Fin-folds and autopods share a conserved Shh-Gremlin-Fgf regulatory network


Meeting Abstract

P2-65  Friday, Jan. 6 15:30 – 17:30  Fin-folds and autopods share a conserved Shh-Gremlin-Fgf regulatory network HOLMQUIST, E*; TULENKO, FJ; KIGUNDU, G; CASS, AN; DAVIS, MC; Kennesaw State University; Monash University; Kennesaw State University; Kennesaw State University; Kennesaw State University eholmqui@students.kennesaw.edu

The morphological transition from fins to limbs involved several key changes in appendage anatomy, including the loss of the distal dermal skeleton and an expansion/remodeling of the endoskeleton to form an autopod (hands/feet) with digits. Under most models, fin-folds and autopods are considered non-homologous, patterned by different developmental modules, and composed of different types of bone, despite similar distal positions in the appendage. Here we present gene expression data from a basal actinopterygian, the American paddlefish Polyodon spathula, that contributes to a growing body of evidence in support of a shared regulatory homology between fin-folds and autopods. The gene regulatory networks that integrate limb bud outgrowth and patterning have been partially characterized in tetrapods, revealing molecular interactions between the posterior limb bud mesenchyme (i.e., the zone of polarizing activity, ZPA) and the distal limb bud ectoderm (the apical ectodermal ridge, AER). In this network, ZPA-derived Shh acts through LIM-homeodomain transcription factors to induce the Bmp antagonist Gremlin. Gremlin, in turn prevents Bmp inhibition of AER-derived Fgf’s, which maintain ZPA-Shh, resulting in a positive regulatory loop that persists through patterning of the digits. Herein, we characterize components of this network in the paired fins of paddlefish and demonstrate an overall pattern similar to that of the autopod. Additionally, we characterize the likely role of Fgf-producing cells of the fin-fold, and use these to test models of fin-fold outgrowth that propose heterochronic shifts in AER signaling that may explain the appendage phenotypes seen in derived lineages.

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