Parental somatogonadal COL2A1 mosaicism contributes to intrafamilial recurrence in a family with type 2 collagenopathy.


Journal

American journal of medical genetics. Part A
ISSN: 1552-4833
Titre abrégé: Am J Med Genet A
Pays: United States
ID NLM: 101235741

Informations de publication

Date de publication:
03 2020
Historique:
received: 20 06 2019
revised: 17 09 2019
accepted: 29 10 2019
pubmed: 20 12 2019
medline: 5 1 2021
entrez: 20 12 2019
Statut: ppublish

Résumé

The COL2A1 gene encodes the alpha-1 chain of procollagen type 2. Pathogenic variants in the COL2A1 gene are associated with several different types of skeletal dysplasia collectively known as type 2 collagenopathies. Type 2 collagenopathies have an autosomal dominant inheritance. Some germline or somatogonadal mosaicism cases have been reported. We investigated whether somatogonadal mosaicism occurred in a family with two children suspected of type 2 collagenopathies or related diseases. First, we detected a pathogenic variant in the COL2A1 gene in the two affected children by whole exome sequencing (WES). Next, we performed targeted deep sequencing to their parents without the variant by WES. A low level of COL2A1 mosaicism was revealed in the mother's tissues. We concluded that the mother had somatogonadal mosaicism with the COL2A1 mutation arose in the epiblast, and that the intrafamilial recurrence rate of the disease by the somatogonadal mosaicism was higher than by the germline mosaicism. This report suggests that parental low-level mosaicism should be evaluated in those parents with children carrying de novo germline mutations and the targeted deep sequencing is useful to detect them.

Identifiants

pubmed: 31854518
doi: 10.1002/ajmg.a.61422
doi:

Substances chimiques

COL2A1 protein, human 0
Collagen Type II 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

454-460

Subventions

Organisme : Japan Agency for Medical Research and Development
ID : 16ek0109166h0002
Pays : International

Commentaires et corrections

Type : CommentIn

Informations de copyright

© 2019 Wiley Periodicals, Inc.

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Auteurs

Kenichi Yamamoto (K)

Department of Pediatrics, Osaka University Graduate School of Medicine, Osaka, Japan.
Department of Statistical Genetics, Osaka University Graduate School of Medicine, Osaka, Japan.

Takuo Kubota (T)

Department of Pediatrics, Osaka University Graduate School of Medicine, Osaka, Japan.

Shinji Takeyari (S)

Department of Pediatrics, Osaka University Graduate School of Medicine, Osaka, Japan.

Taichi Kitaoka (T)

Department of Pediatrics, Osaka University Graduate School of Medicine, Osaka, Japan.

Kei Miyata (K)

Department of Pediatrics, Osaka University Graduate School of Medicine, Osaka, Japan.

Yukako Nakano (Y)

Department of Pediatrics, Osaka University Graduate School of Medicine, Osaka, Japan.

Hirofumi Nakayama (H)

Department of Pediatrics, Osaka University Graduate School of Medicine, Osaka, Japan.

Yasuhisa Ohata (Y)

Department of Pediatrics, Osaka University Graduate School of Medicine, Osaka, Japan.

Kumiko Yanagi (K)

Department of Genome Medicine, National Center for Child Health and Development, Tokyo, Japan.

Tadashi Kaname (T)

Department of Genome Medicine, National Center for Child Health and Development, Tokyo, Japan.

Yukinori Okada (Y)

Department of Statistical Genetics, Osaka University Graduate School of Medicine, Osaka, Japan.

Keiichi Ozono (K)

Department of Pediatrics, Osaka University Graduate School of Medicine, Osaka, Japan.

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