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. 2021 Jan 8;15(1):156–164. doi: 10.1080/19336950.2020.1860383

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© 2021 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 2. — Cell-specific epigenetic factors control functional splicing in nociceptors

Exons 37a and 37b are mutually exclusive in Cacna1b mRNA. Left, in Trpv1 nociceptors, the master chromatin regulator CTCF binds unmethylated e37a locus in Cacna1b gene and promotes e37a inclusion in mRNAs. Ca_V2.2-e37a channels are strongly inhibited by μ-opioid receptor (μOR) activation, promoting morphine analgesia in spinal cord. DNMT3a promotes, and TET1/2 reduces, e37a methylation (5-mC) levels in Cacna1b respectively. Right, following nerve injury that results in neuropathic pain, e37a methylation (5-mC) levels increase, CTCF binding is impaired, and e37a is skipped and e37b is included in mRNAs. Ca_V2.2-e37b channels are weakly inhibited by μOR activation. This disrupted splicing pattern following nerve injury is associated with a concomitant reduced efficacy of morphine in vivo. This figure is modified and reproduced from [25] in accordance with eLife CC-BY license.