Erratum: Corrigendum: Transcriptional regulator PRDM12 is essential for human pain perception

Abstract

In the version of this article initially published, there was an error with the affiliations for author Roman Chrast. His correct affiliations are:

Positive Regulatory Domain I–binding Factor 1 Mediates Peripheral Nerve Injury–induced Nociception in Mice by Repressing Kv4.3 Channel Expression

“…Notably, our findings are also supported by a recent clinical report that reveals that PRDM12 (a member of the PRDI-BF1 and RIZ homology domain-containing family) is essential for human perception of pain, as pathogenic mutations cause a congenital loss of pain perception in humans. 40 This clinical finding further indicates that the PRDI-BF1 and RIZ homology domain-containing family may play a role in pain perception and provides clinical support for our study.…”

Loss of G9a does not phenocopy the requirement for Prdm12 in the development of the nociceptive neuron lineage

“…At the root of the TrkA-lineage, from which emerge most if not all small diameter somatosensory neurons (i.e, nociceptors and C-LTMR), stands the histone methyltransferase (HMT) related transcriptional regulator Prdm12. In the recent years, several studies have shown how much Prdm12 is instrumental in the emergence of the TrkA-lineage, which fails to develop in its absence [10][11][12][13]15]. Mechanistically, Prdm12 appears to act as a pseudo methyltransferase as it has been shown to interact with G9a when overexpress in HEK29T3 cells and to increase H3K9me2 level when overexpressed in Xenopus neuralized animal cap explants [15,22].…”

“…In the recent years, several studies have shown how much Prdm12 is instrumental in the emergence of the TrkA-lineage, which fails to develop in its absence [10][11][12][13]15]. Mechanistically, Prdm12 appears to act as a pseudo methyltransferase as it has been shown to interact with G9a when overexpress in HEK29T3 cells and to increase H3K9me2 level when overexpressed in Xenopus neuralized animal cap explants [15,22]. However, the in vivo relevance of G9a for Prdm12 functions in the emergence of the nociceptive lineage during somatosensory neurogenesis has never been investigated.…”

“…Indeed, Prdm12 function is critical for the emergence of the entire pool of neurons arising from immature TrkA-expressing sensory neuron precursors as well as for TrkA expression itself [10–13]. Accordingly, in human, patients harbouring homozygous mutations of PRDM12 suffer from congenital insensitivity to pain (CIP), a rare developmental disorder associated with depletion of somatosensory fibers allowing the detection of noxious stimuli [14,15]. Moreover, as Prdm12 remains expressed in mature nociceptive neurons and its induced conditional ablation at adulthood alters some pain-related behaviours, it has been hypothesized as a potential new therapeutic target to treat pain related diseases [10,16,17].…”

“…While some PRDM family members possess intrinsic histone methyltransferase activity through their SET related PR domain, it appears not to be the case for Prdm12 which has been shown to be able to form a complex when overexpressed in H2K29T3 cells with G9a, a histone methyltransferase (HMT) that dimethylates histone H3 at lysine 9 (H3K9me2), a hallmark of epigenetic repression [22,23]. While some evidence have been obtained using P rdm12 overexpression experiments in Xenopus suggesting that this interaction with G9a may be functionally relevant for Prdm12’s activity [15,23], no in vivo evidence supporting this hypothesis is available.…”