Genome-wide transcriptomic effects of the foraging gene shed light on genetic pathways that regulate pleiotropy and plasticity

Natural variants of the Drosophila melanogaster foraging (for) gene as a popular model to understand behaviour, plasticity, and pleiotropy at an evolutionary and molecular level. The effects for variants on phenotype, fitness, stimulus-response (e.g., food deprivation), and tissue-specific for expression are well characterized. In contrast, the transcriptome-wide influence that for variants have across different tissues and stimuli remains unknown. In this study, we collected fed and 4-hour food-deprived D. melanogaster samples from the genetic null, the natural sitter variant, and the natural rover variant in the CNS (brain and brain stem), gut, and fat (89 samples total, N=4-5 per condition/genotype/tissue). Paired-end bulk RNA sequencing was then completed in one experimental batch at Genome Quebec using the NovaSeq6000 S4 PE100 Sequencing Lane. Briefly, samples were aligned to the dm6 genome using STAR, duplicates were marked with Picard, and reads that were non-chromosomal, low-quality, or unpaired were filtered with samtools. High-quality reads were then counted to the dm6 genome with the "Drosophila_melanogaster.BDGP6.22.96" genome annotation with featurecounts. These RNA-seq data elucidated how the for locus, and the natural variants of for can influence gene expression and cellular function across tissues and conditions.