Total submissions: 6
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV000482307 | SCV000567022 | pathogenic | not provided | 2015-06-26 | criteria provided, single submitter | clinical testing | The c.1 A>G variant in the SEPN1 gene has been identified previously, both in the compound heterozygousand homozygous state, in patients with SEPN1-related disorders. Patient's presented with multiple featuresincluding rigid spine, nasal speech and various histological findings including minicores (Ferreiro et al., 2002;Maggi et al., 2013). The variant alters the initiator Methionine codon, and the resultant protein would bedescribed as p.Met1?" to signify that it is not known if the loss of Met1 means that all protein translation iscompletely prevented or if an abnormal protein is produced using an alternate Methionine initiator codon.Therefore, c.1 A>G is considered a pathogenic variant." |
Labcorp Genetics |
RCV000004748 | SCV000758294 | pathogenic | Eichsfeld type congenital muscular dystrophy | 2025-01-01 | criteria provided, single submitter | clinical testing | This sequence change affects the initiator methionine of the SELENON mRNA. The next in-frame methionine is located at codon 85. The frequency data for this variant in the population databases is considered unreliable, as metrics indicate poor data quality at this position in the gnomAD database. Disruption of the initiator codon has been observed in individuals with SELENON-related conditions (PMID: 12192640, 23394784, 28558865). ClinVar contains an entry for this variant (Variation ID: 4491). For these reasons, this variant has been classified as Pathogenic. |
MGZ Medical Genetics Center | RCV002288464 | SCV002581201 | pathogenic | Congenital myopathy with fiber type disproportion | 2021-11-15 | criteria provided, single submitter | clinical testing | |
Fulgent Genetics, |
RCV002504747 | SCV002816949 | likely pathogenic | Eichsfeld type congenital muscular dystrophy; Congenital myopathy with fiber type disproportion | 2021-11-15 | criteria provided, single submitter | clinical testing | |
Broad Center for Mendelian Genomics, |
RCV000004748 | SCV006079730 | likely pathogenic | Eichsfeld type congenital muscular dystrophy | 2025-04-29 | criteria provided, single submitter | curation | The heterozygous p.Met1Val variant in SELENON has been reported in at least 7 individuals with rigid spine muscular dystrophy 1 (PMID: 12192640, 16365872, 23394784, 28558865), and has been identified in 0.013% (17406) of East Asian chromosomes by the Genome Aggregation Database (gnomAD, http://gnomad.broadinstitute.org; dbSNP rs121908184). Although this variant has been seen in the general population in a heterozygous state, its frequency is low enough to be consistent with a recessive carrier frequency. This variant has been reported in ClinVar (VCV000004491.15) and has been interpreted as pathogenic/likely pathogenic by multiple submitters. Of the 7 affected individuals, 2 were compound heterozygotes that carried a reported pathogenic variant in trans, which increases the likelihood that the p.Met1Val variant is pathogenic (VCV000373075.21; PMID: 16365872, 28558865). This variant is located in the first amino acid and abolishes the methionine initiation codon. The next in-frame methionine is at amino acid residue 85 and there are multiple reported pathogenic/likely pathogenic variants in ClinVar upstream of this downstream methionine. Loss of function of the SELENON gene is an established disease mechanism in autosomal recessive rigid spine muscular dystrophy 1. In summary, although additional studies are required to fully establish its clinical significance, this variant is likely pathogenic for autosomal recessive rigid spine muscular dystrophy 1. ACMG/AMP Criteria PM3_strong, PVS1_moderate, PM2_supporting (Richards 2015). |
OMIM | RCV000004748 | SCV000024924 | pathogenic | Eichsfeld type congenital muscular dystrophy | 2006-03-01 | no assertion criteria provided | literature only |