Extended Data Fig. 4: Glut1, Hex-C, KATP channel and voltage-gated calcium channel are required in CN neurons to respond to glucose, and the activity of CN neuron is controlled by the internal energy state in live animals.
From: A glucose-sensing neuron pair regulates insulin and glucagon in Drosophila
a, Inactivation of Glut1 by expressing UAS-Glut1 RNAi under the control of CN-Gal4 (but not other glucose transporters) blunts a preference for d-glucose in starved flies. b, Inactivation of Hex-C by expressing UAS-HexC RNAi under the control of CN-Gal4 blunts a preference for d-glucose, but not other hexokinases, in starved flies (Hex-T2 and Hex-A). c, Inactivation of KATP channel or voltage-gated calcium channel by expressing UAS-SUR1 RNAi or UAS-Ca-α1D RNAi by CN-Gal4 blunts a preference for d-glucose in starved flies. d–h, Representative traces (d) and quantifications (e–h) of calcium responses to 1 mM glucose by CN neurons of flies in which Glut1, SUR1 or voltage-gated calcium channel subunit (Ca-α1D) was knocked down by RNAi, or those of control flies. i, j, Representative images (i) and quantifications of native CaLexA-driven GFP intensity from CN cell bodies (j) of fed, starved or refed flies carrying CN-Gal4 and UAS-CaLexA (UAS-mLexA-VP16-NFAT, LexAop-GFP). Cell bodies of CN neurons are stained with anti-Crz (magenta) antibody. Scale bar, 20 µm. Images are z-stacked projections. *P < 0.05, **P < 0.01 and ***P < 0.001; one-way ANOVA with Tukey post hoc test. See Supplementary Table 1 for the sample sizes and statistical analyses.
