Beyond the genome—Towards an epigenetic understanding of handedness ontogenesis. (December 2017)
- Record Type:
- Journal Article
- Title:
- Beyond the genome—Towards an epigenetic understanding of handedness ontogenesis. (December 2017)
- Main Title:
- Beyond the genome—Towards an epigenetic understanding of handedness ontogenesis
- Authors:
- Schmitz, Judith
Metz, Gerlinde A.S.
Güntürkün, Onur
Ocklenburg, Sebastian - Abstract:
- Highlights: The molecular determinants of hemispheric asymmetries are not well understood. Studies revealed few genes accounting for a small part of handedness variance. Family studies indicated heritability of up to 0.66. Epigenetic mechanisms were suggested to contribute to this missing heritability. We review non-genetic influences on handedness and possible epigenetic mechanisms. Abstract: Hemispheric asymmetries represent one of the major organizational principles in vertebrate neurobiology, but their molecular determinants are not well understood. For handedness, the most widely investigated form of hemispheric asymmetries in humans, single gene explanations have been the most popular ontogenetic model in the past. However, molecular genetic studies revealed only few specific genes that explain a small fraction of the phenotypic variance. In contrast, family studies indicated heritability of up to 0.66. It has been suggested that the lack of recognizable genetic heritability is partly accounted for by heritable epigenetic mechanisms. Based on recent neuroscientific findings highlighting the importance of epigenetic mechanisms for brain function and disease, we review recent findings describing non-genetic influences on handedness from conception to childhood. We aim to advance the idea that epigenetic regulation might be the mediating mechanism between environment and phenotype. Recent findings on molecular epigenetic mechanisms indicate that particular asymmetries inHighlights: The molecular determinants of hemispheric asymmetries are not well understood. Studies revealed few genes accounting for a small part of handedness variance. Family studies indicated heritability of up to 0.66. Epigenetic mechanisms were suggested to contribute to this missing heritability. We review non-genetic influences on handedness and possible epigenetic mechanisms. Abstract: Hemispheric asymmetries represent one of the major organizational principles in vertebrate neurobiology, but their molecular determinants are not well understood. For handedness, the most widely investigated form of hemispheric asymmetries in humans, single gene explanations have been the most popular ontogenetic model in the past. However, molecular genetic studies revealed only few specific genes that explain a small fraction of the phenotypic variance. In contrast, family studies indicated heritability of up to 0.66. It has been suggested that the lack of recognizable genetic heritability is partly accounted for by heritable epigenetic mechanisms. Based on recent neuroscientific findings highlighting the importance of epigenetic mechanisms for brain function and disease, we review recent findings describing non-genetic influences on handedness from conception to childhood. We aim to advance the idea that epigenetic regulation might be the mediating mechanism between environment and phenotype. Recent findings on molecular epigenetic mechanisms indicate that particular asymmetries in DNA methylation might affect asymmetric gene expression in the central nervous system that in turn mediates handedness. We propose that an integration of genes and environment is essential to fully comprehend the ontogenesis of handedness and other hemispheric asymmetries. … (more)
- Is Part Of:
- Progress in neurobiology. Volume 159(2017:Dec.)
- Journal:
- Progress in neurobiology
- Issue:
- Volume 159(2017:Dec.)
- Issue Display:
- Volume 159 (2017)
- Year:
- 2017
- Volume:
- 159
- Issue Sort Value:
- 2017-0159-0000-0000
- Page Start:
- 69
- Page End:
- 89
- Publication Date:
- 2017-12
- Subjects:
- ADHD attention deficit hyperactivity disorder -- APOE apolipoprotein E gene -- AR androgen receptor gene -- bdnf brain derived neurotrophic factor -- CAH congenital adrenal hyperplasia -- CAIS complete androgen insensitivity syndrome -- COMT catechol-O-methyltransferase gene -- CYP2E1 cytochrome P450 2E1 gene -- DES diethylstilbestrol -- FKBP5 FK506 binding protein 5 gene -- GR glucocorticoid receptor gene -- IGF1R Insulin-like growth factor 1 receptor gene -- Lefty left-right determination factor -- LRRTM1 leucine rich repeat transmembrane neuronal 1 -- miRNAs microRNAs -- MRI magnetic resonance imaging -- NLH natural left-handers -- Nodal nodal growth differentiation factor -- NRH natural right-handers -- OXTR oxytocin receptor gene -- PCSK6 proprotein convertase subtilisin/kexin type 6 -- PLH pathological left-handedness -- PRH pathological right-handedness -- PRKCZ protein kinase C zeta gene -- SES socioeconomic status -- SETDB2 SET domain bifurcated 2 -- SNP single nucleotide polymorphism -- VIT vitrin gene
Lateralization -- Hemispheric asymmetry -- Functional preference -- Ontogenesis -- Handedness -- Epigenetics
Neurobiology -- Periodicals
Neurology -- Periodicals
Neurology -- Periodicals
Neurobiologie -- Périodiques
612.8 - Journal URLs:
- http://www.sciencedirect.com/science/journal/03010082 ↗
http://www.elsevier.com/journals ↗ - DOI:
- 10.1016/j.pneurobio.2017.10.005 ↗
- Languages:
- English
- ISSNs:
- 0301-0082
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 6870.300000
British Library DSC - BLDSS-3PM
British Library HMNTS - ELD Digital store - Ingest File:
- 5509.xml