Abstract
Behavior is among the most dynamic animal phenotypes, modulated by a variety of internal and external stimuli. Behavioral differences are associated with large-scale changes in gene expression, but little is known about how these changes are regulated. Here we show how a transcription factor (TF), ultraspiracle (usp; the insect homolog of the Retinoid X Receptor), working in complex transcriptional networks, can regulate behavioral plasticity and associated changes in gene expression. We first show that RNAi knockdown of USP in honey bee abdominal fat bodies delayed the transition from working in the hive (primarily “nursing” brood) to foraging outside. We then demonstrate through transcriptomics experiments that USP induced many maturation-related transcriptional changes in the fat bodies by mediating transcriptional responses to juvenile hormone. These maturation-related transcriptional responses to USP occurred without changes in USP's genomic binding sites, as revealed by ChIP–chip. Instead, behaviorally related gene expression is likely determined by combinatorial interactions between USP and other TFs whose cis-regulatory motifs were enriched at USP's binding sites. Many modules of JH– and maturation-related genes were co-regulated in both the fat body and brain, predicting that usp and cofactors influence shared transcriptional networks in both of these maturation-related tissues. Our findings demonstrate how “single gene effects” on behavioral plasticity can involve complex transcriptional networks, in both brain and peripheral tissues.
Highlights
Many studies have demonstrated that certain individual genes can exert strong influences on behavior, including naturallyoccurring behavioral differences [1,2,3,4]
One important class of gene regulators are transcription factors (TF), proteins that orchestrate the expression of tens to thousands of genes
We discovered that ultraspiracle (USP), a TF previously known primarily for its role in development, regulates behavioral change in the honey bee; and we show that USP causes behaviorally related changes in gene expression by mediating responses to an endocrine regulator, juvenile hormone
Summary
Many studies have demonstrated that certain individual genes can exert strong influences on behavior, including naturallyoccurring behavioral differences [1,2,3,4] These results seemingly contrast with quantitative genetic and genomic studies, which have shown that behavioral variation usually involves multiple causal loci [5,6,7] and changes in the expression of hundreds to thousands of genes [8,9]. Combining these perspectives leads to the idea that single genes influence behavior through their interactions with many other genes, but mechanisms linking behavior to single genes and gene networks are not well understood. This is largely the case even for TFs that have been clearly demonstrated to regulate behavioral change (cf. [3,13])
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