FIP1 Plays an Important Role in Nitrate Signaling and Regulates CIPK8 and CIPK23 Expression in Arabidopsis.
FIP1 Plays an Important Role in Nitrate Signaling and Regulates CIPK8 and CIPK23 Expression in Arabidopsis.
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FIP1 在拟南芥硝酸盐信号传导中发挥重要作用并调节 CIPK8 和 CIPK23 表达
DOI：
10.3389/fpls.2018.00593
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发表时间：
2018
影响因子：
5.6
通讯作者：
Wang Y
中科院分区：
文献类型：
--
作者：
Wang C;Zhang W;Li Z;Li Z;Bi Y;Crawford NM;Wang Y
揭示硝酸盐调控的分子机制和破译潜在的遗传网络对于阐明植物对硝酸盐的吸收和利用至关重要。这些知识可以提高农业氮素利用效率。在这里，我们报道了FIP1基因（与poly(A) polymerase 1相互作用的因子）在拟南芥（Arabidopsis thaliana）的硝酸盐信号传导中起重要作用。FIP1编码聚腺苷化因子复合体的一个假定的核心成分。我们发现FIP1与裂解和聚腺苷酸化特异性因子30-L （CPSF30-L）相互作用，CPSF30-L也是硝酸盐信号传导的重要参与者。在fip1突变体中，硝酸盐处理后的硝酸盐应答基因的诱导被抑制。由于fip1幼苗的硝酸盐吸收活性降低，其硝酸盐含量也有所降低。此外，fip1的根中硝酸盐含量较高，而根中硝酸盐含量较低，这可能与NRT1.8的下调和硝酸盐同化基因的上调有关。此外，qPCR分析显示，FIP1负调控CIPK8和CIPK23的表达，这两种蛋白激酶参与硝酸盐信号传导。在fip1突变体中，CIPK23的表达增加可能会影响硝酸盐的吸收，导致其硝酸盐含量降低。遗传和分子证据表明，FIP1和CPSF30-L在相同的硝酸盐信号通路中起作用，FIP1通过与CPSF30-L的相互作用以及对CIPK8和CIPK23的调控介导信号传导。NRT1.1的3 ' -UTR分析显示，fip1突变体的多聚腺苷化位点模式发生了改变。这些发现为硝酸盐调控网络增加了一个新的组成部分，并增强了我们对硝酸盐信号传导潜在机制的理解。
Unraveling the molecular mechanisms of nitrate regulation and deciphering the underlying genetic network is vital for elucidating nitrate uptake and utilization in plants. Such knowledge could lead to the improvement of nitrogen-use efficiency in agriculture. Here, we report that the FIP1 gene (factor interacting with poly(A) polymerase 1) plays an important role in nitrate signaling in Arabidopsis thaliana. FIP1 encodes a putative core component of the polyadenylation factor complex. We found that FIP1 interacts with the cleavage and polyadenylation specificity factor 30-L (CPSF30-L), which is also an essential player in nitrate signaling. The induction of nitrate-responsive genes following nitrate treatment was inhibited in the fip1 mutant. The nitrate content was also reduced in fip1 seedlings due to their decreased nitrate uptake activity. Furthermore, the nitrate content was higher in the roots but lower in the roots of fip1, which may result from the downregulation of NRT1.8 and the upregulation of the nitrate assimilation genes. In addition, qPCR analyses revealed that FIP1 negatively regulated the expression of CIPK8 and CIPK23, two protein kinases involved in nitrate signaling. In the fip1 mutant, the increased expression of CIPK23 may affect nitrate uptake, resulting in its lower nitrate content. Genetic and molecular evidence suggests that FIP1 and CPSF30-L function in the same nitrate-signaling pathway, with FIP1 mediating signaling through its interaction with CPSF30-L and its regulation of CIPK8 and CIPK23. Analysis of the 3′-UTR of NRT1.1 showed that the pattern of polyadenylation sites was altered in the fip1 mutant. These findings add a novel component to the nitrate regulation network and enhance our understanding of the underlying mechanisms for nitrate signaling.
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影响因子：
16.6
作者：
Medici, Anna;Marshall-Colon, Amy;Ronzier, Elsa;Szponarski, Wojciech;Wang, Rongchen;Gojon, Alain;Crawford, Nigel M.;Ruffel, Sandrine;Coruzzi, Gloria M.;Krouk, Gabriel
通讯作者：
Krouk, Gabriel
DOI：
10.1073/pnas.1404657111
发表时间：
2014-07-15
影响因子：
11.1
作者：
Para, Alessia;Li, Ying;Coruzzi, Gloria M.
通讯作者：
Coruzzi, Gloria M.
影响因子：
16.6
作者：
Marchive, Chloe;Roudier, Francois;Krapp, Anne
通讯作者：
Krapp, Anne
影响因子：
7.4
作者：
Bruggeman, Quentin;Garmier, Marie;Delarue, Marianne
通讯作者：
Delarue, Marianne
影响因子：
56.9
作者：
Alonso, JM;Stepanova, AN;Ecker, JR
通讯作者：
Ecker, JR