Conditional Degradation of UNC-31/CAPS Enables Spatiotemporal Analysis of Neuropeptide Function

Rebecca Cornell, Wei Cao, Jie Liu, Roger Pocock

Research output: Contribution to journalArticleResearchpeer-review


Neuropeptide release from dense-core vesicles in Caenorhabditis elegans is promoted by UNC-31, ortholog of the calcium-dependent activator protein for secretion (CAPS). Loss of UNC-31 causes multiple phenotypes in C. elegans including reduced motility, retention of late-stage eggs, and reduction in evoked synaptic release. However, the ability to analyze UNC-31 function over discrete timescales and in specific neurons is lacking. Here, we generated and validated a tool to enable UNC-31 expression and spatiotemporal functional analysis. We show that endogenously tagged UNC-31 is expressed in major ganglia and nerve cords from late embryonic stages through to adult. Using the auxin-inducible degradation system, we depleted UNC-31 postembryonically from the hermaphrodite nervous system and revealed defects in egg laying, locomotion, and vesicle release that were comparable to those in unc-31 null mutant animals. In addition, we found that depleting UNC-31 specifically from the BAG sensory neurons causes increased intestinal fat storage, highlighting the spatial sensitivity of this system. Together, this protein degradation tool may be used to facilitate studies of neuropeptide function at precise cellular and temporal scales.

Original languageEnglish
Pages (from-to)8599-8607
Number of pages9
JournalThe Journal of Neuroscience
Issue number46
Publication statusPublished - 16 Nov 2022


  • behavior
  • Caenorhabditis elegans
  • CAPS
  • neuropeptide
  • physiology
  • UNC-31

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