NtNAC028 and NtNAC080 form heterodimers to regulate jasmonic acid biosynthesis during leaf senescence in Nicotiana tabacum.
NtNAC028 and NtNAC080 form heterodimers to regulate jasmonic acid biosynthesis during leaf senescence in Nicotiana tabacum.
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DOI：
10.1093/jxb/erae006
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发表时间：
2024-01
影响因子：
6.9
通讯作者：
Mingyue Lu;Boyang Fu;Xiao Meng;Tiantian Jia;Xiaoyue Lu;Chaosha Yang;Ke-Lai Li;Pengcheng Yin;Yongfeng Guo;Wei Li;Jina Chi;Geng Wang;Chunjiang Zhou
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文献类型：
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作者：
Mingyue Lu;Boyang Fu;Xiao Meng;Tiantian Jia;Xiaoyue Lu;Chaosha Yang;Ke-Lai Li;Pengcheng Yin;Yongfeng Guo;Wei Li;Jina Chi;Geng Wang;Chunjiang Zhou
植物衰老是一个高度整合的发育阶段，涉及功能退化和养分重新分配。 NAM/ATAF1/CUC (NAC) 转录因子 (TF) 协调各种衰老相关信号并介导植物衰老的微调。先前的数据显示，NtNAC028或NtNAC080的敲除都会导致烟草（Nicotiana tabacum）叶片衰老延迟，这意味着NtNAC028和NtNAC080在叶片衰老的调控中发挥着各自的作用，尽管它们彼此有91.87%的同一性。然而，NtNAC028 和 NtNAC080 调节叶片衰老的机制仍然不清楚。在这里，我们确定 NtNAC028 和 NtNAC080 激活假定的茉莉酸（JA）生物合成基因 NtLOX3，并提高体内 JA 水平。我们发现 NtNAC028 和 NtNAC080 通过其 NA 末端区域彼此相互作用并自身相互作用。值得注意的是，只有 NtNAC028 和 NtNAC080 之间的二聚体刺激了转录激活活性，但不刺激该异二聚体对 NtLOX3 的 DNA 结合活性。代谢组分析表明，NtNAC028 或 NtNAC080 的过度表达会增强衰老阶段尼古丁的生物合成和降解。因此，我们得出结论，NtNAC028与NtNAC080协同形成异二聚体，增强NtLOX3表达和JA生物合成，从而引发叶片衰老并影响烟草的次生代谢。
Plant senescence, as a highly integrated developmental stage, involves functional degeneration and nutrient redistribution. NAM/ATAF1/CUC (NAC) transcription factors (TFs) orchestrate various senescence-related signals and mediate the fine-tuning underlying plant senescence. Previous data revealed that knockout of either NtNAC028 or NtNAC080 leads to delayed leaf senescence in tobacco (Nicotiana tabacum), which implies that NtNAC028 and NtNAC080 play respective roles in the regulation of leaf senescence, although they share 91.87% identity with each other. However, the mechanism underlying NtNAC028- and NtNAC080-regulated leaf senescence remains obscure. Here, we determined that NtNAC028 and NtNAC080 activate a putative jasmonic acid (JA) biosynthetic gene, NtLOX3, and enhance the JA level in vivo. We found that NtNAC028 and NtNAC080 interact with each other and themselves through their NA-terminal region. Remarkably, only the dimerization between NtNAC028 and NtNAC080 stimulated the transcriptional activation activity, but not the DNA binding activity of this heterodimer on NtLOX3. The metabolome analysis indicated that overexpression of either NtNAC028 or NtNAC080 augments both biosynthesis and degradation of nicotine in the senescent stages. Thus, we conclude that NtNAC028 cooperates with NtNAC080 and forms a heterodimer to enhance the NtLOX3 expression and the JA biosynthesis to trigger the onset of leaf senescence and impact the secondary metabolism in tobacco.