During embryogenesis and organ formation, establishing proper gradient is critical for auxin function, which is achieved through coordinated regulation of both auxin metabolism and transport. Expression of auxin biosynthetic genes is often tissue specific and is regulated by environmental signals. However, the underlying regulatory mechanisms remain elusive. Here, we investigated the transcriptional regulation of a key auxin biosynthetic gene, l-Tryptophan aminotransferase of Arabidopsis1 (). A canonical and a novel Arabidopsis () response regulator (ARR) binding site were identified in the promoter and the second intron of , which were required for its tissue-specific expression. C-termini of a subset of the type B ARRs selectively bind to one or both cis elements and activate the expression of We further demonstrated that the ARRs not only mediate the transcriptional regulation of by cytokinins, but also mediate its regulation by ethylene, light, and developmental signals. Through direct protein-protein interactions, the transcriptional activity of ARR1 is enhanced by ARR12, DELLAs, and ethylene-insenstive3 (EIN3). Our study thus revealed the ARR proteins act as key node that mediate the regulation of auxin biosynthesis by various hormonal, environmental, and developmental signals through transcriptional regulation of the key auxin biosynthesis gene.

The phytohormone auxin controls plant growth and development via TIR1-dependent protein degradation of canonical AUX/IAA proteins, which normally repress the activity of auxin response transcription factors (ARFs). IAA33 is a non-canonical AUX/IAA protein lacking a TIR1-binding domain, and its role in auxin signaling and plant development is not well understood. Here, we show that IAA33 maintains root distal stem cell identity and negatively regulates auxin signaling by interacting with ARF10 and ARF16. IAA33 competes with the canonical AUX/IAA repressor IAA5 for binding to ARF10/16 to protect them from IAA5-mediated inhibition. In contrast to auxin-dependent degradation of canonical AUX/IAA proteins, auxin stabilizes IAA33 protein via MITOGEN-ACTI-VATED PROTEIN KINASE 14 (MPK14) and does not affect IAA33 gene expression. Taken together, this study provides insight into the molecular functions of non-canonical AUX/IAA proteins in auxin signaling transduction.

Cytokinins are phytohormones that regulate plant development, growth, and responses to stress. In particular, cytokinin has been reported to negatively regulate plant adaptation to high salinity; however, the molecular mechanisms that counteract cytokinin signaling and enable salt tolerance are not fully understood. Here, we provide evidence that salt stress induces the degradation of the cytokinin signaling components Arabidopsis (Arabidopisis thaliana) response regulator 1 (ARR1), ARR10 and ARR12. Furthermore, the stress‐activated mitogen‐activated protein kinase 3 (MPK3) and MPK6 interact with and phosphorylate ARR1/10/12 to promote their degradation in response to salt stress. As expected, salt tolerance is decreased in the mpk3/6 double mutant, but enhanced upon ectopic MPK3/MPK6 activation in an MKK5DD line. Importantly, salt hypersensitivity phenotypes of the mpk3/6 line were significantly alleviated by mutation of ARR1/12. The above results indicate that MPK3/6 enhance salt tolerance in part via their negative regulation of ARR1/10/12 protein stability. Thus, our work reveals a new molecular mechanism underlying salt‐induced stress adaptation and the inhibition of plant growth, via enhanced degradation of cytokinin signaling components.

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