4.8 Article

Sensory Neuron Fates Are Distinguished by a Transcriptional Switch that Regulates Dendrite Branch Stabilization

期刊

NEURON
卷 79, 期 2, 页码 266-280

出版社

CELL PRESS
DOI: 10.1016/j.neuron.2013.05.009

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资金

  1. National Institutes of Health (NIH) National Center for Research Resources
  2. NIH [R01 NS26115, R01 NS079611, R21 N206882, U01 HG004263, F31 NS071801]
  3. Deutsche Forschungsgemeinschaft [EXC115, GO1011/3-1, GO1011/4-1]
  4. Grants-in-Aid for Scientific Research [24390053] Funding Source: KAKEN
  5. Medical Research Council [MC_U105185857] Funding Source: researchfish
  6. MRC [MC_U105185857] Funding Source: UKRI

向作者/读者索取更多资源

Sensory neurons adopt distinct morphologies and functional modalities to mediate responses to specific stimuli. Transcription factors and their downstream effectors orchestrate this outcome but are incompletely defined. Here, we show that different classes of mechanosensory neurons in C. elegans are distinguished by the combined action of the transcription factors MEC-3, AHR-1, and ZAG-1. Low levels of MEC-3 specify the elaborate branching pattern of PVD nociceptors, whereas high MEC-3 is correlated with the simple morphology of AVM and PVM touch neurons. AHR-1 specifies AVM touch neuron fate by elevating MEC-3 while simultaneously blocking expression of nociceptive genes such as the MEC-3 target, the claudin-like membrane protein HPO-30, that promotes the complex dendritic branching pattern of PVD. ZAG-1 exercises a parallel role to prevent PVM from adopting the PVD fate. The conserved dendritic branching function of the Drosophila AHR-1 homolog, Spineless, argues for similar pathways in mammals.

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