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Fig. 7. Integrins compensate for the absence of PrP^C to support Vn-induced axonal growth. (a) Vn_RGD peptide abrogates Vn-induced axonal growth in cultured ZrchI Prnp^0/0 (grey bars) DRGs at lower concentrations (8 µM) than that (12 µM) necessary for the same effect in Prnp^+/+ (white bars) DRGs. Treatment with the irrelevant peptide Vn_161-174 (12 µM) had no effect. ^*P<0.001 vs poly-L-lysine (Pll) Tukey's test. (b) Exposure to adsorbed Vn_RGD-BSA peptide (0.5, 5, 1 or 10 nmol) increased axonal growth in DRG cells from ZrchI Prnp^0/0 mice, but not from ZrchI Prnp^+/+ mice. ^*P<0.001 vs Pll control, Tukey's test. (c) Adsorbed Vn_RGD-BSA peptide (1 nmol) induced axonal growth in cultured DRG cells from Npu Prnp^–/– mice (black bars) whereas no axonal growth was present at this concentration of absorbed Vn_RGD-BSA peptide in Npu Prnp^+/+ cells (striped bars). ^*P<0.001 vs Pll control, Tukey's test. (d) ZrchI Prnp^0/0 dissociated DRG cells exhibited greater WOW-1 immunoreactivity than those from ZrchI Prnp^+/+ mice, indicating that the knockouts had greater levels of activated _v3 integrin. ^*P<0.001 vs Prnp^+/+, Mann-Whitney's test. (e) Npu Prnp^–/– dissociated DRG cells exhibited greater AP5 immunoreactivity than Npu Prnp^+/+, indicating that the knockouts had greater levels of activated ₃ integrin. ^*P<0.001 vs Npu Prnp^+/+, Mann-Whitney's test.

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