OsHAK1 controls the vegetative growth and panicle fertility of rice by its effect on potassium-mediated sugar metabolism
OsHAK1 controls the vegetative growth and panicle fertility of rice by its effect on potassium-mediated sugar metabolism
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OsHAK1 通过影响钾介导的糖代谢来控制水稻的营养生长和穗肥力
DOI：
10.1016/j.plantsci.2018.05.034
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发表时间：
2018-09-01
期刊：
影响因子：
5.2
通讯作者：
Qian, Qian
中科院分区：
文献类型：
--
作者：
Chen, Guang;Zhang, Yu;Qian, Qian
植物的生长和繁殖都是需要能量的过程;所需的能量由光合作用的产物提供。水稻的营养生长和繁殖成功都受到OsHAK 1基因功能拷贝缺失的影响。在此，野生型水稻和OsHAK 1敲除突变体之间的比较不仅证实了OsHAK 1缺失对根生长、花粉活力和育性的已知不利影响，而且还表明蔗糖磷酸合酶活性降低，并且叶片的蔗糖含量显著增加，这是由于部分阻断了蔗糖向韧皮部的加载。OsHAK 1基因敲除导致根和小穗中糖分配受损，伴随着叶鞘和穗轴中编码蔗糖转运蛋白的基因（SUT基因）的下调，该基因在韧皮部中活跃，以及根和小穗中编码单糖转运蛋白的基因（MST基因）的下调，该基因将己糖转运穿过植物质膜。蔗糖合成酶，酸性转化酶和中性转化酶的活性在过滤阶段测定的突变体植物的根，并在他们的小穗，在灌浆期间测定，显着低于野生型植物的等效器官。其结果是，总可溶性糖，葡萄糖和果糖库器官的供应减少，与根系生长和穗育性的突变的影响一致。与野生型植物相比，突变体在整个植物中积累较少的钾（K）。结论是，未能充分供应的需求，突变体的库器官的同化是负责其受损的表型，和K吸收的缺陷引起的OsHAK 1功能的丧失是负责糖代谢的中断。
Plant growth and reproduction are both energy-requiring processes; the necessary energy is supplied by the products of photosynthesis. Both the vegetative growth and reproductive success of rice are compromised by the absence of a functional copy of the gene OsHAK1. Here, a comparison between wild type rice and OsHAK1 knockout mutants not only confirmed the known detrimental effect of the absence of OsHAK1 on root growth, pollen viability and fertility, but also showed that sucrose phosphate synthase activity was lowered, and the sucrose content of the leaves was markedly increased, due to a partial block on the up-loading of sucrose into the phloem. The impaired allocation of sugar to the roots and spikelets caused by the knocking out of OsHAK1 was accompanied by a down-regulation in the leaf sheaths and panicle axes of genes encoding sucrose transporters (SUT genes), which are active in the phloem, as well as in the roots and spikelets of those encoding monosaccharide transporters (MST genes), which transport hexose sugars across the plant plasma membrane. The activity of sucrose synthase, acid invertase and neutral invertase in the roots of mutant plants assayed at the filtering stage, and in their spikelets, assayed during grain-filling, was significantly lower than in the equivalent organs of wild type plants. As a result, the supply of total soluble sugar, glucose and fructose to sink organs was reduced, consistent with the effect of the mutation on root growth and panicle fertility. Compared to wild type plants, the mutants accumulated less potassium (K) throughout the plant. The conclusion was that the failure to fully supply the demand of the mutant's sink organs for assimilate was responsible for its compromised phenotype, and that the deficiency in K uptake induced by the loss of OsHAK1 functionality was responsible for the disruption of sugar metabolism.