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Biomedical subjects

M A Lieberman

Publications and source records attributed to M A Lieberman.

At least 91 records · Page 5Linked to original sources
PubMed1976

Changes in active transport, intracellular adenosine 5'-triphosphate levels, macromolecular syntheses, and glycolysis in an energy-uncoupled mutant of Escherichia coli.

The temperature-sensitive Escherichia coli mutant ecfts metC (Lieberman and Hong, 1974), previously shown to be defective in the coupling of metabolic energy to active transport, is also altered in a wide variety of cellular activities at the nonpermissive temperature. These alterations include a lowering of intracellular adenosine 5'-triphosphate levels, an alteration of glucose metabolism such that large quantities of pyruvate and dihydroxyacetone phosphate are excreted into the medium, excretion of accumulated potassium ions, and a cessation of deoxyribonucleic acid, ribonucleic acid, and phospholipid synthesis. Since these effects closely mimic the action of colicins E1 and K on E. coli cells, the possibility that the ecf gene product is the primary biochemical target for these colicins is discussed.

Adenosine Triphosphate↗
PubMed1974

A mutant of Escherichia coli defective in the coupling of metabolic energy to active transport.

The isolation of a temperature-sensitive mutant of E. coli K12 whose active transport of amino acids and sugars is not coupled to metabolic energy at 42 degrees is described. This mutant cannot grow on succinate, fumarate, malate, or D-lactate as sole carbon source at 42 degrees and grows on glucose at 42 degrees with a reduced rate and yield. Efflux of accumulated substrate is also demonstrated upon heat inactivation. The defect of this mutant in both growth and transport is not due to a failure in electron transport through the respiratory chain nor the absence of Mg, Ca-ATPase activity. The mutant is thus distinct from the other energy-uncoupled mutants uncA, uncB, or etc. Analysis of spontaneous revertants indicates that the transport defect is caused by two mutations, one in the energy coupling factor gene and the other in the metC gene. The ecf(ts) mutation has been mapped to be in the 54.5- to 60-min region of the E. coli chromosome map. Possible interactions between the metC mutation and the mutated energy coupling factor protein are discussed.

Adenosine Triphosphatases↗