Paul T. Sharpe

TL;DR: The developing tooth has proven to be an excellent model in studies of the molecular basis of patterning and morphogenesis of organs and it can be expected that continuing studies will rapidly increase the understanding of these mechanisms.

TL;DR: Mouse models of several of these syndromes have indicated ways in which conditions could be treated and genes and developmental processes that underlie the many human disorders in which tooth development is defective are identified.

TL;DR: The nested expression patterns of Dlx-1, -2, -3, -5, and -6 provide evidence for a model that predicts the region-specific requirements for each gene, and the DLx-2 and DlX-1 and -2 mutants have ectopic skull components that resemble bones and cartilages found in phylogenetically more primitive vertebrates.

TL;DR: The inhibition of BMP signaling early in mandible development by the action of exogenous Noggin protein resulted in ectopic Barx-1 expression in the distal, presumptive incisor mesenchyme and a transformation of tooth identity from incisors to molar.

TL;DR: A trans-species aneuploid mouse line that stably transmits a freely segregating, almost complete human chromosome 21 (Hsa21) is generated, which is a model of trisomy 21, which manifests as Down syndrome in humans and has phenotypic alterations in behavior, synaptic plasticity, cerebellar neuronal number, heart development, and mandible size that relate to human DS.