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

NLR-1/CASPR Anchors F-Actin to Promote Gap Junction Formation.
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DOI:
10.1016/j.devcel.2020.10.020
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发表时间:
2020-12-07
期刊:
影响因子:
11.8
通讯作者:
Yan D
Yan D
中科院分区:
生物学1区
文献类型:
--
作者:
Meng L;Yan D

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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. Meng et al. reveal the role of the conserved EGF- and Laminin G- domain-containing protein nlr-1/CASPR in control of the formation of gap junctions in multiple tissues across different developmental stages, and show that NLR-1 forms gap junction through recruiting F-actin networks at the gap junction formation plaque
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