Figure 2.

Schematic representation of AFB-Aux/IAA-ARF-mediated auxin response. When auxin levels are low, Aux/IAAs repress ARF-mediated transcriptional activation by dimerising with DNA-bound activating ARFs (ARF^A) and recruiting the corepressor protein TPL (B), or theoretically by sequestering ARF^A from their promoters (E). Although the occurrence and relevance in vivo of Aux/IAA-ARF^R dimers is unknown, Aux/IAAs could affect ARF^R activity by interfering with the formation of ARF ^R dimers through blocking or sequestration (C). When cellular auxin levels increase the affinity of the receptors TIR1/AFB for their substrate Aux/IAA increases, promoting the degradation of Aux/IAA via the proteasome (F). ARF^A are then able to regulate positively transcription (H); it has been shown that some ARFs bind more stably to promoters as dimers (K) and this could increase their transcriptional activity. ARF^R could repress transcription by directly binding to the promoter of target genes (A,G) and importantly, by competing with ARF^A for common target AuxRE binding sites (I), or by interacting with activating ARFs, either on the promoter (L) or as free heterodimers (D,J).