Arabidopsis SMAX1 overaccumulation suppresses rosette shoot branching and promotes leaf and petiole elongation

Arabidopsis: SMAX1/SMXL (SUPPRESSOR OF MAX2 1/SMAX1-LIKE) proteins function as transcriptional repressors in karrikin and strigolactone (SL) signaling pathways and regulate plant architecture. MAX2 is a common factor in the two signaling pathways and a component of the SCF complex that modulates the proteasome-mediated degradation of SMAX1/SMXLs. SMXL6, 7, and 8 proteins promote shoot branching and inhibit petiole elongation. Our study found that the accumulation of SMAX1 suppresses rosette shoot branching and increases cauline branches on the primary inflorescence stem, plant height, petiole length, and leaf length/width ratio. The SMAX1 accumulation enhances the expression of BRC1, HB53, HB40, and HB21 that modulate shoot branching. SMAX1 also regulates the expression of the genes involved in auxin transport, cytokinin signaling pathway, and SL biosynthesis. The expression analyses of these genes suggest that excessive SMAX1 should accelerate the transport of auxin and the biosynthesis of SL in plants. High SL concentration suppresses the bud development in smax1D mutant that accumulates SMAX1 protein in plant. However, the effects of cytokinin and auxin on shoot branching remain elusive in the mutant with excessive SMAX1. SMAX1 regulates leaf shape and petiole length via modulating TCP1 expression. Our findings reveal a novel function of SMAX1 and new mechanism of shoot branching.

Automated summary

Arabidopsis SMAX1/SMXL proteins act as transcriptional repressors in karrikin and strigolactone signaling pathways, regulating plant architecture and shoot branching. Accumulation of SMAX1 promotes plant height, petiole length, and leaf length/width ratio, while enhancing the expression of genes involved in shoot branching. Additionally, SMAX1 modulates the expression of genes related to auxin transport, cytokinin signaling, and strigolactone biosynthesis, suggesting a novel function and mechanism in shoot branching.