(A) The region between positions −96 and −40 mediates the activation of BIK promoter by ∆Np73-α. A luciferase reporter controlled by the indicated portions of the BIK promoter was transfected along with an expression vector for ∆Np73-α (black bars). The luciferase activity relative to the activity of an internal β-galactosidase control [relative luciferase/galactosidase activity (RLA)] in the cell extracts is depicted. (B) Sequence of the region between positions −72 to −38 relative to the transcriptional start of the human BIK gene, and that of the different mutants generated. (C) ∆N isoforms of p73 but neither TAp73 nor p53 activate the region between positions −72 and −38 of BIK promoter. This region confers responsiveness to a heterologous basic promoter driving the luciferase gene. RLA is represented. (D) RLA of the wild-type and mutant 3 (m3) BIK-72/-38 constructs in response to ∆Np73-α (black bars), ∆Np73-β (dark grey bars) or Sp1 (white bars). Mutation 3 greatly impairs basal activity as well as its induction by ∆Np73-α and −β. (E) Induction of luciferase activity in the wild-type and mutant BIK-72/-38 constructs by ∆Np73-α (black bars), ∆Np73-β (dark grey bars) or Sp1 (white bars). Although mutations 1 and 2 barely affect the induction of this region by ∆Np73-α and −β, mutation 3 clearly reduces it. Contrarily, m3 potentiates the activation of this region by Sp1. Fold induction was calculated in relation to empty vector-transfected control cells.