80 - Fibroblast Growth Factor Signaling Affects Tissue Modulus in the Frontonasal Process

Poster Board Number: 80
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Abstract Body : The current paradigm for explaining tissue growth and morphogenesis during development is bulk expansion driven by regional differences in cellular proliferation. However, previous work in our lab found that increasing fibroblast growth factor (FGF) signaling in the Frontonasal Process (FNP) of chicken embryos led to dysmorphogenesis accompanied by decreased proliferation and altered polarity of neural crest cells. Cellular activities that can affect morphogenesis – such as movement, oriented division, and apical-basal polarity – are dependent on physical interaction of cells with their extracellular matrix (ECM). Active feedback between cells and biomechanical properties of ECM may play a role in morphogenesis, and the effect of FGF signaling on craniofacial development may be due in part to changes to the physical environment. Our goal is to determine how the biomechanical properties of the ECM of chicken embryos change after increasing or reducing FGF signaling by placing beads soaked in either FGF2 or SU5402, respectively, into the lateral FNP. Previously we found that reducing FGF signaling increased the concentration of the basement membrane proteins collagen IV and laminin in the lateral sides of the FNP compared to the midline, while increasing FGF signaling had no effect. We have also shown that increasing FGF signaling stimulated collagen crosslinking – which is associated with increased tissue stiffness – in the ectoderm and mesenchyme on the lateral side of the FNP while reducing FGF signaling had no effect. In this study we measured tissue modulus, a size- and shape-independent measure of tissues’ resistance to deform under stress, directly with atomic force microscopy. Our initial results suggest that stimulating FGF signaling tends to increase modulus in the ectoderm on the lateral side of the FNP adjacent to where the beads are placed compared to untreated controls. Increasing FGF signaling had no effect on the modulus of the globular process or midline of the FNP but tended to decrease modulus in both the ectoderm and mesenchyme at the base of the nasal pit. These preliminary results agree with the collagen crosslinking results and suggest that FGF signaling either actively increases crosslinking and modulus to direct morphogenesis or these changes to the biomechanical properties are compensatory mechanisms to constrain overgrowth caused by FGF signaling. These two conclusions will be pursued further by reducing FGF signaling and reducing collagen crosslinking. Future work will directly correlate collagen crosslinking and tissue modulus in adjacent tissue sections.