背景2-PIFs & EIN3: As central transcription factors suppressing light responses, PHYTOCHROME-INTERACTING FACTORs (PIFs) and ETHYLENE-INSENSITIVE 3 (EIN3) actively function in darkness and must be promptly repressed upon light to initiate deetiolation.

背景3-微蛋白: Microproteins are evolutionarily conserved small single-domain proteins that act as posttranslational regulators in eukaryotes.

提出问题：Although hundreds to thousands of microproteins are predicted to exist in plants, their target molecules, biological roles, and mechanisms of action remain largely unknown.

主要发现：Here, we show that two microproteins, miP1a and miP1b (miP1a/b), are robustly stimulated in the dark-to-light transition.

结果-表达模式：miP1a/b are primarily expressed in cotyledons and hypocotyl, exhibiting tissue-specific patterns similar to those of PIFs and EIN3.

结果-生化机制：We demonstrate that PIFs and EIN3 assemble functional oligomers by self-interaction, while miP1a/b directly interact with and disrupt the oligomerization of PIFs and EIN3 by forming nonfunctional protein complexes. As a result, the DNA binding capacity and transcriptional activity of PIFs and EIN3 are predominantly suppressed.

结果-遗传实验：These biochemical findings are further supported by genetic evidence. miP1a/b positively regulate photomorphogenic development, and constitutively expressing miP1a/b rescues the delayed apical hook unfolding and cotyledon development of plants overexpressing PIFs and EIN3.

结论：Our study reveals that microproteins provide a temporal and negative control of the master transcription factors' oligomerization to achieve timely developmental transitions upon environmental changes.

 摘  要 

埋在土下的种子在萌发破土之时会经历剧烈的发育转变。作为抑制光响应的核心转录因子，光敏色素互作因子PIFs与EIN3在黑暗条件下表现活跃，但在植物破土见光之时必须要被抑制，从而起始去黄化。微蛋白是演化上保守的小的、具单个结构域的蛋白，在真核生物中作为翻译后调控因子发挥作用。尽管植物中存在数百至数千个微蛋白，但有关这些植物微蛋白的靶向分子、生物功能以及作用机制都还存在较大的研究空白。本文中，作者发现两个微蛋白miP1a和miP1b在植物由黑暗到光亮的转变时受到强烈刺激。miP1a/b基因主要在子叶和下胚轴中表达，存在与PIFs和EIN3类似的组织特异性表达模式。作者发现PIFs与EIN3能够通过自互作组装形成功能性的寡聚体，而miP1a/b能够直接结合并通过形成非功能性的蛋白复合物来扰乱PIFs和EIN3的寡聚化。因此，PIFs和EIN3的DNA结合能力以及转录活性被极大地抑制了。后续的遗传学实验进一步验证了这些生化发现。miP1a/b能够正向调控光形态发生，并且组成型表达miP1a/b能够拯救过表达PIFs和EIN3基因所导致的顶钩延迟展开和子叶发育的缺陷表型。本文的研究揭示了微蛋白通过对主效转录因子寡聚化的时空负调控，从而在植物遭遇环境变化时确保发育转变成功进行。