The role of Tre6P and SnRK1 in maize early kernel development and events leading to stress-induced kernel abortion.
The role of Tre6P and SnRK1 in maize early kernel development and events leading to stress-induced kernel abortion.
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DOI：
10.1186/s12870-017-1018-2
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发表时间：
2017-04-12
影响因子：
5.3
通讯作者：
Lagrimini LM
中科院分区：
文献类型：
--
作者：
Bledsoe SW;Henry C;Griffiths CA;Paul MJ;Feil R;Lunn JE;Stitt M;Lagrimini LM
开花期间的干旱胁迫是玉米产量损失的主要原因。产量可持续性的遗传和生物技术改进需要了解产量损失的机制。蔗糖饥饿已被认为是导致籽粒败育的原因，然而，尚未确定遗传改良的潜在目标。玉米的田间和温室干旱研究是昂贵的，并且难以重现结果;因此，提出了一种体外籽粒培养方法作为玉米开花时（授粉后3天）发生的干旱胁迫的代表。这种方法是用来专注于干旱对籽粒代谢的影响，海藻糖6-磷酸（Tre 6P）和蔗糖非发酵-1-相关激酶（SnRK 1）作为这种反应的潜在调节剂的作用。在从植物中取出籽粒后的前两个小时内观察到Tre 6P的急剧下降，并且所产生的转录物丰度的变化指示SnRK 1的激活，以及从抗衰老到抗衰老的立即转变。一旦谷粒中的Tre 6P水平耗尽至低于1 nmol·g-1 FW，SnRK 1在整个96小时实验中保持活性，无论培养基中是否存在蔗糖。在富含蔗糖的培养基上的恢复导致蔗糖合成和糖酵解的恢复。生物合成过程，包括柠檬酸循环和蛋白质和淀粉的合成被抑制切除，并不恢复，即使在重新添加蔗糖。还观察到切除诱导糖转运蛋白SUT 1和SWEET 1、蔗糖水解酶细胞壁转化酶2（INCW 2）和蔗糖合成酶1（SUSY 1）、II类海藻糖磷酸合成酶（TPS）、海藻糖酶（TRE）和海藻糖磷酸磷酸酶（ZmTPPA.3）的转录，这些酶先前显示增强耐旱性（Nuccio等人，Nat Biotechnol（October 2014）：1-13，2015）。从穗中切除籽粒的影响引发了一系列事件，这些事件始于Tre 6P水平的急剧下降。据推测，去除Tre 6P对SnRK 1活性的抑制导致了推定的SnRK 1靶基因的转录，以及从生物合成到催化的代谢转变。这突出了Tre 6P在对饥饿的代谢反应中的重要性。我们还提出了证据表明，糖可以介导SnRK 1的激活。Tre 6P的急剧下降对应于ZmTPPA.3转录的大幅增加，表明这种特异性酶可能是Tre 6P去磷酸化的原因。未成熟胚中高水平的Tre 6P对于防止籽粒败育可能是重要的。本文的在线版本（doi：10.1186/s12870-017-1018-2）包含补充材料，可供授权用户使用。
Drought stress during flowering is a major contributor to yield loss in maize. Genetic and biotechnological improvement in yield sustainability requires an understanding of the mechanisms underpinning yield loss. Sucrose starvation has been proposed as the cause for kernel abortion; however, potential targets for genetic improvement have not been identified. Field and greenhouse drought studies with maize are expensive and it can be difficult to reproduce results; therefore, an in vitro kernel culture method is presented as a proxy for drought stress occurring at the time of flowering in maize (3 days after pollination). This method is used to focus on the effects of drought on kernel metabolism, and the role of trehalose 6-phosphate (Tre6P) and the sucrose non-fermenting-1-related kinase (SnRK1) as potential regulators of this response. A precipitous drop in Tre6P is observed during the first two hours after removing the kernels from the plant, and the resulting changes in transcript abundance are indicative of an activation of SnRK1, and an immediate shift from anabolism to catabolism. Once Tre6P levels are depleted to below 1 nmol∙g−1 FW in the kernel, SnRK1 remained active throughout the 96 h experiment, regardless of the presence or absence of sucrose in the medium. Recovery on sucrose enriched medium results in the restoration of sucrose synthesis and glycolysis. Biosynthetic processes including the citric acid cycle and protein and starch synthesis are inhibited by excision, and do not recover even after the re-addition of sucrose. It is also observed that excision induces the transcription of the sugar transporters SUT1 and SWEET1, the sucrose hydrolyzing enzymes CELL WALL INVERTASE 2 (INCW2) and SUCROSE SYNTHASE 1 (SUSY1), the class II TREHALOSE PHOSPHATE SYNTHASES (TPS), TREHALASE (TRE), and TREHALOSE PHOSPHATE PHOSPHATASE (ZmTPPA.3), previously shown to enhance drought tolerance (Nuccio et al., Nat Biotechnol (October 2014):1–13, 2015). The impact of kernel excision from the ear triggers a cascade of events starting with the precipitous drop in Tre6P levels. It is proposed that the removal of Tre6P suppression of SnRK1 activity results in transcription of putative SnRK1 target genes, and the metabolic transition from biosynthesis to catabolism. This highlights the importance of Tre6P in the metabolic response to starvation. We also present evidence that sugars can mediate the activation of SnRK1. The precipitous drop in Tre6P corresponds to a large increase in transcription of ZmTPPA.3, indicating that this specific enzyme may be responsible for the de-phosphorylation of Tre6P. The high levels of Tre6P in the immature embryo are likely important for preventing kernel abortion. The online version of this article (doi:10.1186/s12870-017-1018-2) contains supplementary material, which is available to authorized users.