Supplementary Figure 4: Mical and SelR Redox requirement and the Met-44 residue of actin in Mical/SelR-mediated bristle/actin reorganization.

a, Bristle-specific expression of a Mical transgene with point mutations disrupting Mical’s monooxygenase (Redox) domain (Mical^Δredox) in a wild-type background generates bristle defects similar to when the levels of active SelR are increased in wild-type bristles¹. b-c, Bristle overexpression of high levels of SelR (x2 bristle SelR) in a wild-type background generates severe bristle defects with multiple bends (b) that resemble bristles present in flies homozygous for a point mutation¹⁷ disrupting the Redox domain of Mical (c; Mical redox mutant [Mical^I1367]; ¹). d-e, Elevating the levels of wild-type SelR in bristles markedly suppresses the severe bristle/F-actin alterations ¹ that result from hyperactive Mical Redox signaling (Mical^redoxCH). f, In contrast to its enhancing effects on wild-type Mical in bristles, the SelR mutant (SelR^Delta3/+) suppresses the effects of a loss of Mical activity (Mical^Δredox) in bristles (x1 Bristle Mical^Δredox+SelR^Delta3/+). n = 20 animals per genotype. Replicated in at least 2 independent experiments (separate crosses) per genotype. g, Expressing a non-Mical oxidizable version of actin in bristles (x1 Bristle Actin^M44L) generates bristle defects that are enhanced by SelR (x1 Bristle Actin^M44L+x1Bristle SelR). Chi-Square Test; ^***P<0.0001. n = 10 animals per genotype. Replicated in at least 2 independent experiments (separate crosses) per genotype.