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Mice are arguably the dominant model organisms for studies investigating the effect of genetic traits on the pathways to mammalian skull and teeth development, thus being integral in exploring craniofacial and dental evolution. The aim of this study is to analyse the functional significance of masticatory loads on the mouse mandible and identify critical stress accumulations that could trigger phenotypic and/or growth alterations in mandible-related structures. To achieve this, a 3D model of mouse skulls was reconstructed based on Micro Computed Tomography measurements. Upon segmenting the main hard tissue components of the mandible such as incisors, molars and alveolar bone, boundary conditions were assigned on the basis of the masticatory muscle architecture. The model was subjected to four loading scenarios simulating different feeding ecologies according to the hard or soft type of food and chewing or gnawing biting movement. Chewing and gnawing resulted in varying loading patterns, with biting type exerting a dominant effect on the stress variations experienced by the mandible and loading intensity correlating linearly to the stress increase. The simulation provided refined insight on the mechanobiology of the mouse mandible, indicating that food consistency could influence micro evolutionary divergence patterns in mandible shape of rodents.

During its expansion across the globe, Homo sapiens successfully survived to major adaptive challenges as a species, inviting scientific research to plunge into the particularities of continental settlement dynamics. A recurrent paleoanthropological concern is about the understanding of the great deal of craniofacial diversity that evolved into the Americas, which includes a vector of continuum variation between a generalized morphology observed among humans groups leading the Out-of-Africa dispersion, and a derived set of craniofacial traits classically labeled as ?mongoloid? and that would have arise in Asia during the Holocene. Here, we use geometric morphometric techniques and multivariate statistics along with quantitative genetic approaches to look more closely into the human craniofacial evolutionary history during the Late PleistoceneeEarly Holocene from Asia and the New World. We detected significant signals of deviation of the neutral evolutionary expectations, suggesting an important action of non-stochastic evolution (e.g. natural selection, phenotypic plasticity) in the Americas. We also found further support to the Recurrent Gene Flow model that refers to an ancestral, founder population experiencing a standstill in Beringia, and exhibiting high within-group craniofacial variation. This original, internally variable stock would have been the ancestral source of variation that fuelled the subsequent local micro evolution of other derived phenotypic patterns, giving origin to the craniofacial diversity observed among Holocene Native American samples. © 2015 Elsevier Ltd and INQUA. Fil: de Azevedo, Soledad. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Nacional Patagónico; Argentina Fil: Quinto Sanchez, Mirsha Emmanuel. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Nacional Patagónico; Argentina Fil: Paschetta, Carolina Andrea. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Nacional Patagónico; Argentina Fil: González José, Rolando. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Nacional Patagónico; Argentina

Evolution of facial morphology arises from variation in the activity of developmental regulatory networks that guide the formation of specific craniofacial elements. Importantly, the acquisition of novel morphology must be integrated with a phylogenetically inherited developmental program. We have identified a unique region of the secondary palate associated with the periodic formation of rugae during the rostral outgrowth of the face. Rugae function as SHH signaling centers to pattern the elongating palatal shelves. We have found that a network of signaling genes and transcription factors is spatially organized relative to palatal rugae. Additionally, the first formed ruga is strategically positioned at the presumptive junction of the future hard and soft palate that defines anterior–posterior differences in regional growth, mesenchymal gene expression, and cell fate. We propose a molecular circuit integrating FGF and BMP signaling to control proliferation and differentiation during the sequential formation of rugae and inter-rugae domains in the palatal epithelium. The loss of p63 and Sostdc1 expression and failed rugae differentiation highlight that coordinated epithelial–mesenchymal signaling is lost in the Fgf10 mutant palate. Our results establish a genetic program that reiteratively organizes signaling domains to coordinate the growth of the secondary palate with the elongating midfacial complex.