Cellulose is not only a common component in vascular plants, but also has great economic benefits for paper, wood, and industrial products. In addition, its biosynthesis is highly regulated by carbohydrate metabolism and allocation in plant. MdFRK2, which encodes a key fructokinase (FRK) in apple, showed especially high affinity to fructose and regulated carbohydrate metabolism. It was observed that overexpression of MdFRK2 in apple decreased sucrose (Suc) and fructose (Fru) with augmented FRK activity in stems, and caused the alterations of many phenotypic traits that include increased cellulose content and an increase in thickness of the phloem region. To further investigate the involved mechanisms, we generated FRK2-OE poplar lines OE#1, OE#4 and OE#9 and discovered (1) that overexpression of MdFRK2 resulted in the huge increased cellulose level by shifting the fructose 6-phosphate or glucose 6-phsophate towards UDPG formation, (2) a direct metabolic pathway for the biosynthesis of cellulose is that increased cleavage of Suc into UDP-glucose (UDPG) for cellulose synthesis via the increased sucrose synthase (SUSY) activity and transcript levels of PtrSUSY1, (3) that the increased FRK activity increases the sink strength overall so there is more carbohydrate available to fuel increased cambial activity and that resulted in more secondary phloem. These results demonstrated that MdFRK2 overexpression would significantly changes the photosynthetic carbon flux from sucrose and hexose to UDPG for increased cellulose synthesis. The present data indicated that MdFRK2 overexpression in apple and poplar changes the photosynthetic carbon flux from sucrose and hexose to UDPG for stem cellulose synthesis. A strategy is proposed to increase cellulose production by regulating sugar metabolism as a whole.

中文翻译：

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MdFRK2介导的糖代谢加速苹果和杨树的纤维素积累

纤维素不仅是维管植物中的常见成分，而且对造纸、木材和工业产品具有巨大的经济效益。此外，其生物合成受到植物中碳水化合物代谢和分配的高度调节。MdFRK2 编码苹果中的关键果糖激酶 (FRK)，对果糖表现出特别高的亲和力并调节碳水化合物代谢。据观察，苹果中 MdFRK2 的过表达降低了蔗糖 (Suc) 和果糖 (Fru)，并增强了茎中的 FRK 活性，并导致了许​​多表型性状的改变，包括纤维素含量增加和韧皮部区域厚度增加。为了进一步研究所涉及的机制，我们生成了 FRK2-OE 杨树品系 OE#1，OE#4 和 OE#9 并发现 (1) MdFRK2 的过表达通过将 6-磷酸果糖或 6-磷酸葡萄糖转移到 UDPG 形成，导致纤维素水平大幅增加，(2) 直接代谢途径用于生物合成纤维素是通过增加蔗糖合酶 (SUSY) 活性和 PtrSUSY1 的转录水平，增加 Suc 裂解为 UDP-葡萄糖 (UDPG) 以进行纤维素合成，(3) 增加的 FRK 活性增加了整体的汇强度，因此有更多的碳水化合物可用于促进形成层活动的增加，从而导致更多的次生韧皮部。这些结果表明，MdFRK2 过表达会显着改变从蔗糖和己糖到 UDPG 的光合碳通量，以增加纤维素合成。目前的数据表明，苹果和杨树中的 MdFRK2 过表达将光合碳通量从蔗糖和己糖改变为用于茎纤维素合成的 UDPG。提出了一种通过整体调节糖代谢来增加纤维素产量的策略。