Transcriptional regulator PRDM12 is essential for human pain perception
Geoffrey Woods, Jan Senderek and colleagues show that biallelic mutations in PRDM12 cause congenital insensitivity to pain. They further show that PRDM12 is expressed in nociceptors and their progenitors and participates in sensory neuron development in Xenopus . Pain perception has evolved as a war...
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| Published in | Nature genetics Vol. 47; no. 7; pp. 803 - 808 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
New York
Nature Publishing Group US
01.07.2015
Nature Publishing Group |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Geoffrey Woods, Jan Senderek and colleagues show that biallelic mutations in
PRDM12
cause congenital insensitivity to pain. They further show that PRDM12 is expressed in nociceptors and their progenitors and participates in sensory neuron development in
Xenopus
.
Pain perception has evolved as a warning mechanism to alert organisms to tissue damage and dangerous environments
1
,
2
. In humans, however, undesirable, excessive or chronic pain is a common and major societal burden for which available medical treatments are currently suboptimal
3
,
4
. New therapeutic options have recently been derived from studies of individuals with congenital insensitivity to pain (CIP)
5
,
6
. Here we identified 10 different homozygous mutations in
PRDM12
(encoding PRDI-BF1 and RIZ homology domain-containing protein 12) in subjects with CIP from 11 families. Prdm proteins are a family of epigenetic regulators that control neural specification and neurogenesis
7
,
8
. We determined that Prdm12 is expressed in nociceptors and their progenitors and participates in the development of sensory neurons in
Xenopus
embryos. Moreover, CIP-associated mutants abrogate the histone-modifying potential associated with wild-type Prdm12. Prdm12 emerges as a key factor in the orchestration of sensory neurogenesis and may hold promise as a target for new pain therapeutics
9
,
10
. |
|---|---|
| AbstractList | Pain perception has evolved as a warning mechanism to alert organisms to tissue damage and dangerous environments (1,2). In humans, however, undesirable, excessive or chronic pain is a common and major societal burden for which available medical treatments are currently suboptimal (3,4). New therapeutic options have recently been derived from studies of individuals with congenital insensitivity to pain (CIP) (5,6). Here we identified 10 different homozygous mutations in PRDM12 (encoding PRDI-BF1 and RIZ homology domain-containing protein 12) in subjects with CIP from 11 families. Prdm proteins are a family of epigenetic regulators that control neural specification and neurogenesis (7,8). We determined that Prdm12 is expressed in nociceptors and their progenitors and participates in the development of sensory neurons in Xenopus embryos. Moreover, CIP-associated mutants abrogate the histone-modifying potential associated with wild-type Prdm12. Prdm12 emerges as a key factor in the orchestration of sensory neurogenesis and may hold promise as a target for new pain therapeutics (9,10). Pain perception has evolved as a warning mechanism to alert organisms to tissue damage and dangerous environments. In humans, however, undesirable, excessive or chronic pain is a common and major societal burden for which available medical treatments are currently suboptimal. New therapeutic options have recently been derived from studies of individuals with congenital insensitivity to pain (CIP). Here we identified 10 different homozygous mutations in PRDM12 (encoding PRDI-BF1 and RIZ homology domain-containing protein 12) in subjects with CIP from 11 families. Prdm proteins are a family of epigenetic regulators that control neural specification and neurogenesis. We determined that Prdm12 is expressed in nociceptors and their progenitors and participates in the development of sensory neurons in Xenopus embryos. Moreover, CIP-associated mutants abrogate the histone-modifying potential associated with wild-type Prdm12. Prdm12 emerges as a key factor in the orchestration of sensory neurogenesis and may hold promise as a target for new pain therapeutics. Pain perception has evolved as a warning mechanism to alert organisms to tissue damage and dangerous environments 1 , 2 . In humans, however, undesirable, excessive or chronic pain is a common and major societal burden for which available medical treatments are currently suboptimal 3 , 4 . New therapeutic options have recently been derived from studies of individuals with congenital insensitivity to pain (CIP) 5 , 6 . Here we identified 10 different homozygous mutations in PRDM12 (encoding PRDI-BF1 and RIZ homology domain-containing protein 12) in subjects with CIP from 11 families. Prdm proteins are a family of epigenetic regulators that control neural specification and neurogenesis 7 , 8 . We determined that Prdm12 is expressed in nociceptors and their progenitors and participates in the development of sensory neurons in Xenopus embryos. Moreover, CIP-associated mutants abrogate the histone-modifying potential associated with wild-type Prdm12. Prdm12 emerges as a key factor in the orchestration of sensory neurogenesis and may hold promise as a target for new pain therapeutics 9 , 10 . Pain perception has evolved as a warning mechanism to alert organisms to tissue damage and dangerous environments1,2. In humans, however, undesirable, excessive or chronic pain is a common and major