ILK regulates PNS remyelination. (A) Cre-mediated recombination was induced in 2-mo-old control and mutant mice by five daily consecutive tamoxifen injections. A period of 2 mo was allowed for recombination and protein depletion before assays were performed. Cre Rec., Cre recombinase; 2MPC, 2 mo post-CI; 4MPC, 4 mo post-CI. (B) Western blots performed on protein lysates obtained from contralateral and crushed nerves show a reduction in ILK levels in mutant (mut) nerves compared with those of controls (cont). PINCH1 and AKT phosphorylation levels are reduced in mutant nerves compared with controls. (C) Semithin sections of SNs collected 2 and 4 mo after CI. In contrast to controls (a, c, and g), mutant nerves show a significant reduction in the number of remyelinated axons at 2 and 4 mo after CI (b, d, and g; n = 3, P < 0.0001). In d, the low magnification EM insert shows that in mutant SNs, virtually all axons are engaged by SCs (arrowheads) but only very few went on to myelinate (arrow). (e) Tamoxifen (TAM) treatment does not affect myelination. (f) Noninjured mutant nerves collected 6 mo after tamoxifen induction show no structural abnormalities, implying that ILK is not necessary for the maintenance of the myelin membrane. (h) There was no difference in the axonal number in mutant crushed nerves when compared with control crushed nerves. (D) Oct6 immunohistochemistry on 2-mo post-CI cryosections. Oct6 is virtually absent in control nerves, whereas levels are still high in mutant nerves. Error bars indicate ± SEM. ***, P < 0.001. Bars: (C) 10 µm; (D) 50 µm.