{"title":"Studies on the glucose-transport system in Escherichia coli with α-methylglucoside as substrate","authors":"H. Hagihira, T.H. Wilson, E.C.C. Lin","doi":"10.1016/0006-3002(63)90912-0","DOIUrl":null,"url":null,"abstract":"<div><p>The properties of the glucose-transport system of <em>Escherichia coli</em> K10 were studied by following intracellular accumulation of <sup>14</sup>C-labeled α-methylglucoside. A mutant defective in the uptake of glucose was found to be unable to accumulate α-methylglucoside to a significant level, confirming the view that the carrier for glucose also acts on α-methylglucoside. Although the glucoside was not incorporated into cellular constituents or metabolized for energy, about one-half of the accumulated molecules underwent phosphorylation while one-half remained as the free glucoside. Studies on the inhibition of uptake of the glucoside showed that the affinity of the compound depended upon the substituents on C-2, C-3 and C-6. Structural modifications at C-1, on the other hand, had relatively little effect on the affinity unless a large aglycone was added. α-Methylglucoside accumulated by the cells was gradually lost upon dilution of the cells in simple inorganic medium. The rate of exit could be accelerated by two groups of compounds: non-metabolizable structural analogs with affinity for the transport carrier and metabolizable compounds which entered the cell by other routes. The effect of the latter group depended upon their further metabolism within the cell rather than their own direct effects on the carrier system.</p></div>","PeriodicalId":94301,"journal":{"name":"Biochimica et biophysica acta","volume":"78 3","pages":"Pages 505-515"},"PeriodicalIF":0.0000,"publicationDate":"1963-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0006-3002(63)90912-0","citationCount":"60","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biochimica et biophysica acta","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/0006300263909120","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 60
Abstract
The properties of the glucose-transport system of Escherichia coli K10 were studied by following intracellular accumulation of 14C-labeled α-methylglucoside. A mutant defective in the uptake of glucose was found to be unable to accumulate α-methylglucoside to a significant level, confirming the view that the carrier for glucose also acts on α-methylglucoside. Although the glucoside was not incorporated into cellular constituents or metabolized for energy, about one-half of the accumulated molecules underwent phosphorylation while one-half remained as the free glucoside. Studies on the inhibition of uptake of the glucoside showed that the affinity of the compound depended upon the substituents on C-2, C-3 and C-6. Structural modifications at C-1, on the other hand, had relatively little effect on the affinity unless a large aglycone was added. α-Methylglucoside accumulated by the cells was gradually lost upon dilution of the cells in simple inorganic medium. The rate of exit could be accelerated by two groups of compounds: non-metabolizable structural analogs with affinity for the transport carrier and metabolizable compounds which entered the cell by other routes. The effect of the latter group depended upon their further metabolism within the cell rather than their own direct effects on the carrier system.