Double vision: pigment genes do more than just color

Abstract

The use of P element collections led to the discovery of unanticipated effects from common genetic background mutants white, brown, and rosy in our previously reported model of tauopathy that expresses full-length human tau in the fly eye, in which mutant rosy suppresses mutant white and brown worsening of tau-induced toxicity (Ambegaokar & Jackson, 2010, Genetics, v. 186, p. 435-42). Here we discuss further possible effects of mini-white and evidence for autophagy as a mediator of white enhancement of tau toxicity.

Figure 1

(A) Multiple mini-white genes suppress tau-induced toxicity. Scanning electron micrographs (SEM) demonstrating the gl-tau eye phenotype is partially suppressed when combined with a GMR-GAL4 transgene, which like the gl-tau transgene, bears one copy of mini-white as a marker gene. (B) Increased temperature partially suppresses tau-induced toxicity. gl-tau flies raised at 25°C show a mild suppression of roughness compared to flies raised at 22°C. The gl-tau eye shows marked roughness in the anterior portion of the eye, while the posterior region is generally protected. The double-headed arrows depict maximal eye diameter and the area of the eye that that is protected from tau-induced degeneration. (C) Flies that are white homozygotes (w¹¹¹⁸/w¹¹¹⁸) show decreased phosphorylation of p70 ribosomal S6 kinase (S6K) than white heterozygotes (w¹¹¹⁸/+) (n = 3; p = 0.01), indicating white homozygotes have increased tOr inhibition and thus increased autophagy initiation; β-tubulin shown as loading control.