Labeling of the ATP synthase of Escherichia coli from the head-group region of the lipid bilayer

Biochemistry ◽  
1987 ◽  
Vol 26 (22) ◽  
pp. 7107-7113 ◽  
Author(s):  
Robert Aggeler ◽  
Yu Zhong Zhang ◽  
Roderick A. Capaldi
Keyword(s):  
Escherichia Coli ◽  
Lipid Bilayer ◽  
Atp Synthase ◽  
Head Group

scholarly journals The Regulatory C-Terminal Domain of Subunit   of FoF1 ATP Synthase Is Dispensable for Growth and Survival of Escherichia coli

2011 ◽  
Vol 193 (8) ◽  
pp. 2046-2052 ◽  
Author(s):  
N. Taniguchi ◽  
T. Suzuki ◽  
M. Berney ◽  
M. Yoshida ◽  
G. M. Cook
Keyword(s):  
Escherichia Coli ◽  
Atp Synthase ◽  
Growth And Survival ◽  
Terminal Domain ◽  
Fof1 Atp Synthase

scholarly journals Genome-Wide Screening Identifies Six Genes That Are Associated with Susceptibility to Escherichia coli Microcin PDI

2015 ◽  
Vol 81 (20) ◽  
pp. 6953-6963 ◽  
Author(s):  
Zhe Zhao ◽  
Lauren J. Eberhart ◽  
Lisa H. Orfe ◽  
Shao-Yeh Lu ◽  
Thomas E. Besser ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Atp Synthase ◽  
Disulfide Bonds ◽  
Gene Knockout ◽  
Single Gene ◽  
Site Directed Mutagenesis ◽  
Content Type ◽  
E Coli ◽  
Synthase Inhibitor ◽  
Loss Of Susceptibility

ABSTRACTThe microcin PDI inhibits a diverse group of pathogenicEscherichia colistrains. Coculture of a single-gene knockout library (BW25113;n= 3,985 mutants) against a microcin PDI-producing strain (E. coli25) identified six mutants that were not susceptible (ΔatpA, ΔatpF, ΔdsbA, ΔdsbB, ΔompF, and ΔompR). Complementation of these genes restored susceptibility in all cases, and the loss of susceptibility was confirmed through independent gene knockouts inE. coliO157:H7 Sakai. Heterologous expression ofE. coliompFconferred susceptibility toSalmonella entericaandYersinia enterocoliticastrains that are normally unaffected by microcin PDI. The expression of chimeric OmpF and site-directed mutagenesis revealed that the K47G48N49region within the first extracellular loop ofE. coliOmpF is a putative binding site for microcin PDI. OmpR is a transcriptional regulator forompF, and consequently loss of susceptibility by the ΔompRstrain most likely is related to this function. Deletion of AtpA and AtpF, as well as AtpE and AtpH (missed in the original library screen), resulted in the loss of susceptibility to microcin PDI and the loss of ATP synthase function. Coculture of a susceptible strain in the presence of an ATP synthase inhibitor resulted in a loss of susceptibility, confirming that a functional ATP synthase complex is required for microcin PDI activity. Intransexpression ofompFin the ΔdsbAand ΔdsbBstrains did not restore a susceptible phenotype, indicating that these proteins are probably involved with the formation of disulfide bonds for OmpF or microcin PDI.

scholarly journals Overproduction and purification of the uncI gene product of the ATP synthase of Escherichia coli.

1990 ◽  
Vol 265 (1) ◽  
pp. 389-395
Author(s):  
B Schneppe ◽  
G Deckers-Hebestreit ◽  
K Altendorf
Keyword(s):  
Escherichia Coli ◽  
Gene Product ◽  
Atp Synthase
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