Abstract
The question of phenotypic convergence across a signalling pathway has important implications for both developmental and evolutionary biology. The ERK-MAPK cascade is known to play a central role in dental development, but the relative roles of its components remain unknown. Here we investigate the diversity of dental phenotypes in Spry2−/−, Spry4−/−, and Rsk2−/Y mice, including the incidence of extra teeth, which were lost in the mouse lineage 45 million years ago (Ma). In addition, Sprouty-specific anomalies mimic a phenotype that is absent in extant mice but present in mouse ancestors prior to 9 Ma. Although the mutant lines studied display convergent phenotypes, each gene has a specific role in tooth number determination and crown patterning. The similarities found between teeth in fossils and mutants highlight the pivotal role of the ERK-MAPK cascade during the evolution of the dentition in rodents.
Highlights
The question of phenotypic convergence across a signalling pathway has important implications for both developmental and evolutionary biology
This cascade is typically initiated by the binding of a growth factor to a receptor tyrosine kinase (RTK), which triggers the phosphorylation of successive kinases and culminates in activation of effector kinases and the transcription of target genes (Fig. 1)[1]
After stimulation by growth factors, the Sprouty proteins have been proposed to function by translocating to the plasma membrane, where their phosphorylation prevents the formation of an FGFR adaptor complex[20]; the biochemistry of the Sprouty proteins is still the subject of much debate
Summary
The question of phenotypic convergence across a signalling pathway has important implications for both developmental and evolutionary biology. The extracellular signal-regulated kinase/mitogen-activated protein kinase (ERK-MAPK) pathway is a central regulator of tooth development. This cascade is typically initiated by the binding of a growth factor to a receptor tyrosine kinase (RTK), which triggers the phosphorylation of successive kinases and culminates in activation of effector kinases and the transcription of target genes (Fig. 1)[1]. Whereas the morphogenesis of molar teeth in Spry1−/− mice has not yet been examined, Spry2−/− and Spry4−/− mice are known to have abnormal dentition, which sometimes includes supernumerary teeth (ST) located immediately in front of the first lower molar[7] These supernumerary teeth, which occur at differing frequencies depending on the genetic background[7,22,23], are believed to derive from evolutionary vestigial tooth buds that normally undergo apoptosis in wild-type embryos[24,25,26]. The role of Spry[1], Spry[2] and Spry[4] in the development of upper molars is not known, and the adult molar morphology has not been scrutinised in these mutants
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