Structural Asymmetry in the Frontal and Temporal Lobes Is Associated with PCSK6 VNTR Polymorphism.
Language
Laterality
PCSK6
Superior temporal sulcus
VNTR
Journal
Molecular neurobiology
ISSN: 1559-1182
Titre abrégé: Mol Neurobiol
Pays: United States
ID NLM: 8900963
Informations de publication
Date de publication:
Nov 2019
Nov 2019
Historique:
received:
04
03
2019
accepted:
10
05
2019
pubmed:
23
5
2019
medline:
13
3
2020
entrez:
23
5
2019
Statut:
ppublish
Résumé
The nodal cascade influences the development of bodily asymmetries in humans and other vertebrates. The gene PCSK6 has shown a regulatory function during left-right axis formation and is therefore thought to influence bodily left-right asymmetries. However, it is not clear if variation in this gene is also associated with structural asymmetries in the brain. We genotyped an intronic 33bp PCSK6 variable number tandem repeat (VNTR) polymorphism that has been associated with handedness in a cohort of healthy adults. We acquired T1-weighted structural MRI images of 320 participants and defined cortical surface and thickness for each HCP region. The results demonstrate a significant association between PCSK6 VNTR genotypes and gray matter asymmetry in the superior temporal sulcus, which is involved in voice perception. Heterozygous individuals who carry a short (≤ 6 repeats) and a long (≥ 9 repeats) PCSK6 VNTR allele show stronger rightward asymmetry. Further associations were evident in the dorsolateral prefrontal cortex. Here, individuals homozygous for short alleles show a more pronounced asymmetry. This shows that PCSK6, a gene that has been implicated in the ontogenesis of bodily asymmetries by regulating the nodal cascade, is also relevant for structural asymmetries in the human brain.
Identifiants
pubmed: 31115778
doi: 10.1007/s12035-019-01646-1
pii: 10.1007/s12035-019-01646-1
doi:
Substances chimiques
PCSK6 protein, human
EC 3.4.21.-
Proprotein Convertases
EC 3.4.21.-
Serine Endopeptidases
EC 3.4.21.-
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
7765-7773Subventions
Organisme : Deutsche Forschungsgemeinschaft
ID : OC 127/9-1
Organisme : Deutsche Forschungsgemeinschaft
ID : GU 227/16-1
Organisme : Deutsche Forschungsgemeinschaft
ID : GE 2777/2-1
Organisme : Deutsche Forschungsgemeinschaft
ID : SFB 940
Organisme : Deutsche Forschungsgemeinschaft
ID : SFB 1280 project A03
Organisme : Mercur Foundation
ID : An-2015-0044
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