Evidence map›Paper›PMID 15883838›Full record

ArticleHuman genetics2005

Anatomy of a founder effect: myotonic dystrophy in Northeastern Quebec.

Vania Yotova, Damian Labuda, Ewa Zietkiewicz, Dominik Gehl, Alan Lovell, Jean-François Lefebvre, Stéphane Bourgeois, Emilie Lemieux-Blanchard, Marcin Labuda, Hélène Vézina and 6 more

Abstract read
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In one paragraph

Article in Human genetics, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Myotonic dystrophy type 1.CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne · 2016
    Article
  15. Myotonic dystrophy.Neurologic clinics · 2014
    Review
  16. Observational
  17. Article
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors.

Vania YotovaCentre de recherche, Hôpital Sainte-Justine, 3175 Côte Sainte-Catherine, Montréal, PQ, Canada, H3T 1C5.
Damian Labuda
Ewa Zietkiewicz
Dominik Gehl
Alan Lovell
Jean-François Lefebvre
Stéphane Bourgeois
Emilie Lemieux-Blanchard
Marcin Labuda
Hélène Vézina
Louis Houde
Marc Tremblay
Bruno Toupance
Evelyne Heyer
Thomas J Hudson
Claude Laberge

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Founder effects are largely responsible for changes in frequency profiles of genetic variants in local populations or isolates. They are often recognized by elevated incidence of certain hereditary disorders as observed in regions of Charlevoix and Saguenay-Lac-Saint-Jean (SLSJ) in Northeastern Quebec. Dominantly transmitted myotonic dystrophy (DM1) is highly prevalent in SLSJ where its carrier rate reaches 1/550, compared with 1/5,000 to 1/50,000 elsewhere. To shed light on the origin of DM1 in this region, we have screened 50 nuclear DM1 families from SLSJ and studied the genetic variation in a 2.05 Mb (2.9 cM) segment spanning the site of the expansion mutation. The markers analyzed included 22 biallelic SNPs and two microsatellites. Among 50 independent DM1 chromosomes, we distinguished ten DM1-associated haplotypes and grouped them into three haplotype families, A, B and C, based on the relevant extent of allele sharing between them. To test whether the data were consistent with a single entry of the mutation into SLSJ, we evaluated the age of the founder effect from the proportion of recombinant haplotypes. Taking the prevalent haplotype A1_21 (58%) as ancestral to all the disease-associated haplotypes in this study, the estimated age of the founder effect was 19 generations, long predating the colonization of Nouvelle-France. In contrast, considering A1_21 as ancestral to the haplotype family A only, yielded the estimated founder age of nine generations, consistent with the settlement of Charlevoix at the turn of 17th century and subsequent colonization of SLSJ. We conclude that it was the carrier of haplotype A (present day carrier rate of 1/730) that was a "driver" of the founder effect, while minor haplotypes B and C, with corresponding carrier rates of 1/3,000 and 1/10,000, respectively, contribute DM1 to the incidence level known in other populations. Other studies confirm that this might be a general scenario in which a major "driver" mutation/haplotype issued from a founder effect is found accompanied by distinct minor mutations/haplotypes occurring at background population frequencies.

Indexed as

AllelesFounder EffectPolymorphism, Single NucleotideFemaleHaplotypesHeterozygoteHumansMaleMicrosatellite RepeatsMutationMyotonic DystrophyQuebec

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.