1Department of Anatomy and Neurobiology, Washington University School of Medicine, 2Department of Molecular and Human Genetics, Baylor College of Medicine, 3Department of Genetics, Texas Biomedical Research Institute
Friday 2:15-2:30, 200ABC
Elevated cognition is a hallmark of the primate clade. Cognitive capacity is determined both by number of neurons in the brain and the network of information exchange between brain regions. Increased folding (gyrification) of cerebral cortex allows more neurons to fit within the skull with minimal overall volume increase. The arrangement of folds (sulci) across cerebral cortex indicates the connectivity network; due to selection for the most efficient information-processing strategy, regions experiencing the highest level of crosstalk tend to be anatomically co-located along a gyrus and those least connected functionally tend to be separated anatomically by a sulcus. Despite its importance, the genetic and evolutionary underpinnings of primate brain gyrification remain unknown.
In this project, we answer pivotal questions about the genetic architecture of baboon cortical gyrification, differing cognitive strategies across the primate clade, and the evolutionary mechanisms responsible for their formation. We use a pedigreed baboon population (N=980) to assess the genetic basis, modularity, and morphological integration of cortical folding in primates and identify the chromosomal regions and candidate genes affecting these traits. Heritability of 25 brain traits has been quantified (average h2= 31.1%) in the population, asymmetry assessed (Pearson’s T-test p=0.0345) and phenotypic variation mapped to the genome using QTL analysis (highest peak: trait Left acruate rectus spur; baboon chromosome 4, 628Mb-707Mb). Four genes of interest are present in this region, including brain-specific angiogenesis inhibitor 3.
This project was funded by the National Science Foundation, grant BCS-0725068.