Validation of <i>dNf1</i> modifiers involved in Jeb/dAlk/Ras/ERK and cAMP signaling.

<p>(A) Neuronal expression of <i>dAlk</i> RNAi using <i>Ras2-Gal4</i>, <i>Ras2-Gal4</i>+<i>UAS-Dcr-2</i>, <i>c23-Gal4</i> or <i>n-syb-Gal4</i> drivers suppresses the <i>dNf1</i> size defect. Expression of <i>jeb</i> RNAi with the same neuronal drivers also suppresses. Weaker suppression is observed when <i>jeb</i> RNAi expression is controlled by the pan-glial <i>repo</i>-<i>Gal4</i> driver. Dark grey bars are control measurements of Gal4 drivers in the <i>dNf1</i> background. Light grey bars are sizes of wild-type (<i>w¹¹¹⁸</i>) and <i>dNf1^E2</i> controls. (B) Suppression of the <i>dNf1</i> size defect by the indicated <i>jeb</i>, <i>cnk</i>, <i>Dsor1</i> and <i>amx</i> alleles. (C) Neuronal <i>cnk</i>, <i>Dsor1</i> or <i>amx</i> knockdown suppressed the <i>dNf1</i> size defect. In the case of <i>Dsor1 v107276</i> and <i>amx</i>, cultures were maintained at 18°C to prevent lethality observed at 25°C. Some RNAi transgene/driver combinations were lethal (†) even at 18°C. (D) Validation of <i>dnc</i> and <i>Pka-C1</i> as <i>dNf1</i> modifiers was obtained in crosses with <i>dnc^M14</i>, <i>dnc^ML</i>, <i>Pka-C1⁶³⁵³</i> and <i>Pka-C1^BG02142</i> loss-of-function alleles. In this and subsequent figures, * and ** denote <i>p</i>-values<0.05 and <0.01, respectively.