Evidence That Non-Syndromic Familial Tall Stature Has an Oligogenic Origin Including Ciliary Genes.


Journal

Frontiers in endocrinology
ISSN: 1664-2392
Titre abrégé: Front Endocrinol (Lausanne)
Pays: Switzerland
ID NLM: 101555782

Informations de publication

Date de publication:
2021
Historique:
received: 29 01 2021
accepted: 04 05 2021
entrez: 1 7 2021
pubmed: 2 7 2021
medline: 13 1 2022
Statut: epublish

Résumé

Human growth is a complex trait. A considerable number of gene defects have been shown to cause short stature, but there are only few examples of genetic causes of non-syndromic tall stature. Besides rare variants with large effects and common risk alleles with small effect size, oligogenic effects may contribute to this phenotype. Exome sequencing was carried out in a tall male (height 3.5 SDS) and his parents. Filtered damaging variants with high CADD scores were validated by Sanger sequencing in the trio and three other affected and one unaffected family members. Network analysis was carried out to assess links between the candidate genes, and the transcriptome of murine growth plate was analyzed by microarray as well as RNA Seq. Heterozygous gene variants in

Identifiants

pubmed: 34194391
doi: 10.3389/fendo.2021.660731
pmc: PMC8237855
doi:

Substances chimiques

CROCC protein, human 0
Carrier Proteins 0
Cell Cycle Proteins 0
Cep104 protein, human 0
Cytoskeletal Proteins 0
TOM1L2 protein, human 0
NEK1 protein, human EC 2.7.11.1
NIMA-Related Kinase 1 EC 2.7.11.1
Thiosulfate Sulfurtransferase EC 2.8.1.1

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

660731

Informations de copyright

Copyright © 2021 Weiss, Eberle, Roeth, de Bruin, Lui, Paramasivam, Hinderhofer, van Duyvenvoorde, Baron, Wit and Rappold.

Déclaration de conflit d'intérêts

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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Auteurs

Birgit Weiss (B)

Department of Human Molecular Genetics, Institute of Human Genetics, Ruprecht Karls University Heidelberg, Heidelberg, Germany.

Birgit Eberle (B)

Department of Human Molecular Genetics, Institute of Human Genetics, Ruprecht Karls University Heidelberg, Heidelberg, Germany.

Ralph Roeth (R)

Department of Human Molecular Genetics, Institute of Human Genetics, Ruprecht Karls University Heidelberg, Heidelberg, Germany.

Christiaan de Bruin (C)

Department of Pediatrics, Leiden University Medical Center, Leiden, Netherlands.

Julian C Lui (JC)

Section on Growth and Development, National Institute of Health, Bethesda, MD, United States.

Nagarajan Paramasivam (N)

Computational Oncology Group, Molecular Diagnostics Program at the National Center for Tumor Diseases (NCT) and German Cancer Research Center (DKFZ), Heidelberg, Germany.

Katrin Hinderhofer (K)

Institute of Human Genetics, Ruprecht Karls University Heidelberg, Heidelberg, Germany.

Hermine A van Duyvenvoorde (HA)

Department of Clinical Genetics, Leiden University Medical Center, Leiden, Netherlands.

Jeffrey Baron (J)

Section on Growth and Development, National Institute of Health, Bethesda, MD, United States.

Jan M Wit (JM)

Department of Pediatrics, Leiden University Medical Center, Leiden, Netherlands.

Gudrun A Rappold (GA)

Department of Human Molecular Genetics, Institute of Human Genetics, Ruprecht Karls University Heidelberg, Heidelberg, Germany.

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Classifications MeSH