A molecular framework underlying low-nitrogen- induced early leaf senescence in Arabidopsis thaliana
A molecular framework underlying low-nitrogen- induced early leaf senescence in Arabidopsis thaliana
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DOI：
10.1016/j.molp.2023.03.006
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发表时间：
2023-04-03
期刊：
影响因子：
27.5
通讯作者：
Wang，Yong
中科院分区：
文献类型：
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作者：
Fan，Hongmei;Quan，Shuxuan;Wang，Yong
氮 (N) 缺乏会导致叶片提前衰老，从而加速整个植物的成熟并严重降低作物产量。然而，缺氮引起的早期叶片衰老的分子机制仍不清楚，即使在模式物种拟南芥中也是如此。在这项研究中，我们通过酵母单杂交筛选，使用来自 NRT2.1 启动子的 NO3− 增强子片段，确定了生长、发育和剪接 1 (GDS1)（一种先前报道的转录因子）作为硝酸盐 (NO3−) 信号的新调节因子。我们发现，GDS1 通过影响多个 NO3−调节基因（包括硝酸盐调节基因 2 (NRG2)）的表达来促进 NO3−信号传导、吸收和同化。有趣的是，我们观察到gds1突变体在缺氮条件下表现出叶片早期衰老以及NO3含量和氮吸收减少。进一步的分析表明，GDS1 与几个衰老相关基因的启动子结合，包括光敏色素相互作用转录因子 4 和 5（PIF4 和 PIF5），并抑制其表达。有趣的是，我们发现缺氮会减少 GDS1 蛋白的积累，并且 GDS1 可以与后期促进复合体亚基 10 (APC10) 相互作用。遗传和生化实验表明，后期促进复合物或环体 (APC/C) 在缺氮条件下促进 GDS1 泛素化和降解，导致 PIF4 和 PIF5 抑制消失，从而导致叶片提前衰老。此外，我们发现GDS1的过度表达可以延缓拟南芥叶片衰老并提高种子产量和氮利用效率（NUE）。总之，我们的研究揭示了一个分子框架，说明了低氮诱导叶片早期衰老的新机制，并为提高产量和氮利用效率的作物品种遗传改良提供了潜在目标。
Nitrogen (N) deficiency causes early leaf senescence, resulting in accelerated whole-plant maturation and severely reduced crop yield. However, the molecular mechanisms underlying N-deficiency-induced early leaf senescence remain unclear, even in the model speciesArabidopsis thaliana. In this study, we identified Growth, Development and Splicing 1 (GDS1), a previously reported transcription factor, as a new regulator of nitrate (NO3−) signaling by a yeast-one-hybrid screen using a NO3−enhancer fragment from the promoter ofNRT2.1. We showed that GDS1 promotes NO3−signaling, absorption and assimilation by affecting the expression of multiple NO3−regulatory genes, includingNitrate Regulatory Gene2(NRG2). Interestingly, we observed thatgds1mutants show early leaf senescence as well as reduced NO3−content and N uptake under N-deficient conditions. Further analyses indicated that GDS1 binds to the promoters of several senescence-related genes, includingPhytochrome-Interacting Transcription Factors 4and5(PIF4andPIF5) and represses their expression. Interestingly, we found that N deficiency decreases GDS1 protein accumulation, and GDS1 could interact with Anaphase Promoting Complex Subunit 10 (APC10). Genetic and biochemical experiments demonstrated that Anaphase Promoting Complex or Cyclosome (APC/C) promotes the ubiquitination and degradation of GDS1 under N deficiency, resulting in loss ofPIF4andPIF5repression and consequent early leaf senescence. Furthermore, we discovered that overexpression ofGDS1could delay leaf senescence and improve seed yield and N-use efficiency (NUE) inArabidopsis. In summary, our study uncovers a molecular framework illustrating a new mechanism underlying low-N-induced early leaf senescence and provides potential targets for genetic improvement of crop varieties with increased yield and NUE.