De novo FA synthesis in SCs is required for correct PNS function. (a) Conditional Fasn allele inactivation in vivo upon Dhh-driven Cre expression. (b) FASN immunoblot and quantification graph, normalized to β-actin, of protein lysates of sciatic nerves (P40). n = 3 blots, each data point represents an independent experiment with an independent set of lysates from three control (CT) and three conditional mutant (cMU) mice (unpaired two-tailed two sample Student’s t test, P = 0.0044, t = 5.816); **, P < 0.01. (c) Aberrant hindlimb clasping in cMU mice by tail lift. (d) Representative immunostaining of cross sectioned sciatic nerves from P14 CT and cMU mice; n = 3 mice for each, CT and cMU. Note the prominent cytoplasmic FASN expression in SCs of nerves of CT but not cMU mice. Myelin marker: myelin basic protein, MBP; axonal marker: neurofilament M, NF-M; nuclear marker: DAPI. Bars, 10 µm. (e and f) P40 cMU mice showed reduced grip strength (unpaired two-tailed two sample Student’s t test, P = 0.0044, t = 3.310); **, P < 0.01, and decreased latency to fall from a Rotarod (two-way ANOVA, trials P = 0.0333, F3,24 = 3.424, Genotype P = 0.01, F1,8 = 11.25, with Bonferroni’s multiple comparisons test, trial 1 P < 0.0001, t = 5.284; trial 2 P = 0.0033, t = 3.819; trial 3 P = 0.0001, t = 5.140; trial 4 P = 0.0003, t = 4.747); **, P < 0.01; ***, P < 0.001, compared with CT. Data points represent n = 9 mice for each, CT and cMU. Bars represent mean ± SEM.