Transcriptional profile of SCs upon nerve injury or under myelinating conditions after cAMP treatment. (A) ISH for Artn and GDNF genes on Junf/f and JunΔSC uninjured sciatic nerves or 7 d post-crush in proximal and distal stumps from the injury site. Rectangles indicate area shown with higher magnification on the last panel to the right. (B) Q-PCR showing changes in gene expression of injured sciatic nerves 7 d post-crush compared with uninjured wild-type nerves (baseline value uninjured nerve, 1; numbers shown are mean of three replicates, n = 5 injured or control wild-type animals, representative experiment out of two experiments). (C) Q-PCR in primary SC cultures upon treatment with cAMP for 5 d (baseline value untreated, 1). Values plotted are the mean of the means from two independent experiments with three replicates each. Within each experiment, samples from individual pups were pooled. Across the two independent experiments, 10 P2-P5 pups were analyzed for each condition. Error bars represent the SD of the two means. *, P < 0.05 (Student’s t test). (D) Q-PCR of SC primary cultures isolated from wild-type mice. The graph shows fold gene expression when comparing cultures that overexpress c-Jun (adenovirus–c-Jun) versus mock-infected cultures (adenovirus-GFP). Numbers are mean of three replicates, n = 10 P2-P5 pups pooled for each condition, representative experiment out of two experiments. (E) Assessment of Ret activation and downstream signaling in facial motoneurons in axotomized facial nerve of control and c-Jun deleted mutant mice. Cohorts from both genotypes were subjected to facial nerve axotomy and the axotomized facial nucleus was microdissected 7 d after injury. Extracts were then analyzed by Western blot using antibodies for the indicated proteins. Uninjured mice with Ret neuronal deletion were used as a negative control for total and p-Tyr905 Ret Western blots. Bars: (A; bottom left applies to the low magnification three first columns) 150 µm; (high magnification series, top right column) 25 µm.