Massachusetts Institute of Technology

education 📍 Cambridge, United States
Massachusetts Institute of Technology
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Associated Institutions

Broad Institute
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McGovern Institute for Brain Research
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Ragon Institute of MGH, MIT and Harvard
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Massachusetts Green High Performance Computing Center
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Massachusetts Space Grant Consortium
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Publications

Gene variants associated with pediatric-onset erythromelalgia: Mendelian and rare-variant association analyses.

Yonas MC, Ocay DD, Genetti CA, Lobo K, Fernandes M , et al.
Pain reports •

Erythromelalgia is a descriptive term for burning pain and erythema in distal extremities, often worsened by heat and improved by cold. Inherited erythromelalgia has been primarily linked to gain-of-function variants in , encoding voltage-gated sodium channel NaV1.7. However, approximately 65% to 85% of patients with erythromelalgia do not have pathogenic variants. The objective of this study was to uncover and assess gene variants potentially associated with pediatric-onset erythromelalgia. With IRB approval and informed consent, probands and families with erythromelalgia underwent next-generation sequencing. A list of genes of interest was produced based on Mendelian inheritance models. Selected gene candidates were assessed using the Sequence Kernel Association Test-Optimal (SKAT-O). Sixty-two probands with erythromelalgia and their relatives were included in Mendelian analysis, which identified variants in PR domain zinc finger protein 12 () and dihydropyrimidinase-like protein 2 (). In a targeted 12-gene rare-variant set analysis using SKAT-O, zinc finger homeobox protein 2 () showed evidence of association ( = 6.9 × 10), surpassing Bonferroni correction for 12 tests (α = 4.17 × 10), whereas showed only a nominal association signal ( = 0.03) that did not survive multiple-testing correction. Genes associated with both increased and decreased pain sensitivity are of considerable interest for elucidating pain mechanisms and analgesic development. As rare variants in and were identified in a pediatric erythromelalgia cohort and a gene-based rare-variant association signal for was identified, replication and functional validation are needed.

Erythromelalgia caused by the missense mutation p.Arg220Pro in an alternatively spliced exon of SCN9A (NaV1.7).

Deuis JR, Kumble S, Keramidas A, Ragnarsson L, Simons C , et al.
Human molecular genetics •

Erythromelalgia (EM), is a familial pain syndrome characterized by episodic 'burning' pain, warmth, and erythema. EM is caused by monoallelic variants in SCN9A, which encodes the voltage-gated sodium channel (NaV) NaV1.7. Over 25 different SCN9A mutations attributed to EM have been described to date, all identified in the SCN9A transcript utilizing exon 6N. Here we report a novel SCN9A missense variant identified in seven related individuals with stereotypic episodes of bilateral lower limb pain presenting in childhood. The variant, XM_011511617.3:c.659G>C;p.(Arg220Pro), resides in the exon 6A of SCN9A, an exon previously shown to be selectively incorporated by developmentally regulated alternative splicing. The mutation is located in the voltage-sensing S4 segment of domain I, which is important for regulating channel activation. Functional analysis showed the p.Arg220Pro mutation altered voltage-dependent activation and delayed channel inactivation, consistent with a NaV1.7 gain-of-function molecular phenotype. These results demonstrate that alternatively spliced isoforms of SCN9A should be included in all genomic testing of EM.