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.

半球不对称是脊椎动物神经生物学的主要组织原理之一，但其分子决定因素尚未得到很好的理解。对于惯用性，这是人类半球不对称最广泛研究的形式，单基因解释在过去是最流行的本体模型。但是，分子遗传学研究仅揭示了解释少数表型变异的特定基因。相反，家庭研究表明遗传力高达0.66。已经提出，可识别的遗传遗传力的缺乏部分是由可遗传的表观遗传机制引起的。根据最近的神经科学发现强调了表观遗传机制对脑功能和疾病的重要性，我们回顾了最近的发现，这些发现描述了从概念到童年对惯用性的非遗传影响。我们旨在提出表观遗传调控可能是环境和表型之间的中介机制的想法。关于分子表观遗传机制的最新发现表明，DNA甲基化中的特定不对称性可能会影响中枢神经系统中不对称基因的表达，进而介导上手性。我们提出基因和环境的整合对于充分理解手性和其他半球不对称的本体是必不可少的。关于分子表观遗传机制的最新发现表明，DNA甲基化中的特定不对称性可能会影响中枢神经系统中不对称基因的表达，进而介导上手性。我们建议基因和环境的整合对于充分理解手性和其他半球不对称性的本体形成是必不可少的。关于分子表观遗传机制的最新发现表明，DNA甲基化中的特定不对称性可能会影响中枢神经系统中不对称基因的表达，进而介导上手性。我们提出基因和环境的整合对于充分理解手性和其他半球不对称的本体是必不可少的。