NLR-1/CASPR Anchors F-Actin to Promote Gap Junction Formation.

Journal Article (Journal Article)

Gap junctions are present in most tissues and play essential roles in various biological processes. However, we know surprisingly little about the molecular mechanisms underlying gap junction formation. Here, we uncover the essential role of a conserved EGF- and laminin-G-domain-containing protein nlr-1/CASPR in the regulation of gap junction formation in multiple tissues across different developmental stages in C. elegans. NLR-1 is located in the gap junction perinexus, a region adjacent to but not overlapping with gap junctions, and forms puncta before the clusters of gap junction channels appear on the membrane. We show that NLR-1 can directly bind to actin to recruit F-actin networks at the gap junction formation plaque, and the formation of F-actin patches plays a critical role in the assembly of gap junction channels. Our findings demonstrate that nlr-1/CASPR acts as an early stage signal for gap junction formation through anchoring of F-actin networks.

Full Text

Duke Authors

Cited Authors

  • Meng, L; Yan, D

Published Date

  • December 7, 2020

Published In

Volume / Issue

  • 55 / 5

Start / End Page

  • 574 - 587.e3

PubMed ID

  • 33238150

Pubmed Central ID

  • PMC7725993

Electronic International Standard Serial Number (EISSN)

  • 1878-1551

Digital Object Identifier (DOI)

  • 10.1016/j.devcel.2020.10.020


  • eng

Conference Location

  • United States