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A Neuronal Signaling Pathway of CaMKII and Gq  Regulates Experience-Dependent Transcription of tph-1

Qin, Y. ; Zhang, X. ; Zhang, Y.

Journal of Neuroscience, 01/16/2013, Vol.33(3), pp.925-935 [Tạp chí có phản biện]

ISSN: 0270-6474 ; E-ISSN: 1529-2401 ; DOI: http://dx.doi.org/10.1523/JNEUROSCI.2355-12.2013

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  • Nhan đề:
    A Neuronal Signaling Pathway of CaMKII and Gq  Regulates Experience-Dependent Transcription of tph-1
  • Tác giả: Qin, Y. ; Zhang, X. ; Zhang, Y.
  • Chủ đề: Mimicry ; Learning ; Olfactory Receptor Neurons ; Sensory Neurons ; Tryptophan Hydroxylase ; Transcription ; Enzymes ; Pathogens ; Serotonin ; Nervous System ; Neurogenesis ; Aversion ; Gene Regulation ; Plasticity (Behavioral) ; Ca Super(2+)/Calmodulin-Dependent Protein Kinase II ; Signal Transduction ; Caenorhabditis Elegans ; Behavioral and Cognitive Neuroscience
  • Là 1 phần của: Journal of Neuroscience, 01/16/2013, Vol.33(3), pp.925-935
  • Mô tả: Dynamic serotonin biosynthesis is important for serotonin function; however, the mechanisms that underlie experience-dependent transcriptional regulation of the rate-limiting serotonin biosynthetic enzyme tryptophan hydroxylase (TPH) are poorly understood. Here, we characterize the molecular and cellular mechanisms that regulate increased transcription of Caenorhabditis elegans tph-1 in a pair of serotonergic neurons ADF during an aversive experience with pathogenic bacteria, a common environmental peril for worms. Training with pathogenic bacteria induces a learned aversion to the smell of the pathogen, a behavioral plasticity that depends on the serotonin signal from ADF neurons. We demonstrate that pathogen training increases ADF neuronal activity. While activating ADF increases tph-1 transcription, inhibiting ADF activity abolishes the training effect on tph-1, demonstrating the dependence of tph-1 transcriptional regulation on ADF neural activity. At the molecular level, the C. elegans homolog of CaMKII, UNC-43, functions cell-autonomously in ADF neurons to generate training-dependent enhancement in neuronal activity and tph-1 transcription, and this cell-autonomous function of UNC-43 is required for learning. Furthermore, selective expression of an activated form of UNC-43 in ADF neurons is sufficient to increase ADF activity and tph-1 transcription, mimicking the training effect. Upstream of ADF, the Gq alpha protein EGL-30 facilitates training-dependent induction of tph-1 by functional regulation of olfactory sensory neurons, which underscores the importance of sensory experience. Together, our work elucidates the molecular and cellular mechanisms whereby experience modulates tph-1 transcription.
  • Ngôn ngữ: English
  • Số nhận dạng: ISSN: 0270-6474 ; E-ISSN: 1529-2401 ; DOI: http://dx.doi.org/10.1523/JNEUROSCI.2355-12.2013

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