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Wnt 分泌受四跨膜蛋白 HIC-1 与其相互作用蛋白 Neurabin/NAB-1 调节。

Wnt Secretion Is Regulated by the Tetraspan Protein HIC-1 through Its Interaction with Neurabin/NAB-1.

机构信息

Indian Institute of Science Education and Research (IISER) Mohali, Knowledge City, Sector 81, SAS Nagar, Manauli PO 140306, Punjab, India.

Queensland Brain Institute, Clem Jones Centre for Ageing Dementia Research (CJCADR), University of Queensland, Upland Road 79, St. Lucia, QLD 4072, Australia.

出版信息

Cell Rep. 2018 Nov 13;25(7):1856-1871.e6. doi: 10.1016/j.celrep.2018.10.053.

DOI:10.1016/j.celrep.2018.10.053
PMID:30428353
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6258899/
Abstract

The aberrant regulation of Wnt secretion is implicated in various neurological diseases. However, the mechanisms of Wnt release are still largely unknown. Here we describe the role of a C. elegans tetraspan protein, HIC-1, in maintaining normal Wnt release. We show that HIC-1 is expressed in cholinergic synapses and that mutants in hic-1 show increased levels of the acetylcholine receptor AChR/ACR-16. Our results suggest that HIC-1 maintains normal AChR/ACR-16 levels by regulating normal Wnt release from presynaptic neurons, as hic-1 mutants show an increase in secreted Wnt from cholinergic neurons. We further show that HIC-1 affects Wnt secretion by modulating the actin cytoskeleton through its interaction with the actin-binding protein NAB-1. In summary, we describe a protein, HIC-1, that functions as a neuromodulator by affecting postsynaptic AChR/ACR-16 levels by regulating presynaptic Wnt release from cholinergic motor neurons.

摘要

Wnt 分泌的异常调节与各种神经疾病有关。然而，Wnt 释放的机制在很大程度上仍然未知。在这里，我们描述了线虫中的一种四跨膜蛋白 HIC-1 在维持正常 Wnt 释放中的作用。我们发现 HIC-1 在胆碱能突触中表达，hic-1 突变体中乙酰胆碱受体 AChR/ACR-16 的水平升高。我们的结果表明，HIC-1 通过调节来自突触前神经元的正常 Wnt 释放来维持正常的 AChR/ACR-16 水平，因为 hic-1 突变体显示出胆碱能神经元分泌的 Wnt 增加。我们进一步表明，HIC-1 通过与肌动蛋白结合蛋白 NAB-1 的相互作用来调节肌动蛋白细胞骨架，从而影响 Wnt 的分泌。总之，我们描述了一种蛋白质 HIC-1，它通过调节来自胆碱能运动神经元的突触前 Wnt 释放来影响突触后 AChR/ACR-16 水平，从而作为神经调节剂发挥作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27d2/6258899/55da87845725/emss-80601-f007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27d2/6258899/3d37e780b181/emss-80601-f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27d2/6258899/6f9d752a55cb/emss-80601-f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27d2/6258899/0e4f748f820e/emss-80601-f003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27d2/6258899/ff30f4cd799b/emss-80601-f004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27d2/6258899/d2d31beab625/emss-80601-f005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27d2/6258899/59b199606ebf/emss-80601-f006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27d2/6258899/55da87845725/emss-80601-f007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27d2/6258899/3d37e780b181/emss-80601-f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27d2/6258899/6f9d752a55cb/emss-80601-f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27d2/6258899/0e4f748f820e/emss-80601-f003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27d2/6258899/ff30f4cd799b/emss-80601-f004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27d2/6258899/d2d31beab625/emss-80601-f005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27d2/6258899/59b199606ebf/emss-80601-f006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27d2/6258899/55da87845725/emss-80601-f007.jpg

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