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Adam MP, Feldman J, Mirzaa GM, et al., editors. GeneReviews® [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2024.

Resources for Genetics Professionals — Genetic Disorders Associated with Founder Variants Common in the Gitxsan Population

, MD
Senior Editor, GeneReviews
Clinical Professor, Department of Pediatrics
University of Washington
Seattle, Washington
, PhD
Consulting Editor, GeneReviews
Variant Scientist, Department of Laboratories
Seattle Children’s Hospital
Seattle, Washington

Initial Posting: .

Estimated reading time: 1 minute

A founder variant is a pathogenic variant observed at high frequency in a specific population due to the presence of the variant in a single ancestor or small number of ancestors. The presence of a founder variant can affect the approach to molecular genetic testing. When one or more founder variants account for a large percentage of all pathogenic variants found in a population, testing for the founder variant(s) may be performed first.

The table below includes common founder variants – here defined as three or fewer variants that account for >50% of the pathogenic variants identified in a single gene in individuals of a specific ancestry – in individuals of Gitxsan ancestry. Note: Pathogenic variants that are common worldwide due to a DNA sequence hot spot are not considered founder variants and thus are not included.

Table.

Genetic Disorders Associated with Founder Variants Common in the Gitxsan Population

GeneDisorderMOIDNA Nucleotide ChangePredicted Protein Change% of Pathogenic Variants in Gene 1Carrier FrequencyEthnicityReference SequencesReferences
ANK2 Long QT syndrome 4 (OMIM 600919)ADc.1937C>Tp.Ser646Phe<100%NAGitxsan NM_001148​.6
NP_001139​.3
Swayne et al [2017]
KCNQ1 Long QT syndrome 1 (OMIM 192500)ADc.613G>Ap.Val205Met<100%NAGitxsan NM_000218​.3
NP_000209​.2
Arbour et al [2008], Jackson et al [2014]

Included if ≤3 pathogenic variants account for ≥50% of variants identified in a specific ethnic group

AD = autosomal dominant; MOI = mode of inheritance; NA = not applicable

1.

This percentage does not account for the possibility of rare de novo pathogenic variants occurring in this population.

References

  • Arbour L, Rezazadeh S, Eldstrom J, Weget-Simms G, Rupps R, Dyer Z, Tibbits G, Accili E, Casey B, Kmetic A, Sanatani S, Fedida D. A. KCNQ1 V205M missense mutation causes a high rate of long QT syndrome in a First Nations community of northern British Columbia: a community-based approach to understanding the impact. Genet Med. 2008;10:545–50. [PubMed: 18580685]
  • Jackson HA, McIntosh S, Whittome B, Asuri S, Casey B, Kerr C, Tang A, Arbour LT. LQTS in northern BC: homozygosity for KCNQ1 V205M presents with a more severe cardiac phenotype but with minimal impact on auditory function. Clin Genet. 2014;86:85–90. [PubMed: 23844633]
  • Swayne LA, Murphy NP, Asuri S, Chen L, Xu X, McIntosh S, Wang C, Lancione PJ, Roberts JD, Kerr C, Sanatani S, Sherwin E, Kline CF, Zhang M, Mohler PJ, Arbour LT. Novel variant in the ANK2 membrane-binding domain is associated with ankyrin-B syndrome and structural heart disease in a First Nations population with a high rate of long QT syndrome. Circ Cardiovasc Genet. 2017;10:e001537. [PMC free article: PMC5312931] [PubMed: 28196901]

Revision History

  • 11 August 2022 (sw) Initial posting
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