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Sugar sensing responses to low and high light in leaves of the C4 model grass Setaria viridis.
Journal of Experimental Botany ( IF 5.6 ) Pub Date : 2020-01-23 , DOI: 10.1093/jxb/erz495
Clémence Henry 1 , Alexander Watson-Lazowski 1 , Maria Oszvald 2 , Cara Griffiths 2 , Matthew J Paul 2 , Robert T Furbank 3 , Oula Ghannoum 1
Affiliation  

Although sugar regulates photosynthesis, the signalling pathways underlying this process remain elusive, especially for C4 crops. To address this knowledge gap and identify potential candidate genes, we treated Setaria viridis (C4 model) plants acclimated to medium light intensity (ML, 500 µmol m-2 s-1) with low (LL, 50 µmol m-2 s-1) or high (HL, 1000 µmol m-2 s-1) light for 4 d and observed the consequences on carbon metabolism and the transcriptome of source leaves. LL impaired photosynthesis and reduced leaf content of signalling sugars (glucose, sucrose, and trehalose-6-phosphate). In contrast, HL strongly induced sugar accumulation without repressing photosynthesis. LL more profoundly impacted the leaf transcriptome, including photosynthetic genes. LL and HL contrastingly altered the expression of hexokinase (HXK) and sucrose-non-fermenting 1 (Snf1)-related protein kinase 1 (SnRK1) sugar sensors and trehalose pathway genes. The expression of key target genes of HXK and SnRK1 were affected by LL and sugar depletion, while surprisingly HL and strong sugar accumulation only slightly repressed the SnRK1 signalling pathway. In conclusion, we demonstrate that LL profoundly impacted photosynthesis and the transcriptome of S. viridis source leaves, while HL altered sugar levels more than LL. We also present the first evidence that sugar signalling pathways in C4 source leaves may respond to light intensity and sugar accumulation differently from C3 source leaves.

中文翻译:

C4模型草狗尾草叶片中糖对低光和高光的响应。

尽管糖调节着光合作用,但这一过程的信号传导途径仍然难以捉摸,尤其是对于C4作物。为了解决这一知识鸿沟并确定潜在的候选基因,我们处理了适应中等光强度(ML,500 µmol m-2 s-1)和低(LL,50 µmol m-2 s-1)的狗尾草(C4模型)植物)或高光(HL,1000 µmol m-2 s-1)照射4 d,观察到对碳代谢和源叶片转录组的影响。LL损害了光合作用,降低了信号糖(葡萄糖,蔗糖和6磷酸海藻糖)的叶片含量。相反,HL强烈诱导糖积累而不抑制光合作用。LL更深刻地影响了叶片的转录组,包括光合作用基因。LL和HL分别改变了己糖激酶(HXK)和蔗糖非发酵1(Snf1)相关蛋白激酶1(SnRK1)糖传感器和海藻糖途径基因的表达。HXK和SnRK1关键靶基因的表达受LL和糖耗竭的影响,而令人惊讶的是HL和强糖的积累仅轻微抑制了SnRK1信号通路。总之,我们证明LL深刻影响了S. viridis源叶的光合作用和转录组,而HL改变的糖含量比LL更大。我们还提供了第一个证据,表明C4源叶中的糖信号通路可能对光强度和糖积累的响应不同于C3源叶。HXK和SnRK1关键靶基因的表达受LL和糖耗竭的影响,而令人惊讶的是HL和强糖的积累仅轻微抑制了SnRK1信号通路。总之,我们证明LL深刻影响了S. viridis源叶的光合作用和转录组,而HL改变的糖含量比LL更大。我们还提供了第一个证据,表明C4源叶中的糖信号通路可能对光强度和糖积累的响应不同于C3源叶。HXK和SnRK1关键靶基因的表达受LL和糖耗竭的影响,而令人惊讶的是HL和强糖的积累仅轻微抑制了SnRK1信号通路。总之,我们证明LL深刻影响了S. viridis源叶的光合作用和转录组,而HL改变的糖含量比LL更大。我们还提供了第一个证据,表明C4源叶中的糖信号通路可能对光强度和糖积累的响应不同于C3源叶。
更新日期:2020-01-24
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