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Abstract
背景回顾：Hormone-activated proteolysis is a recurring theme of plant hormone signaling mechanisms. In strigolactone signaling, the enzyme-receptor DWARF14 (D14) and an F-box protein, MORE AXILLARY GROWTH2 (MAX2), mark SUPPRESSOR OF MAX2 1-LIKE (SMXL) family proteins SMXL6, SMXL7, and SMXL8 for rapid degradation. Removal of these transcriptional corepressors initiates downstream growth responses.
提出问题：The homologous proteins SMXL3, SMXL4, and SMXL5, however, are resistant to MAX2-mediated degradation.
结果1-SMXL5功能：We discovered that the smxl4 smxl5 mutant has enhanced responses to strigolactone. SMXL5 attenuates strigolactone signaling by interfering with AtD14-SMXL7 interactions. SMXL5 interacts with AtD14 and SMXL7, providing two possible ways to inhibit SMXL7 degradation.
结果2-EAR功能：SMXL5 function is partially dependent on an EAR motif that typically mediates interactions with the TOPLESS family of transcriptional corepressors. However, we find that loss of the EAR motif reduces SMXL5-SMXL7 interactions and the attenuation of strigolactone signaling by SMXL5.
结果3-作用机制：We hypothesize that integration of SMXL5 into heteromeric SMXL complexes reduces the susceptibility of SMXL6/7/8 proteins to strigolactone-activated degradation, and that the EAR motif promotes the formation or stability of these complexes.
结论：This mechanism may provide a way to spatially or temporally fine-tune strigolactone signaling through the regulation of SMXL5 expression or translation.
Two hypotheses of how SMXL5 attenuates strigolactone signaling.
摘 要
激素激活的蛋白水解是植物激素信号转导机制的不变主题。在独脚金内酯信号转导中，酶受体D14和一个F-box蛋白MAX2能够标记SMXL家族的SMXL6/7/8使其快速降解。移除掉这些转录共抑制因子会起始下游的生长响应。但是，SMXL家族SMXL3/4/5蛋白并不会受到MAX2介导的降解途径的影响。作者发现smxl4 smxl5双突对于独脚金内酯的响应增强了。SMXL5会通过干扰AtD14-SMXL7的互作，从而扰乱独脚金内酯信号转导。SMXL5与AtD14和SMXL7互作，因此可能会从两条途径来抑制SMXL7的降解。SMXL5的功能部分依赖于一个EAR基序，该基序能够介导与TPL家族转录共抑制子的互作。但是，作者发现丢失EAR基序会导致SMXL5-SMXL7互作的减弱，并且通过SMXL5来扰乱独脚金内酯信号转导。作者假设SMXL5加入到异源多聚复合体中会降低SMXL6/7/8蛋白对于受独脚金内酯激活的降解途径的敏感性，而EAR基序促进了这些复合体的形成或稳定。本文的研究显示可以通过调控SMXL5基因的表达或翻译，实现独脚金内酯信号转导的时空精确调控。
美国加州大学河滨分校David C. Nelson教授、湖南大学姚瑞枫教授以及崖州湾国家实验室青年科学家李擎天为该论文的共同通讯作者，李擎天、湖南大学博士生余海洋和中科院遗传发育所博士生常文文为该论文共同第一作者。该研究得到了美国国家科学基金会、海南省种业实验室、中国国家重点研发计划、深圳市科技创新委员会、中国国家自然科学基金、河北省自然科学基金以及德国科学基金会的资助。
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