foundational research in translational model organisms. Research into the etiology of human obesity and nutritional regulation of hormones and development is supported by this work.


Diet; Ecdysone; Evolution; Exaptation; Fat; Protein


Ecology and Evolutionary Biology | Evolution | Medical Physiology | Molecular Biology | Physiology

File Format


File Size

3300 KB

Degree Grantor

University of Nevada, Las Vegas




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