UC Irvine

The molecular mechanisms underlying adaptation have eluded evolutionary biologists even with the advent of new sequencing technology. Many attempts to address this issue have focused on using knockout or knock-down genes in inbred populations, but have failed to fully characterize how molecular changes ultimately effect phenotypic changes. These systems likely fall short because inbred populations give variable and inconsistent results, while knockout and knock-down genes have unknown pleiotropic effects.

Experimental evolution in Drosophila features replicated outbred populations with easy access to both phenotypic and molecular characterization. Experimentally evolved Drosophila populations are outbred and offer ample replication which is necessary when using statistical learning tools to search for the molecular basis for phenotypic change. My work chiefly focuses on 20 experimentally evolved Drosophila populations, ten selected for short life-cycles and ten selected for long life-cycles. Using these 20 populations, I find that phenotypic divergence from an ancestral population occurs rapidly, within dozens of generations, regardless of evolutionary history and similarly, populations sharing a selection treatment converge on common phenotypes in the same time frame (Chapter 1). From the same 20 populations, I find that traits are heavily influenced by selection regime when the trait is fitness-related; conversely, when the trait is not fitness-related, evolutionary history takes precedent (Chapter 2). Next, I sequenced the transcriptome from these 20 populations and found evidence for convergence within each group of populations undergoing the same selection regime, and moderate differentiation between the two groups of populations (Chapter 3). Lastly, I applied statistical learning tools to genomic, transcriptomic, and phenotypic data obtained from these 20 populations. I found that (a) the transcriptome is static in adult Drosophila, (b) both genome and transcriptome can be good predictors for phenotypic characters, and (c) gene expression is influenced by genomic sites found all across the genome (Chapter 4).