High impact information on DRE2

• DNA-binding preferences of DBFs were analysed by electrophoretic mobility shift assays, and showed that both DBF1 and DBF2 bound to the wild-type DRE2 element, but not to the DRE2 mutant or to the DRE1 element which differs only in a single nucleotide [1].
• The promoter of SNM1 contains a 15 bp motif, which shows homology to the DRE2 box of the RAD2 promoter [2].
• However, our results show that DRE1 and DRE2 each function as a UAS (upstream activating sequence) rather than a URS and are also required for DNA-damage inducibility of the gene [3].
• Two elements, designated DRE1 and DRE2 (for damage-responsive element), match a decamer consensus URS (upstream repressing sequence) found in the promoters of many other DNA repair and metabolism genes from S. cerevisiae [3].
• Deletion of the element DRE2 increased the UV sensitivity of cells in both the G1/early S and S/G2 phases of the cell cycle as well as in stationary phase [4].

Biological context of DRE2

• Transactivation activity using particle bombardment showed that DBF1 functioned as activator of DRE2-dependent transcription of rab17 promoter by ABA, whereas DBF2 overexpression had a repression action downregulating not only the basal promoter activity, but also the ABA effect [1].

Other interactions of DRE2

• Finally, mutations in three genes of unknown function were isolated (NBP35, DRE2, TAH18) [5].

References