Mutations in PRDM12 cause congenital insensitivity to pain, yet the mechanistic insights on the causative deficits are missing. Here we report that loss of PRDM12 function in mice results in a complete, selective absence of nociceptive neurons. Forcing PRDM12 expression in neural crest cells alters their neurogenic potential, but is not sufficient to drive the nociceptive neuron fate. These data reveal that PRDM12 is necessary for the generation of pain initiating neuron types during development.

PRDM12 is required for initiation of the nociceptive neuron lineage during neurogenesis / Bartesaghi, Luca; Wang, Yiqiao; Fontanet, Paula; Wanderoy, Simone; Berger, Finja; Wu, Haohao; Akkuratova, Natalia; Bouçanova, Filipa; Médard, Jean-Jacques; Petitpré, Charles; Landy, Mark A.; Zhang, Ming-Dong; Harrer, Philip; Stendel, Claudia; Stucka, Rolf; Dusl, Marina; Eleni Kastriti, Maria; Croci, Laura; Lai, Helen C.; Consalez, GIANGIACOMO GERMANO; Pattyn, Alexandre; Ernfors, Patrik; Senderek, Jan; Adameyko, Igor; Lallemend, Francois; Hadjab, Saida; Chrast, Roman. - In: CELL REPORTS. - ISSN 2211-1247. - 26:13(2019), pp. 3484-3492. [10.1016/j.celrep.2019.02.098]

PRDM12 is required for initiation of the nociceptive neuron lineage during neurogenesis

Gian Giacomo Consalez;
2019-01-01

Abstract

Mutations in PRDM12 cause congenital insensitivity to pain, yet the mechanistic insights on the causative deficits are missing. Here we report that loss of PRDM12 function in mice results in a complete, selective absence of nociceptive neurons. Forcing PRDM12 expression in neural crest cells alters their neurogenic potential, but is not sufficient to drive the nociceptive neuron fate. These data reveal that PRDM12 is necessary for the generation of pain initiating neuron types during development.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.11768/87138
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