Developmental Basis for Evolutionary Variation in Craniofacial Shape

Embryonic Variation in Cell Signaling and Craniofacial Shape

A major challenge in evolutionary biology is to understand how phenotypic variation is generated both within and among species. For example, how are common developmental processes (e.g., cell proliferation, death, and differentiation) affected by modulation of cell-signaling pathways (Shh, Fgfs, Bmps, Wnts), and how does this impact phenotypic variation? Using a population-level approach to developmental biology, I focus on the developmental basis for evolutionary variation in the principal axes of facial shape (e.g., width, length, height and depth). My research shows that activity levels of key pathways can predict embryonic facial growth, shape, and postnatal phenotype. Sonic Hedgehog (SHH) signaling in the embryonic brain regulates formation of a signaling center in the face (the frontonasal ectodermal zone or "FEZ") that controls normal facial patterning and growth in both the chicken and mouse. Variation in the activity and spatial organization of this broadly conserved signaling center contributes to an axis of midfacial shape variation common to all amniote species. Current work is focused on comparing embryonic variation in brain, face, and FEZ shape from a targeted sample of amniote species (reptiles, avians, and mammals). If FEZ organization and activity varies across amniotes, then SHH-signaling variation likely affects differential growth in the facial mesenchyme, and altering SHH-signaling variation from the brain should affect variation in midfacial shape. To test this idea, I am using an innovative combination of modern experimental developmental biology with high resolution three-dimensional digital imaging, quantitative gene expression, and landmark-based geometric morphometric analyses of shape.

Evolution of the Human & Ape Postcranium

Variability and Evolvability of Human and Primate Postcrania

Humans are unique among primates in behaviors like committed bipedalism, endurance running, and complex tool use, all of which are reflected in our relatively long legs and short arms. How did these features evolve, and what impact did our last common ancestor with African apes have on this process? Interestingly, living apes share postcranial adaptations that emphasize independent use of the limbs, such as brachiation and hanging, that appear to serve as “pre”-adaptations in human ancestors. Among these, my work demonstrates that ape shoulders and limbs exhibit weaker morphological integration and canalization of shape and size compared to quadrupedal taxa, suggesting that apes experience weaker stabilizing selection compared to monkeys. Humans benefited from this change because weaker integration increases the independent evolvability of postcrania, and could have facilitated the mosaic evolution seen in ancestral hominins. This result also yields testable predictions about lineage-specific patterns on a macroevolutionary scale. For example, differences in evolvability are reflected in the relative diversity of limb proportions in primate taxa (e.g., apes are more diverse than monkeys). It also suggests a novel explanation for why fossil human and ape postcranial evolution is so hard to understand: many of the features likely evolved in mosaic fashion, with increased “experimentation” of postcranial adaptations. To further test these ideas I have ongoing projects to better understand the evolution of postcranial integration in living humans and fossil apes.