Like TIRs in rain

Abstract

The canonical auxin pathway in the Arabidopsis nucleus was characterized two decades ago: auxin acts as a molecular glue to bind the TIR1 F-box auxin receptor (and five AFB homologues) to small auxin and indole-3-acetic acid (Aux/IAA) proteins. These Aux/IAA proteins are then marked for degradation by ubiquitination. As they are degraded, they stop repressing ARF transcription factors, which are then free to activate downstream auxin genes. This model of signalling by degradation of transcriptional repressors was found to be conserved in several other hormone signalling pathways.

It was recently shown by the same team that TIR1 and AFBs have an unexpected auxin-induced adenylate cyclase (AC) activity that arises from a small domain near their C terminus, and that this activity producing cAMP is needed for root growth response to auxin. Now, the authors perform a set of clever experiments, including the use of an engineered orthogonal TIR1–auxin pair that works without interference from the constant endogenous auxin signalling background, the mutational uncoupling of TIR1 AC activity from its ubiquitin ligase activity, abolishing auxin-induced cAMP production but still allowing the degradation of Aux/IAA proteins, various auxin reporters, and many mutants and transgenic lines. Reading this study feels like observing a watchmaker digging into the precise clockwork mechanism of this signalling pathway, removing or replacing one cog at a time to see what happens.