Karrikins and strigolactones govern plant development and environmental responses through closely related signaling pathways. The transcriptional repressor proteins SUPPRESSOR OF MAX2 1 (SMAX1), SMAX1-like2 (SMXL2), and D53-like SMXLs mediate karrikin and strigolactone signaling by directly binding downstream genes or by inhibiting the activities of transcription factors. In this study, we characterized the non-transcriptional regulatory activities of SMXL proteins in . We discovered that SMAX1 and SMXL2 with mutations in their ethylene-response factor-associated amphiphilic repression (EAR) motif had undetectable or weak transcriptional repression activities but still partially rescued the hypocotyl elongation defects and fully reversed the cotyledon epinasty defects of the mutant. SMAX1 and SMXL2 directly interact with PHYTOCHROME INTERACTION FACTOR 4 (PIF4) and PIF5 to enhance their protein stability by interacting with phytochrome B (phyB) and suppressing the association of phyB with PIF4 and PIF5. The karrikin-responsive genes were then identified by treatment with GR24, a GR24 analog showing karrikin activity. Interestingly, () expression was repressed by GR24 treatment in a PIF4- and PIF5-dependent and EAR-independent manner, whereas () expression was induced in a PIF4- and PIF5-independent and EAR-dependent manner. Furthermore, the non-transcriptional regulatory activity of SMAX1, which is independent of the EAR motif, had a global effect on gene expression. Taken together, these results indicate that non-transcriptional regulatory activities of SMAX1 and SMXL2 mediate karrikin-regulated seedling response to red light.

中文翻译：

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SMAX1 和 SMXL2 的非转录调节活性介导拟南芥中 karrikin 调节的幼苗对红光的反应


Karrikins 和独脚金内酯通过密切相关的信号通路控制植物发育和环境反应。转录阻遏蛋白 SUPPRESSOR OF MAX2 1 (SMAX1)、SMAX1-like2 (SMXL2) 和 D53-like SMXL 通过直接结合下游基因或抑制转录因子的活性来介导 karrikin 和独脚金内酯信号传导。在这项研究中，我们表征了 SMXL 蛋白的非转录调节活性。我们发现，乙烯反应因子相关的两亲性抑制（EAR）基序发生突变的SMAX1和SMXL2具有不可检测或微弱的转录抑制活性，但仍部分挽救了突变体的下胚轴伸长缺陷并完全逆转了子叶上上缺陷。 SMAX1 和 SMXL2 直接与 PHYTOCHROME INTERACTION FACTOR 4 (PIF4) 和 PIF5 相互作用，通过与光敏色素 B (phyB) 相互作用并抑制 phyB 与 PIF4 和 PIF5 的结合来增强其蛋白质稳定性。然后通过用 GR24（一种显示 karrikin 活性的 GR24 类似物）处理来鉴定 karrikin 反应基因。有趣的是，GR24 处理以 PIF4 和 PIF5 依赖且 EAR 独立的方式抑制 () 表达，而 () 表达以 PIF4 和 PIF5 独立且 EAR 依赖的方式诱导。此外，SMAX1 的非转录调控活性独立于 EAR 基序，对基因表达具有全局影响。综上所述，这些结果表明 SMAX1 和 SMXL2 的非转录调节活性介导 karrikin 调节的幼苗对红光的反应。