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The Venn Overlap Rule, as manifest in the control of wing blade identity by vestigial (vg) and scalloped (sd).
a, b. Regions where vg and sd are normally transcribed (black areas). These regions are plotted on a schematic map (key in a) where the derivatives of eye, wing, and leg discs are outlined by thick lines, and subregions (A = antenna, H = head capsule, E = eye, N = notum, W = wing) are partitioned by thin lines. a. The vg gene is transcribed throughout the wing and in small areas of the hinge and notum (not shown; cf. Fig. 6.2) . b. The sd gene is transcribed throughout the vg-ON territory, as well as in eye and leg discs . Although expression in eyes per se is well documented , the antennal, head, and leg areas plotted here are only guesses based on the ability of ectopic vg to induce wing tissue wherever sd is already ON [2219, 3936].
c. Venn diagram of the logic. Only when Vg and Sd are co-expressed (black area of overlap) will wing tissue be formed. Put more generally, the Venn Overlap Rule states that when two or more genes interact cooperatively, they only activate target genes where their domains of expression overlap .
d-f. Cartoons which show how the rule is implemented at a molecular level. d. When a cell expresses vg alone, Vg resides mainly in the cytoplasm [1686, 3936]. Even those Vg molecules that do enter the nucleus are impotent because they can't bind DNA without help from Sd. e. When both Vg and Sd are present, Vg binds Sd , and the Vg-Sd complex is found mainly in the nucleus. Nuclear localization could be due to escorted import (as shown) or to selective retention after import. The Vg-Sd complex binds a DNA sequence (gray box) near target genes like blistered (bs) . Some of those genes (not bs itself) execute wing identity. Whether the Vg-Sd dimers activate transcription directly or merely allow other trans-activators to turn ON bs, etc., is unknown. f. When a cell expresses sd alone, Sd binds those same sites. In the absence of Vg, trans-activators like Ci cannot turn ON a target gene via Ci-binding sites in its cis-enhancer region (not shown) . See also App. 7.