societal burden for which available medical treatments are currently suboptimal3,4. New therapeutic options have recently been derived from studies of individuals with congenital insensitivity to pain (CIP)5,6. Here we identified 10 different homozygous mutations in PRDM12 (encoding PRDI-BF1 and RIZ homology domain-containing protein 12) in subjects with CIP from 11 families. Prdm proteins are a family of epigenetic regulators that control neural specification and neurogenesis7,8. We determined that Prdm12 is expressed in nociceptors and their progenitors and participates in the development of sensory neurons in Xenopus embryos. Moreover, CIP-associated mutants abrogate the histone-modifying potential associated with wild-type Prdm12. Prdm12 emerges as a key factor in the orchestration of sensory neurogenesis and may hold promise as a target for new pain therapeutics9,10. Geoffrey Woods, Jan Senderek and colleagues show that biallelic mutations in PRDM12 cause congenital insensitivity to pain. They further show that PRDM12 is expressed in nociceptors and their progenitors and participates in sensory neuron development in Xenopus . Pain perception has evolved as a warning mechanism to alert organisms to tissue damage and dangerous environments 1 , 2 . In humans, however, undesirable, excessive or chronic pain is a common and major societal burden for which available medical treatments are currently suboptimal 3 , 4 . New therapeutic options have recently been derived from studies of individuals with congenital insensitivity to pain (CIP) 5 , 6 . Here we identified 10 different homozygous mutations in PRDM12 (encoding PRDI-BF1 and RIZ homology domain-containing protein 12) in subjects with CIP from 11 families. Prdm proteins are a family of epigenetic regulators that control neural specification and neurogenesis 7 , 8 . We determined that Prdm12 is expressed in nociceptors and their progenitors and participates in the development of sensory neurons in Xenopus embryos. Moreover, CIP-associated mutants abrogate the histone-modifying potential associated with wild-type Prdm12. Prdm12 emerges as a key factor in the orchestration of sensory neurogenesis and may hold promise as a target for new pain therapeutics 9 , 10 . |
| Audience | Academic |
| Author | von Au, Katja Stendel, Claudia Weiss, Caecilia Katona, Istvan Parman, Yesim Chen, Ya-Chun Samara, Chrysanthi Schmid, Annina B Weis, Joachim Zitzelsberger, Manuela Baumgartner, Manuela Murphy, Sinead M Irvine, Alan D Young, Gareth T Kropatsch, Regina Auer-Grumbach, Michaela Senderek, Jan Cho, Lily Ting-Yin Themistocleous, Andreas C Valente, Enza Maria Carvalho, Ofélia P Moore, Adrian W Shaikh, Samiha S Karbani, Gulshan Stucka, Rolf Willems, Patrick J Restrepo, Carlos M Nahorski, Michael S Rautenstrauss, Bernd Chrast, Roman Nicholas, Adeline K Bergmann, Carsten McHugh, John C Reimann, Frank Jensen, Uffe Birk Reilly, Mary M Woods, C Geoffrey Cilio, Maria Roberta Watson, Rosemarie M Matsukawa, Shinya De Jonghe, Peter Michiue, Tatsuo Strom, Tim M Pereira, Diego Schabhüttl, Maria Bennett, David L H Graul-Neumann, Luitgard Dusl, Marina Finke, Christian Hertz, Jens Michael Kurth, Ingo Wieland, Thomas Moog, Ute Baets, Jonathan McAleer, Maeve A Passarge, Eberhard Stafford, Fay Heinritz, Wolfram Windhager, Reinhard |
| AuthorAffiliation | 48 Department of Human Genetics, Ruhr-University Bochum, Bochum, Germany 9 Institute of Human Genetics, Technische Universität München, Munich, Germany 23 Neurogenetics Unit, Casa Sollievo della Sofferenza, San Giovanni Rotondo, Italy 25 Unidad de Genética, Universidad del Rosario, Bogotá, Colombia 7 Brain Function Research Group, School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa 34 Department of Neuroscience, Bambino Gesù Children’s Hospital and Research Institute, Rome, Italy 51 Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden 46 Department of Neurology, Antwerp University Hospital, Antwerp, Belgium 49 Institute of Human Genetics, Jena University Hospital, Jena, Germany 15 Ambulantes Gesundheitszentrum der Charité Campus Virchow (Humangenetik), Universitätsmedizin Berlin, Berlin, Germany 44 Neurogenetics Group, VIB Department of Molecular Genetics, University of Antwerp, Antwerp, Belgium 1 Department of Med |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/26005867$$D View this record in MEDLINE/PubMed http://kipublications.ki.se/Default.aspx?queryparsed=id:131562917$$DView record from Swedish Publication Index |
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| Snippet | Geoffrey Woods, Jan Senderek and colleagues show that biallelic mutations in
PRDM12
cause congenital insensitivity to pain. They further show that PRDM12 is... Pain perception has evolved as a warning mechanism to alert organisms to tissue damage and dangerous environments. In humans, however, undesirable, excessive... Pain perception has evolved as a warning mechanism to alert organisms to tissue damage and dangerous environments (1,2). In humans, however, undesirable,... Pain perception has evolved as a warning mechanism to alert organisms to tissue damage and dangerous environments1,2. In humans, however, undesirable,... Pain perception has evolved as a warning mechanism to alert organisms to tissue damage and dangerous environments 1 , 2 . In humans, however, undesirable,... |
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| Title | Transcriptional regulator PRDM12 is essential for human pain perception |
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