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J L Flagg

Publications and source records attributed to J L Flagg.

5 recordsLinked to original sources

A novel type of coupling between proline and galactoside transport in Escherichia coli.

Exit of thiomethylgalactoside (TMG) from preloaded cells induced the accumulation of proline. Likewise, proline exit stimulated TMG accumulation. Since a proton ionophore (carbonylcyanide-m-chlorophenylhydrazone) abolished these effects, a protonmotive force was implicated as the "intermediate" in the coupling reaction. The evidence suggests that the exit of TMG resulted in proton exit, which produced either a membrane potential (inside negative or a pH gradient (outside acid) or both. This inwardly directed protonmotive force provided the energy for proline entry and accumulation. Thus the energy coupling was not via a common transport protein but by proton movements which coupled the two separate H+-dependent transport processes.

Biological Transport↗

A protonmotive force as the source of energy for galactoside transport in energy depleted Escherichia coli.

An artificially produced electrochemical potential difference for protons (portonmotive force) provided the energy for the transport of galactosides in Escherichia coli cells which were depleted of their endogenous energy reserves. The driving force for the entry of protons was provided by either a transmembrane pH gradient or a membrane potential. The pH gradient across the membrane was created by acidifying the external medium. The membrane potential (inside negative) was established by the outward diffusion of potassium (in the presence of valinomycin) or by the inward diffusion of the permeant thiocyanate ion. The magnitude of the electrochemical potential difference for protons agreed well with magnitude of the chemical potential difference of the lactose analog, thiomethylgalactoside. The observations are consistent with the view that the carrier-mediated entry of each galactoside molecule is accompanied by the entry of one proton.

Adenosine Triphosphate↗

lacY mutant of Escherichia coli with altered physiology of lactose induction.

A mutant of Escherichia coli is described that grew on lactose only in the presence of isopropylthiogalactoside. This cell contained a defect in the lacY gene that resulted in the formation of a transport system with a poor affinity for lactose. The inability to grow on lactose alone was due to the failure of induction by this disaccharide. This failure of inducation was presumably due to a defect in lactose accumulation which resulted in significant reduction in the formation of allo-lactose, the true inducer of lac operon. These results are consistent with the view that the capacity to accumulate lactose plays an important physiological role in the induction of the enzymes necessary for its utilization.

Biological Transport, Active↗