Inactivation of VCP/ter94 Suppresses Retinal Pathology Caused by Misfolded Rhodopsin in Drosophila
Figure 5
Suppression of Rh1P37H-induced retinal degeneration by VCP loss-of-function alleles.
(A–F) Photomicrographs of toluidine blue-stained semithin eye sections of Rh1P37H;Rh1+/+ (A,D), Rh1P37H;VCP26-8/+;Rh1+/+ (B,E) and Rh1P37H;VCPk15502/+;Rh1+/+ (C,F) flies after 20 (A–C) or 30 (D–F) days of light exposure (dle). Scale bar is 50 µm. (G) Quantification of average number of photoreceptors/ommatidium (P/O) (n>7 animals/group, * p<0.05, ** p<0.01 and *** p<0.001 t-test). Decreasing VCP function potently suppresses retinal degeneration caused by Rh1P37H. (H) Immunoblot revealing the levels of VCP in Rh1WT;Rh1+/+ and Rh1P37H;Rh1+/+ retinas, exposed to light for increasing durations. Rh1P37H;Rh1+/+ display a 2.25-fold increase of VCP levels relative to Rh1WT;Rh1+/+ retinas after 1 dle. β-Tubulin (β-Tub) served as loading control. (I) Quantification of VCP expression levels revealed higher VCP levels in Rh1P37H;Rh1+/+ flies after 1 dle. VCP levels were averaged from three independent experiments (** p<0.01 t-test).