Key Laboratory of Ministry of Education for Genetics, Breeding and Multiple Utilization of Crops, College of Agriculture, Fujian Agriculture and Forestry University, Fuzhou, 350002, China.
Key Laboratory of Ministry of Education for Genetics, Breeding and Multiple Utilization of Crops, College of Agriculture, Fujian Agriculture and Forestry University, Fuzhou, 350002, China.
Biochem Biophys Res Commun. 2021 May 14;553:44-50. doi: 10.1016/j.bbrc.2021.03.006. Epub 2021 Mar 20.
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.
SMAX1/SMXL（MAX2 抑制因子 1/SMAX1 样）蛋白在卡列金和独脚金内酯（SL）信号通路中作为转录抑制剂发挥作用，并调节植物的结构。MAX2 是这两个信号通路的共同因子，也是调节 SMAX1/SMXLs 蛋白酶体介导降解的 SCF 复合物的组成部分。SMXL6、7 和 8 蛋白促进分枝并抑制叶柄伸长。我们的研究发现，SMAX1 的积累抑制了莲座丛分枝，并增加了主花序茎上的茎生分枝、株高、叶柄长度和叶长/宽比。SMAX1 的积累增强了调节分枝的 BRC1、HB53、HB40 和 HB21 的表达。SMAX1 还调节参与生长素运输、细胞分裂素信号通路和 SL 生物合成的基因的表达。这些基因的表达分析表明，过量的 SMAX1 应该加速植物中生长素的运输和 SL 的生物合成。高 SL 浓度抑制在植物中积累 SMAX1 蛋白的 smax1D 突变体中的芽发育。然而，在过量 SMAX1 的突变体中，细胞分裂素和生长素对分枝的影响仍不清楚。SMAX1 通过调节 TCP1 的表达来调节叶片形状和叶柄长度。我们的研究结果揭示了 SMAX1 的新功能和分枝的新机制。
