Arabidopsis PCaP2 Plays an Important Role in Chilling Tolerance and ABA Response by Activating CBF- and SnRK2-Mediated Transcriptional Regulatory Network.

Arabidopsis PCaP2 Plays an Important Role in Chilling Tolerance and ABA Response by Activating CBF- and SnRK2-Mediated Transcriptional Regulatory Network.
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拟南芥 PCaP2 通过激活 CBF 和 SnRK2 介导的转录调控网络在耐冷性和 ABA 响应中发挥重要作用

DOI:
10.3389/fpls.2018.00215
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发表时间:
2018
影响因子:
5.6
通讯作者:
Wang C
Wang C
中科院分区:
生物学2区
文献类型:
--
作者:
Wang X;Wang L;Wang Y;Liu H;Hu D;Zhang N;Zhang S;Cao H;Cao Q;Zhang Z;Tang S;Song D;Wang C

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低温胁迫影响植物生长和生产力。然而,抗寒性的多个潜在机制还没有得到很好的理解。拟南芥PCaP 2参与调控微管(MTs)和F-actin的动态变化以及与Ca ~(2+)结合的能力。结果表明,低温胁迫下,PCaP 2在根、子叶、真叶、侧根和花中的表达均被诱导。与野生型相比,PCaP 2过表达的拟南芥表现出更强的耐冷性,而其RNAi和突变体在拟南芥种子萌发、幼苗生长和生殖生长过程中表现出更强的耐冷性。此外,通过分析PCaP 2的表达以及PCaP 2过表达植株、突变体和RNAi植株在阿坝处理下的表型,发现PCaP 2也是阿坝信号通路的正调控因子。有趣的是,PCaP 2的破坏抑制CBF 1,-3和CBF-targetCOR基因的表达,而CBF 2的表达增加响应冷或阿坝。PCaP 2突变体下调SnRK 2. 2、-2. 3和SnRK 2介导的下游基因ABF 2、RD 29 A、KIN 1、KIN 2的转录水平,上调SnRK 2.6、ABF 1、-3、-4在阿坝和低温处理中的转录水平。PCaP 2作为一种钙离子结合蛋白,通过调控基因的表达来提高植物的耐冷性。我们进一步的研究表明,MT去稳定PCaP 2的活性,而不是F-肌动蛋白切断功能,可能参与低温胁迫。综上所述,我们的研究结果表明PCaP 2通过激活CBF和SnRK 2介导的转录调控途径,在植物的耐冷性和阿坝反应中发挥重要作用,为低温胁迫下多途径调控机制的研究提供了新的证据。
Chilling stress affects plant growth and productivity. However, the multi-underlying mechanisms of chilling tolerance are not well understood. Arabidopsis PCaP2 is involved in regulating the dynamic of microtubules (MTs) and F-actin and Ca2+-binding ability. Here, the results showed that thePCaP2expression was highly induced in roots, cotyledons, true leaves, lateral roots and flowers under cold stress. Compared with the wild type,PCaP2-overexpressing plants displayed the enhanced tolerance, whereas its RNAi and mutant were more sensitive in seed germination, seedling and reproductive growth under chilling stress in Arabidopsis. In addition, PCaP2 was also a positive regulator of ABA signaling pathway by analyzing the expression ofPCaP2and the phenotypes of PCaP2-overexpressing, mutant and RNAi plants under ABA treatment. Interestingly, disruption ofPCaP2inhibited the expression ofCBF1,-3and CBF-targetCORgenes, while increased theCBF2expression in response to cold or ABA. Moreover, we found that SnRK2s were involved in cold stress andPCaP2mutants down-regulated the transcription level of SnRK2.2, -2.3 and SnRK2-mediated downstream genes includingABF2,RD29A,KIN1,KIN2, but up-regulatedSnRK2.6,ABF1,-3,-4in ABA and cold treatments. It is well-accepted that PCaP2 as a Ca2+-binding protein triggers the gene expression to enhance plant chilling tolerance. Our further studies showed that MT destabilizing activity of PCaP2, but not F-actin-severing function, may be involved in chilling stress. Taken together, our results highlight that PCaP2 plays an important role in chilling tolerance and ABA response by triggering the CBF- and SnRK2-meditated transcriptional regulatory pathways, providing novel evidences of underlying mechanisms of multi-pathways in chilling stress.
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