Citrus sinensis CBF1 Functions in Cold Tolerance by Modulating Putrescine Biosynthesis Through Regulation of ARGININE DECARBOXYLASE.
Citrus sinensis CBF1 Functions in Cold Tolerance by Modulating Putrescine Biosynthesis Through Regulation of ARGININE DECARBOXYLASE.
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DOI：
10.1093/pcp/pcab135
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发表时间：
2021-09
影响因子：
4.9
通讯作者：
Jie Song;Hao Wu;F. He;Jing Qu;Yue Wang;Chunlong Li;Ji-Hong Liu
中科院分区：
文献类型：
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作者：
Jie Song;Hao Wu;F. He;Jing Qu;Yue Wang;Chunlong Li;Ji-Hong Liu
C-repeat（CRT）结合因子（CBF）是已知的在冷应激反应中起重要作用的转录因子。精氨酸脱羧酶（ADC）介导的腐胺生物合成已被报道在暴露于寒冷条件下的植物中被激活，但CBFs是否可以调节ADC的表达和腐胺积累仍然是难以捉摸的。在本研究中，我们发现，冷上调ADC基因（CsADC）和提高内源腐胺含量的甜橙子（柑橘）。CsADC的启动子包含两个CRT序列，它们是CBF识别的典型元件。甜橙子基因组含有4个CBF（CsCBF 1 -4），其中CsCBF 1受冷诱导显著。CsCBF 1位于细胞核内，与CsADC启动子直接特异性结合，是一种转录激活因子。在甜橙子中，CsCBF 1的过量表达导致转基因植株中CsADC和腐胺水平显著升高，沿着的是其抗寒性显著增强。然而，预处理与D-精氨酸，ADC抑制剂，引起显着降低内源腐胺水平的过表达线，伴随着极大地损害耐冷性。综上所述，这些结果表明，甜橙子的CBF 1直接调节ADC的表达和调节腐胺的合成，以协调耐冷性。我们的研究结果揭示了通过靶向ADC基因在冷应激的存在下腐胺积累的转录调控。同时，本研究也阐明了脑血流介导的冷应激反应的新机制。
C-repeat (CRT) binding factors (CBFs) are well known to act as crucial transcription factors that function in cold stress response. Arginine decarboxylase (ADC)-mediated putrescine biosynthesis has been reported to be activated in plants exposed to cold conditions, but it remains elusive whether CBFs can regulate ADC expression and putrescine accumulation. In this study, we show that cold up-regulated ADC gene (CsADC) and elevation of endogenous putrescine content in sweet orange (Citrus sinensis). Promoter of CsADC contains two CRT sequences that are canonical elements recognized by CBFs. Sweet orange genome contains four CBFs (CsCBF1-4), in which CsCBF1 was significantly induced by cold. CsCBF1, located in the nucleus, was demonstrated to bind directly and specifically to the promoter of CsADC and acted as a transcriptional activator. Overexpression of CsCBF1 led to notable elevation of CsADC and putrescine level in sweet orange transgenic plants, along with remarkably enhanced cold tolerance, relative to the wild type (WT). However, pretreatment with D-arginine, an ADC inhibitor, caused prominent reduction of endogenous putrescine level in the overexpressing lines, accompanied by greatly compromised cold tolerance. Taken together, these results demonstrate that CBF1 of sweet orange directly regulates ADC expression and modulates putrescine synthesis for orchestrating the cold tolerance. Our findings shed light into the transcriptional regulation of putrescine accumulation through targeting the ADC gene in the presence of cold stress. Meanwhile, this study illustrates a new mechanism underlying the CBF-mediated cold stress response.