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质体叶酸可防止糖流入拟南芥非光合质体引发的淀粉生物合成。

Plastidial Folate Prevents Starch Biosynthesis Triggered by Sugar Influx into Non-Photosynthetic Plastids of Arabidopsis.

机构信息

Department of Bioscience, Nagahama Institute of Bioscience and Technology, Tamura 1266, Nagahama, Shiga 526-0829, Japan.

Department of Cell Biology, National Institute for Basic Biology, Okazaki 444-8585, Japan.

出版信息

Plant Cell Physiol. 2017 Aug 1;58(8):1328-1338. doi: 10.1093/pcp/pcx076.

Abstract

Regulation of sucrose-starch interconversion in plants is important to maintain energy supplies necessary for viability and growth. Arabidopsis mutants were screened for aberrant responses to sucrose to identify candidates with a defect in the regulation of starch biosynthesis. One such mutant, fpgs1-4, accumulated substantial amounts of starch in non-photosynthetic cells. Dark-grown mutant seedlings exhibited shortened hypocotyls and accumulated starch in etioplasts when supplied with exogenous sucrose/glucose. Similar starch accumulation from exogenous sucrose was observed in mutant chloroplasts, when photosynthesis was prevented by organ culture in darkness. Molecular genetic analyses revealed that the mutant was defective in plastidial folylpolyglutamate synthetase, one of the enzymes engaged in folate biosynthesis. Active folate derivatives are important biomolecules that function as cofactors for a variety of enzymes. Exogenously supplied 5-formyl-tetrahydrofolate abrogated the mutant phenotypes, indicating that the fpgs1-4 mutant produced insufficient folate derivative levels. In addition, the antifolate agents methotrexate and 5-fluorouracil induced starch accumulation from exogenously supplied sucrose in dark-grown seedlings of wild-type Arabidopsis. These results indicate that plastidial folate suppresses starch biosynthesis triggered by sugar influx into non-photosynthetic cells, demonstrating a hitherto unsuspected link between plastidial folate and starch metabolism.

摘要

植物中蔗糖-淀粉相互转化的调控对于维持生存和生长所需的能量供应非常重要。筛选拟南芥突变体以研究其对蔗糖的异常反应,以鉴定在淀粉生物合成调控中存在缺陷的候选物。一个这样的突变体,fpgs1-4,在非光合细胞中积累了大量的淀粉。黑暗生长的突变体幼苗在供应外源蔗糖/葡萄糖时,表现出短化的下胚轴,并在黄化质体中积累淀粉。当光合作用被黑暗中的器官培养所阻止时,类似的淀粉积累也发生在突变体叶绿体中。分子遗传学分析表明,该突变体在质体叶酰多谷氨酸合成酶中有缺陷,该酶参与叶酸生物合成。活性叶酸衍生物是重要的生物分子,作为多种酶的辅助因子发挥作用。外源 5-甲酰四氢叶酸消除了突变体表型,表明 fpgs1-4 突变体产生的叶酸衍生物水平不足。此外,抗叶酸剂氨甲蝶呤和 5-氟尿嘧啶在黑暗生长的拟南芥野生型幼苗中诱导外源供应的蔗糖积累淀粉。这些结果表明质体叶酸抑制了糖流入非光合细胞所引发的淀粉生物合成,表明质体叶酸和淀粉代谢之间存在以前未被怀疑的联系。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ad2/5921527/76690be79853/pcx076f1.jpg

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