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. 2012 May 1;139(9):1611–1619. doi: 10.1242/dev.077842

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Fig. 3. — abd-A and hth regulate RhoAAA-lacZ in abdominal SOPs. (A) The RhoA wild type and Hox, Exd, Hth and Sens mutations tested in DNA-binding and reporter assays. The Pax2, Sens, Exd, Hth and Hox sites are highlighted, and the column on the right summarizes the effect each mutation has on abdominal SOP reporter activity. (B) Lateral view of a stage 11 RhoAAA-lacZ;abd-A^M1 embryo immunostained for β-gal (green) and Abd-A (red) reveals a loss of RhoAAA-lacZ activity (A1 segment indicated). (C,D) Lateral views of stage 11 RhoAAA-lacZ;PrdG4;UAS-MycAbd-A (C) or RhoAAA-lacZ;PrdG4;UAS-MycAntp (D) embryos immunostained for β-gal (green) and Abd-A (red). (E) Lateral view of a stage 11 RhoAAA-lacZ;hth^p2 embryo immunostained for β-gal (green) and Abd-A (red) reveals a loss of RhoAAA-lacZ activity (A1 segment indicated). (F) Lateral view of a stage 11 RhoAAA_HthM-lacZ embryo immunostained for β-gal (green) and Abd-A (red) reveals relatively normal β-gal expression in the abdomen (A1 segment indicated) and de-repression in the thorax (white arrows). Thoracic de-repression correlates with a loss of DNA binding to the HthM site by the Sens repressor (Li-Kroeger et al., 2008). (G) Lateral view of a stage 11 RhoAAA-lacZ;hth^100.1 embryo immunostained for β-gal (green) and Abd-A (red) reveals normal β-gal expression in the abdomen (A1 segment indicated).