Figure 1 .

(A) The regulatory output of the IAB5 and IAB2 enhancers is determined by specific TF inputs. The pair-rule TF FUSHI-TARAZU (FTZ) acts as an activator of IAB5 in alternating body segments of the embryo, whereas KRUPPEL (KR) and HUNCHBACK (HB) act as repressors at the BX-C enhancers in broad regions of the embryo. The activator for IAB2 is currently unknown. (B) Model of TFBS redundancy at an enhancer (orange rectangle). In the upper panel, the distance between two neighboring binding sites (x) is close enough so that the loss of one site can be functionally compensated for by the adjacent site. In the lower panel, the distances to the neighboring sites (y and z) are too great to allow functional redundancy. (C) The calculated ratio of TFBS spacing for the entire BX-C (excluding all enhancers); the IAB8, IAB7, and IAB6 enhancers grouped together (Enhancers); IAB5 and IAB2 for KR (at high stringency [ln(p) < −9.0] and low stringency [ln(p) < −7.4]), HB, and FTZ are shown. A value >1 indicates that binding sites are closer together, and a value <1 indicates that sites are more distantly spaced relative to the expected spacing (= size of the entire BX-C/total number of binding sites).