Bergman Matthew E, Evans Sonia E, Kuai Xiahezi, Franks Anya E, Despres Charles, Phillips Michael A
Department of Cell and Systems Biology, University of Toronto, Toronto, ON M5S 3G5, Canada.
Department of Biological Sciences, Brock University, St. Catharines, ON L2S 3A1, Canada.
Plants (Basel). 2023 Sep 16;12(18):3284. doi: 10.3390/plants12183284.
Salicylic acid (SA) is produced by plants in response to pathogen infection. SA binds the NONEXPRESSOR OF PATHOGENESIS-RELATED GENES (NPR) family of receptors to regulate both positive (NPR1) and negative (NPR3/4) plant immune responses by interacting with the clade II TGACG (TGA) motif-binding transcription factors (TGA2, TGA5, and TGA6). Here, we report that the principal metabolome-level response to SA treatment in Arabidopsis is a reduction in sucrose and other free sugars. We observed nearly identical effects in the triple mutant, which lacks all clade II TGA transcription factors. The mutant presents reduced leaf blade development and elongated hypocotyls, roots, and petioles consistent with sucrose starvation. No changes were detected in auxin levels, and mutant seedling growth could be restored to that of wild-type by sucrose supplementation. Although the retrograde signal 2--methyl-D-erythritol-2,4-cyclodiphosphate is known to stimulate SA biosynthesis and defense signaling, we detected no negative feedback by SA on this or any other intermediate of the 2--methyl-D-erythritol-4-phosphate pathway. Trehalose, a proxy for the sucrose regulator trehalose-6-phosphate (T6P), was highly reduced in , suggesting that defense-related reductions in sugar availability may be controlled by changes in T6P levels. We conclude that the negative regulatory roles of TGA2/5/6 include maintaining sucrose levels in healthy plants. Disruption of TGA2/5/6-NPR3/4 inhibitory complexes by mutation or SA triggers sucrose reductions in Arabidopsis leaves, consistent with the 'pathogen starvation' hypothesis. These findings highlight sucrose availability as a mechanism by which TGA2/5/6 balance defense and development.
水杨酸（SA）是植物在病原体感染时产生的。SA与病程相关基因非表达子（NPR）家族受体结合，通过与II类TGACG（TGA）基序结合转录因子（TGA2、TGA5和TGA6）相互作用来调节植物的正向（NPR1）和负向（NPR3/4）免疫反应。在此，我们报告拟南芥中对SA处理的主要代谢组水平反应是蔗糖和其他游离糖的减少。我们在缺乏所有II类TGA转录因子的三重突变体中观察到了几乎相同的效果。该突变体叶片发育减少，下胚轴、根和叶柄伸长，这与蔗糖饥饿一致。生长素水平未检测到变化，通过补充蔗糖，突变体幼苗的生长可以恢复到野生型水平。尽管已知逆行信号2-甲基-D-赤藓糖醇-2,4-环二磷酸可刺激SA生物合成和防御信号传导，但我们未检测到SA对2-甲基-D-赤藓糖醇-4-磷酸途径的该中间体或任何其他中间体的负反馈。海藻糖是蔗糖调节剂海藻糖-6-磷酸（T6P）的替代物，在该突变体中高度降低，这表明与防御相关的糖可用性降低可能受T6P水平变化的控制。我们得出结论，TGA2/5/6的负调控作用包括维持健康植物中的蔗糖水平。通过突变或SA破坏TGA2/5/6-NPR3/4抑制复合物会引发拟南芥叶片中蔗糖减少，这与“病原体饥饿”假说一致。这些发现突出了蔗糖可用性是TGA2/5/6平衡防御和发育的一种机制。
