1959
DOI: 10.1073/pnas.45.12.1786
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Hereditary Defects in Galactose Metabolism in Escherichia Coli Mutants, Ii. Galactose-Induced Sensitivity

Abstract: 26 The composition per liter volume is as follows: galactose, 10 gm.; casein digest, 8 gm.; yeast extract, 1 gm.; sodium chloride, 5 gm.; K3HPO4, 2 gm.; eosin Y, 0.4 gm.; methylene blue, 0.065 gm. and agar 15 gm.; 20 to 25 ml. was used for a Petri plate, according to Lederberg, J.

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Cited by 98 publications
(76 citation statements)
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“…This result suggests that the enzyme is primarily involved in biosynthetic pathways rather than in the metabolism of galactose from external or internal sources. Bacterial and yeast mutants deficient in UDP-Glc epimerase are highly sensitive to galactose (Douglas and Hawthorne, 1964;Yarmolinsky et al, 1959). It has also long been known that many plants are sensitive to external application of galactose (e.g.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…This result suggests that the enzyme is primarily involved in biosynthetic pathways rather than in the metabolism of galactose from external or internal sources. Bacterial and yeast mutants deficient in UDP-Glc epimerase are highly sensitive to galactose (Douglas and Hawthorne, 1964;Yarmolinsky et al, 1959). It has also long been known that many plants are sensitive to external application of galactose (e.g.…”
Section: Discussionmentioning
confidence: 99%
“…Mutants of Escherichia coli or yeast affected in galE or gal10, respectively, are characterized by their inability to grow on media containing galactose (Douglas and Hawthorne, 1964;Yarmolinsky et al, 1959). In humans, certain forms of galactosaemia, a pathological increase of galactose content in the blood, are caused by a defect in the UDP-Glc epimerase gene (Daude et al, 1995).…”
Section: Introductionmentioning
confidence: 99%
“…Second, an h8-derived triple mutant, with mutations in fda gnd pgi, which does not convert glucose into fructose-6-phosphate because of blocks in the glucose-6-phosphate isomerase and the 6-phosphogluconate dehydrogenase, and therefore does not accumulate fructose-1,6-diphosphate, can grow on glucose at 42°C (50 diphosphate is toxic to cells. Accumulation of phosphorylated metabolic intermediates following growth on galactose, arabinose, or glycerol can be toxic to growing cells (9,14,15,18,31,61). The mode of action of toxic intermediates has not been determined for these systems.…”
Section: Jxci Of L-[35slmethionine-l-[35slcysteine Trans Labelmentioning
confidence: 99%
“…Thus, ppGpp is not an obligatory component of this control system. Although the effector for growth rate regulation is unknown, the fraction of ribosomes involved in active translation seems to be one element in this internal signal transduction pathway (8,29,61). Both the growth-rate and stringent responses are regulated at the level of transcription initiation (6,13,24,34,42,49,54).…”
mentioning
confidence: 99%
“…Although it has been the subject of decades of research, knowledge of the mechanisms controlling glycolytic flux are still incomplete, even in the well studied model organism Escherichia coli. Numerous studies have noted that bacterial strains with an impaired capacity to metabolize phosphorylated sugars (including some of the substrates of glycolysis) often show strong phenotypes of growth inhibition or in some cases cell lysis (1)(2)(3). However, until recently, little was known about the mechanisms used by bacterial cells to deal with metabolic stress associated with intracellular phosphosugar accumulation.…”
mentioning
confidence: 99%