DYRK1A Overexpression in Mice Downregulates the Gonadotropic Axis and Disturbs Early Stages of Spermatogenesis.


Journal

Genes
ISSN: 2073-4425
Titre abrégé: Genes (Basel)
Pays: Switzerland
ID NLM: 101551097

Informations de publication

Date de publication:
16 11 2021
Historique:
received: 24 10 2021
revised: 08 11 2021
accepted: 12 11 2021
entrez: 27 11 2021
pubmed: 28 11 2021
medline: 10 2 2022
Statut: epublish

Résumé

Down syndrome (DS) is the most common chromosomal disorder. It is responsible for intellectual disability (ID) and several medical conditions. Although men with DS are thought to be infertile, some spontaneous paternities have been reported. The few studies of the mechanism of infertility in men with DS are now dated. Recent research in zebrafish has indicated that overexpression of DYRK1A (the protein primarily responsible for ID in DS) impairs gonadogenesis at the embryonic stage. To better ascertain DYRK1A's role in infertility in DS, we investigated the effect of DYRK1A overexpression in a transgenic mouse model. We found that overexpression of DYRK1A impairs fertility in transgenic male mice. Interestingly, the mechanism in mice differs slightly from that observed in zebrafish but, with disruption of the early stages of spermatogenesis, is similar to that seen in humans. Unexpectedly, we observed hypogonadotropic hypogonadism in the transgenic mice.

Identifiants

pubmed: 34828406
pii: genes12111800
doi: 10.3390/genes12111800
pmc: PMC8621272
pii:
doi:

Substances chimiques

Protein-Tyrosine Kinases EC 2.7.10.1
Protein Serine-Threonine Kinases EC 2.7.11.1

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

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Auteurs

Rodolphe Dard (R)

Laboratoire Processus Dégénératifs, Stress et Vieillissement, Unité de Biologie Fonctionnelle et Adaptative (BFA), UMR 8251 CNRS, Université de Paris, 75205 Paris, France.
Université Paris-Saclay, UVSQ, INRAE, ENVA, BREED, 78350 Jouy-en-Josas, France.
Département de Génétique, CHI de Poissy St Germain en Laye, 78300 Poissy, France.

Manon Moreau (M)

Laboratoire Processus Dégénératifs, Stress et Vieillissement, Unité de Biologie Fonctionnelle et Adaptative (BFA), UMR 8251 CNRS, Université de Paris, 75205 Paris, France.

Estelle Parizot (E)

Laboratoire Processus Dégénératifs, Stress et Vieillissement, Unité de Biologie Fonctionnelle et Adaptative (BFA), UMR 8251 CNRS, Université de Paris, 75205 Paris, France.
Université Paris-Saclay, UVSQ, INRAE, ENVA, BREED, 78350 Jouy-en-Josas, France.

Farah Ghieh (F)

Université Paris-Saclay, UVSQ, INRAE, ENVA, BREED, 78350 Jouy-en-Josas, France.

Leslie Brehier (L)

Université Paris-Saclay, UVSQ, INRAE, ENVA, BREED, 78350 Jouy-en-Josas, France.

Nadim Kassis (N)

Laboratoire Processus Dégénératifs, Stress et Vieillissement, Unité de Biologie Fonctionnelle et Adaptative (BFA), UMR 8251 CNRS, Université de Paris, 75205 Paris, France.

Valérie Serazin (V)

Département de Génétique, CHI de Poissy St Germain en Laye, 78300 Poissy, France.

Antonin Lamaziere (A)

Centre de Recherche Saint-Antoine (CRSA), Sorbonne Université-INSERM, 75012 Paris, France.

Chrystèle Racine (C)

Centre de Recherche Saint-Antoine (CRSA), Sorbonne Université-INSERM, 75012 Paris, France.

Nathalie di Clemente (N)

Centre de Recherche Saint-Antoine (CRSA), Sorbonne Université-INSERM, 75012 Paris, France.

François Vialard (F)

Université Paris-Saclay, UVSQ, INRAE, ENVA, BREED, 78350 Jouy-en-Josas, France.
Département de Génétique, CHI de Poissy St Germain en Laye, 78300 Poissy, France.

Nathalie Janel (N)

Laboratoire Processus Dégénératifs, Stress et Vieillissement, Unité de Biologie Fonctionnelle et Adaptative (BFA), UMR 8251 CNRS, Université de Paris, 75205 Paris, France.

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Classifications MeSH