Anthropology, Stony Brook University, Stony Brook, New York, USA.
Cell Biology and Anatomy, University of Calgary Cumming School of Medicine, Calgary, Canada.
J Anat. 2022 Aug;241(2):211-229. doi: 10.1111/joa.13657. Epub 2022 Mar 31.
Brain and skull tissues interact through molecular signalling and mechanical forces during head development, leading to a strong correlation between the neurocranium and the external brain surface. Therefore, when brain tissue is unavailable, neurocranial endocasts are often used to approximate brain size and shape. Evolutionary changes in brain morphology may have resulted in secondary changes to neurocranial morphology, but the developmental and genetic processes underlying this relationship are not well understood. Using automated phenotyping methods, we quantified the genetic basis of endocast variation across large genetically varied populations of laboratory mice in two ways: (1) to determine the contributions of various genetic factors to neurocranial form and (2) to help clarify whether a neurocranial variation is based on genetic variation that primarily impacts bone development or on genetic variation that primarily impacts brain development, leading to secondary changes in bone morphology. Our results indicate that endocast size is highly heritable and is primarily determined by additive genetic factors. In addition, a non-additive inbreeding effect led to founder strains with lower neurocranial size, but relatively large brains compared to skull size; suggesting stronger canalization of brain size and/or a general allometric effect. Within an outbred sample of mice, we identified a locus on mouse chromosome 1 that is significantly associated with variation in several positively correlated endocast size measures. Because the protein-coding genes at this locus have been previously associated with brain development and not with bone development, we propose that genetic variation at this locus leads primarily to variation in brain volume that secondarily leads to changes in neurocranial globularity. We identify a strain-specific missense mutation within Akt3 that is a strong causal candidate for this genetic effect. Whilst it is not appropriate to generalize our hypothesis for this single locus to all other loci that also contribute to the complex trait of neurocranial skull morphology, our results further reveal the genetic basis of neurocranial variation and highlight the importance of the mechanical influence of brain growth in determining skull morphology.
脑和颅骨组织在头部发育过程中通过分子信号和机械力相互作用,导致神经颅和外部脑表面之间存在很强的相关性。因此,当脑组织不可用时,通常使用神经颅内面铸型来近似脑的大小和形状。脑形态的进化变化可能导致神经颅形态的继发变化,但这种关系的发育和遗传过程尚不清楚。使用自动化表型方法,我们通过两种方式量化了实验室小鼠大型遗传多样化群体中内面铸型变异的遗传基础:(1)确定各种遗传因素对神经颅形态的贡献;(2)帮助澄清神经颅变异是基于主要影响骨骼发育的遗传变异,还是基于主要影响大脑发育的遗传变异,从而导致骨骼形态的继发变化。我们的研究结果表明,内面铸型大小具有高度遗传性,主要由加性遗传因素决定。此外,非加性近交效应导致创始株具有较小的神经颅大小,但与颅骨大小相比,大脑相对较大;这表明大脑大小的 canalization 更强,或存在一般的异速生长效应。在一个杂交的小鼠样本中,我们在小鼠染色体 1 上确定了一个与几个正相关的内面铸型大小度量值变异显著相关的基因座。由于该基因座的蛋白质编码基因以前与大脑发育有关,而与骨骼发育无关,我们提出该基因座的遗传变异主要导致大脑体积的变化,从而导致神经颅球形度的变化。我们在 Akt3 内发现了一个与该遗传效应密切相关的种系特异性错义突变。虽然不能将我们关于该单一基因座的假设推广到对神经颅颅骨形态这一复杂特征有贡献的所有其他基因座,但我们的结果进一步揭示了神经颅变异的遗传基础,并强调了脑生长的机械影响在确定颅骨形态方面的重要性。