Loss of Whirlin in the peripheral nervous system results in disrupted paranodal compaction. A–H. 4, 6, 8-week-old teased sciatic nerve fibers either wild-type (Aa–Ad, Ca–Cd, Fa–Fd) or Whrn knockout (Ba–Bd, Da–Dd, Ea–Ed, Ga–Gd, Ha–Hd) immunostained against Kv1.2 (Aa-Da, Fa, Ga, red), NFCt (Ea, Ha, red), Caspr (Ab–Hb, green), NF186 (Ac-Dc, Fc, Gc, blue), AnkG (Ec, Hc, blue), and merged images (Ad–Hd). In all Whrn mutant panels, Caspr (Bb, Bd; Db, Dd; Eb, Ed; Gb, Gd; Hb, Hd, green) and paranodal NF155 (NFCt) (Ea, Ed; Ha, Hd, red) fail to compact properly at the paranodes. Nodal NF186 or AnkG are not affected (Ac,d–Hc,d, blue). Scale bars (Ad-Hd) = 5 μm. I. Sample image shows parameters of various domain measurements in (nodal gap in white, paranodal diameter in blue, paranodal width in red, and counting of spring-like phenotype in purple) using ~10 micron caliber, Caspr-immunostained wild-type and Whrn−/− fibers. J-L. No statistically significant differences were observed comparing 4, 6, and 8-week-old wild-type and mutant fibers with concern to nodal gap (J), paranodal diameter (K), or paranodal width (L) (N=20 for each genotype/age combination). Note the greater percentage of paranodes with compaction issues in mutant fibers (M, light purple bars) likely contributes to the increased deviation in paranodal widths (L, light red bars).
Green et al. BMC Neuroscience 2013 14:96 doi:10.1186/1471-2202-14-96