7 Very Important Elements For SRT1720

, 1991?and?Phillips and Whittle, 1993). Anti-��-gal antibody staining revealed a regular pattern of SOPs in wild-type discs ( Fig.?2A). Sulf1 mutants exhibited an increase in SOP number (average number?=?20.5, n?=?27) when compared to wild-type (average number?=?18.4, n?=?21, p?this website distribution of wing margin bristles observed in Sulf1 mutant adults. We next analyzed expression of Distal-less (Dll), a low-threshold target gene of Wg signaling. We found that Dll levels were consistently elevated in Sulf1 mutant wing discs compared to the wild-type counterparts ( Figs.?2C and D). To confirm this result, Sulf1 mutant clones were generated by somatic recombination and their effects on Dll expression was examined. Figs.?2E�CE�� show a wing disc that has a large Sulf1 mutant clone covering almost the entire posterior compartment. The area of cells positive for anti-Dll antibody staining was remarkably expanded in the mutant see more clone compared to wild-type control region. Thus, Wg signaling is up-regulated throughout Sulf1 mutant wing discs, indicating that Sulf1 is a novel negative regulator of Wg signaling. Based on the observation that Wg signaling is elevated in Sulf1 mutant discs, we hypothesized that Sulf1 overexpression would disrupt Wg signaling. To test this idea, a UAS-Sulf1 transgene was driven in the wing disc by various Gal4 drivers. We found that Sulf1-overexpressing adult wings exhibited a wide range of phenotypes. Sulf1 expression at a moderate level using C96-Gal4, a driver for the DV border of the wing disc, or A9-Gal4, a driver for the entire wing disc, resulted in a significantly reduced number of wing margin bristles ( Figs.?3A and B). Sulf1 expression at higher levels, driven by en-Gal4 or hh-Gal4, led to notched wings (penetrance: 96%, n?=?27; Fig.?3C). These phenotypes are consistent with compromised Wg signaling ( Phillips and Whittle, 1993). To determine if Sulf1 overexpression indeed affects Wg signaling, larval wing discs were stained for Dll. Sulf1 misexpression in the D compartment driven by ap-Gal4 abrogated Dll expression ( Fig.?3D), confirming that Sulf1 inhibits Wg UNC2881 signaling. On the other hand, the effect of Sulf1 overexpression on Senseless (Sens), a high-threshold target for Wg signaling, was less evident ( Fig.?3D��). Similarly, Sens expression was not obviously affected by Sulf1 overexpression by hh-Gal4 ( Figs.?3E and E��). Thus, low- and high-threshold markers exhibited different sensitivities to alterations of Sulf1 activity. Collectively, these results are consistent with the idea that Sulf1 is a novel negative regulator of Wg signaling at the DV boundary of the developing wing.