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. Author manuscript; available in PMC: 2011 Aug 15.
Published in final edited form as: Dev Biol. 2010 May 15;344(2):1060–1070. doi: 10.1016/j.ydbio.2010.05.011

Figure 6. Ato decreases the ability of Senseless to bind RhoA.

Figure 6

A. Sequence of wild type RhoA element highlighting the presence of the Sens, Exd, Hth, and Hox binding sites. The red nucleotides denote a mis-match to the consensus Sens binding site. The SensS sequence is shown. B. Gel shift assays showing that Ato and Da do not bind RhoA. The Ato and Da proteins are able to bind a positive control probe (AtoRE). C. Gel shift assays showing that Ato and Da significantly decrease the ability of Sens to bind RhoA but not the optimized SensS probe. D. Gel shift assays showing that Ato and Da have no significant effect on Exd/Hth or Exd/Hth/Abd-A binding to RhoA. E-E’. Lateral view of a stage 11 RhoAAASensS-lacZ embryo immunostained for β-gal (green) and Abd-A (purple) revealing that strengthening of the Sens site in all three copies of RhoA results in decreased β-gal activity in the abdomen. F-F’’’. Lateral view of three abdominal PrdG4;UAS-Ato;UAS-GFP segments (stage 11) immunostained for β-gal (green), GFP (blue), and Ato (red). Note that while GFP is detected in the β-gal positive C1 cells, Ato expression is low (arrows). However, Ato protein is detected in many other cells of the PrdG4-on stripe.