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神经元钙调蛋白水平受 CAMTA 转录因子控制。

Neuronal calmodulin levels are controlled by CAMTA transcription factors.

机构信息

Cell Biology Division, Medical Research Council Laboratory of Molecular Biology, Cambridge, United Kingdom.

Institute of Science and Technology Austria (IST Austria), Klosterneuburg, Austria.

出版信息

Elife. 2021 Sep 9;10:e68238. doi: 10.7554/eLife.68238.

DOI:10.7554/eLife.68238
PMID:34499028
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8428840/
Abstract

The ubiquitous Ca sensor calmodulin (CaM) binds and regulates many proteins, including ion channels, CaM kinases, and calcineurin, according to Ca-CaM levels. What regulates neuronal CaM levels, is, however, unclear. CaM-binding transcription activators (CAMTAs) are ancient proteins expressed broadly in nervous systems and whose loss confers pleiotropic behavioral defects in flies, mice, and humans. Using and , we show that CAMTAs control neuronal CaM levels. The behavioral and neuronal Ca signaling defects in mutants lacking the sole CAMTA, can be rescued by supplementing neuronal CaM. CAMT-1 binds multiple sites in the CaM promoter and deleting these sites phenocopies . Our data suggest CAMTAs mediate a conserved and general mechanism that controls neuronal CaM levels, thereby regulating Ca signaling, physiology, and behavior.

摘要

普遍存在的钙传感器钙调蛋白 (CaM) 根据 Ca-CaM 水平结合并调节许多蛋白质，包括离子通道、CaM 激酶和钙调神经磷酸酶。然而，调节神经元 CaM 水平的机制尚不清楚。CaM 结合转录激活因子 (CAMTAs) 是在神经系统中广泛表达的古老蛋白质，其缺失会导致果蝇、小鼠和人类出现多种行为缺陷。使用 和 ，我们表明 CAMTAs 控制神经元 CaM 水平。缺乏唯一的 CAMTA 的突变体的行为和神经元 Ca 信号缺陷可以通过补充神经元 CaM 来挽救。CAMT-1 结合 CaM 启动子中的多个位点，并且删除这些位点模拟 。我们的数据表明，CAMTAs 介导一种保守且普遍的机制，控制神经元 CaM 水平，从而调节 Ca 信号、生理学和行为。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc36/8428840/c299d567d7c3/elife-68238-fig7-figsupp1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc36/8428840/c299d567d7c3/elife-68238-fig7-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc36/8428840/32e8a5038ce8/elife-68238-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc36/8428840/a5232a7de144/elife-68238-fig1-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc36/8428840/1b5e7db55960/elife-68238-fig1-figsupp2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc36/8428840/9960b4b2029f/elife-68238-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc36/8428840/2d2187ec41c3/elife-68238-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc36/8428840/2f311c47d12c/elife-68238-fig3-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc36/8428840/6a94473a1c42/elife-68238-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc36/8428840/f1fc0370dffd/elife-68238-fig4-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc36/8428840/d8cd9f50cd8d/elife-68238-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc36/8428840/2b40137abe1f/elife-68238-fig5-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc36/8428840/68e06d7f0bf4/elife-68238-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc36/8428840/57e3758d69e9/elife-68238-fig6-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc36/8428840/0bb4783de775/elife-68238-fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc36/8428840/c299d567d7c3/elife-68238-fig7-figsupp1.jpg

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