Search

Janus kinase (JAK) and signal transducer and activator of transcription (STAT) signaling affect social aggregation, mood and psychiatric disorders, nociceptive and depressive behaviors. Olfactory dysfunction is one of the distinct symptoms of these behaviors, but function and mechanism of JAK and STAT in modulating olfaction remain largely unknown. Migratory locusts show olfactory preference for their own volatiles. We thus use this animal model to explore functions and mechanisms of JAK and STAT5B in mediating olfaction response to their own volatiles. Tissue distribution study shows that JAK and STAT5B express in antennae and brains, especially in antennal lobes and mushroom bodies in locust brains, and knockdown of these two genes by RNA interference (RNAi) in antennae and brains results in the loss of olfactory preference for locust volatiles, including chemical odorants indole and β-ionone. RNA-seq analysis reveals that JAK and STAT5B RNAi knockdown downregulates a functional class of transcripts in nucleoprotein complex, including heterogeneous nuclear ribonucleoprotein C (hnRNPC) and small nuclear ribonucleoprotein polypeptide F (SNRPF). HnRNPC and SNRPF mRNAs and proteins are also expressed in antennae and brains, and RNAi knockdown of these two genes reduces the percentage of locusts preferring volatiles, including chemical odorants indole and β-ionone. Furthermore, RNAi knockdown of dopamine receptor 1 (DopR1) results in the decrease of JAK mRNA level in antennae, and JAK/STAT5B, hnRNPC and SNRPF are required for dopamine receptor 1 (DopR1) to modulate olfactory preference for their own volatiles. This study confirms that JAK/STAT5B signaling modulates olfaction by affecting expression levels of hnRNPC and SNRPF , and this pathway is also required for DopR1 to modulate olfactory preference for their own volatiles. These findings highlight novel roles of JAK and STAT5B in modulating olfactory preference. This study provides novel insights into functional links among JAK/STAT5B signaling, RNA binding proteins and DopR1 underlying the modulation of olfactory behaviors. [Display omitted] • JAK/STAT5B signaling in migratory locusts mediates olfactory preference for locust volatiles. • HnRNPC and SNRPF are potentially the critical targets in JAK/STAT5B signaling for olfaction. • JAK/STAT5B, hnRNPC and SNRPF are required for DopR1 to mediate olfactory preference for volatiles. [ABSTRACT FROM AUTHOR]

Animals communicate with each other in aggregating for survival and adaptation. Solitary locusts show an olfactory transition from repulsion to attraction in aggregation. However, the molecular mechanism underlying this transition is less well known. In this study, we explored differentially expressed transcripts (DETs) during locust aggregation and identified that a functional class of general metabolism encompassed the largest number of DETs among all analyzed gene classes. Within this functional class of general metabolism, oxidoreductase mediates synthesis of retinoic acid (RA) from vitamin A and other metabolites derived from carbohydrates. The expression levels of retinaldehyde hydroxylase 1 (raldh1) and retinoid X receptor (rxr) , which are two crucial genes for RA synthesis and signaling, were upregulated during 4 h of crowding. Knockdown of raldh1 and rxr by RNA interference (RNAi) in the brains resulted in the loss of olfactory attraction. Moreover, inhibition of RXR by RNAi resulted in downregulated expression of Gna14 , a member of the Gα subfamily that transduces signals in G protein-coupled receptor (GPCR) pathways. Abrogating RXR signaling and Gna1 4 by RNAi knockdown inhibited the function of dopamine receptor 1 (DopR1) and octopamine receptor α1 (OctαR1) in modulating olfactory attraction. RXR signaling is essential for DopR1 and OctαR1 to mediate olfactory attraction. This study showed that RXR signaling mediates attraction by Gα signaling and confirmed a novel link between nuclear receptor RXR and the membrane receptor GPCRs in modulating olfactory attraction. Image 1 • Retinoid X receptor (RXR) and retinaldehyde hydroxylase 1(raldh1) mediate olfactory attraction. • RXR affects the expression level of Gna14 in G protein-coupled receptor (GPCR) signaling pathway. • The deficiency of RXR abrogates the roles of DopR1 and OctαR1 in the modulation of olfactory attraction. [ABSTRACT FROM AUTHOR]

Cellular retinaldehyde-binding protein (CRALBP) is abundantly expressed in retina and its mutations are associated with visual impairments. The functions of CRALBP are less known in extra retinal tissues. Herein, we study the function of CRALBP in modulating olfactory behaviors in gregarious and solitary locusts. The expressions of cralbp mRNA and protein were enriched in locust brains and antennae. RNAi knockdown of cralbp in gregarious locusts decreased their attractive response to gregarious volatiles. RNA-seq and quantitative PCR confirmed that cralbp mRNA and protein expression levels were upregulated and downregulated after octopamine receptor α1 (OctαR1) activation and inhibition, respectively. Gene network analysis revealed that cralbp is the core hub gene in the interactive network among differentially expressed transcripts (DETs) resulting from activating and inhibiting OctαR1. Moreover, cralbp RNAi knockdown inhibited the induction of olfactory attraction by octopamine (OA)-OctαR1 signaling. CRALBP helped to transmit OA signals to mediate olfactory attraction response to guaiacol and veratrole, which are two odorant components in gregarious volatiles. This study suggested that CRALBP may act as a novel effector protein in OctαR1 signaling to mediate olfactory attraction. This study indicated that CRALBP modulates olfactory attraction in extra retina tissues and retinaldehyde metabolism may be crucial for olfactory attraction modulation. Image 1 • CRALBP is enriched in the brains and affects their olfactory attraction. • OctαR1 activation and inhibition upregulates and downregulates CRALBP expression, respectively. • CRALBP acts as a critical target in OctαR1 signaling to mediate olfactory attraction. [ABSTRACT FROM AUTHOR]