Abstract
Gene expression changes in neural systems are essential for environment-induced behavioral plasticity in animals; however, neuronal signaling pathways mediating the effect of external stimuli on transcriptional changes are largely unknown. Recently, we have demonstrated that the neuropeptide F (NPF)/nitric oxide (NO) signaling pathway plays a regulatory role in phase-related locomotor plasticity in the migratory locust, Locusta migratoria. Here, we report that a conserved transcription factor, cAMP response element-binding protein B (CREB-B), is a key mediator involved in the signaling pathway from NPF2 to NOS in the migratory locust, triggering locomotor activity shift between solitarious and gregarious phases. We find that CREB-B directly activates brain NOS expression by interacting with NOS promoter region. The phosphorylation at serine 110 site of CREB-B dynamically changes in response to population density variation and is negatively controlled by NPF2. The involvement of CREB-B in NPF2-regulated locomotor plasticity is further validated by RNAi experiment and behavioral assay. Furthermore, we reveal that protein kinase A mediates the regulatory effects of NPF2 on CREB-B phosphorylation and NOS transcription. These findings highlight a precise signal cascade underlying environment-induced behavioral plasticity.
Highlights
Animals can adjust to a changing environment by developing alternative behavioral phenotypes that improve their fitness; this phenomenon is known as “behavioral plasticity” [1,2,3]
Our previous finding shows that NPF2-regulated nitric oxide synthase (NOS) transcription plays important roles in phase-related locomotor plasticity in the locust
We further demonstrate that phosphorylated cAMP response element-binding protein B (CREB-B) directly activates NOS transcription in the pars intercerebralis, mediates phase-related locomotor plasticity
Summary
Animals can adjust to a changing environment by developing alternative behavioral phenotypes that improve their fitness; this phenomenon is known as “behavioral plasticity” [1,2,3]. Environmental stimuli acts directly on the nervous system and induces short-term changes in neural and endocrine activity, or long-term changes in gene expression, lead to behavioral alterations at different time scales [4, 5]. Long-term behavioral plasticity is greatly shaped by transcriptional changes in key genes that are governed intricately by the interactions of neural modulators in the brain [9,10,11]. TFs undergo either expression alteration or protein modification changes that affect their subcellular location, binding activity, or stability; and result in transcriptional changes of downstream behaviorrelated genes [16,17,18]. Uncovering the precise signaling cascade by which TFs respond to upstream signal and regulate downstream gene transcription will provide insights into the regulatory mechanism underlying environment-induced behavioral plasticity
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