A comparative examination of odontogenic markers in both toothed and toothless amniotes (344.3)

Abstract

It is a well‐known tenet of murine tooth development that BMP4 and FGF8 antagonistically initiate odontogenesis, but it is largely unexplored whether this tenet is conserved across amniotes. Additionally, changes in BMP4‐signaling have previously been implicated in evolutionary tooth loss in Aves. Here we demonstrate that Bmp4, Msx1, and Msx2 expression is limited proximally in the red‐eared slider turtle (Trachemys scripta) mandible, at stages equivalent to those at which tooth development is initiated in mice, similar to previously reported results in chicks. To address the question of whether the limited domains shared between the turtle and the chicken are indicative of an evolutionary molecular parallelism that resulted in the loss of the dentition, or whether the domains simply constitute an ancestral phenotype, we assessed expression of Bmp4, Msx1, Msx2, and Fgf8 expression in a toothed reptile (the American alligator, Alligator mississippiensis) and a toothed non‐placental mammal (the Gray short‐tailed opossum, Monodelphis domestica). We demonstrate that the Bmp4 domain is limited proximally in M. domestica and that the Fgf8 domain is limited distally in A. mississippiensis just preceding odontogenesis. Additionally, we show that Msx1 and Msx2 expression patterns in these species differ from those found in mice. Our data suggest that a limited Bmp4 domain does not necessarily correlate with edentulism, and reveal that the initiation of odontogenesis in non‐murine amniotes may be more complex than previously imagined. Our data also suggest a partially conserved odontogenic program in T. scripta, as indicated by the conserved mandibular expression domains of Pitx2, Pax9, and Barx1 and by the presence of Shh‐expressing palatal epithelium in some Yntema stage 17 (Y17) T. scripta specimens, which we hypothesize may represent potential dental rudiments based on the fossil record of Testudinata.Grant Funding Source: Supported by NIH‐NIDCR‐R01DE018234 and NSF‐BSC‐0616308 with REU supplement.