Genome-wide screen for Escherichia coli genes involved in repressing cell-to-cell transfer of non-conjugative plasmids.

Acquiring new genetic traits by lateral gene transfer is a bacterial strategy for environment adaptation. We previously showed that Escherichia coli could laterally transmit non-conjugative plasmids in co-cultures containing strains with and without the plasmid. In this study, using the Keio collection, a comprehensive library of E. coli knock-out mutants for non-essential genes, we screened for genes responsible for repressing cell-to-cell plasmid transfer in recipient cells. By stepwise screening, we identified 55 'transfer-up' mutants that exhibited approximately 2- to 30-fold increased activities. We confirmed plasmid acquisition by these 'up' mutants and revealed that there were no significant changes in antibiotic resistance in the original Keio strains. The presumed functions of these gene products covered a wide range of activities, including metabolism and synthesis, transport, transcription or translation and others. Two competence-gene homologues (ybaV and yhiR) were identified from among these genes. The presumed localizations of these 55 gene products were estimated to be 34 cytoplasmic proteins, 20 in or around the cell surface and 1 unknown location. Our results suggest that these 55 genes may be involved in repressing plasmid uptake during cell-to-cell plasmid transfer.

Effects of vasodilators on fibrin-induced pulmonary edema, so-called neurogenic pulmonary edema, in the rat.

The present study was undertaken to evaluate the effects of vasodilators on the development of neurogenic pulmonary edema. Pulmonary edema was induced by injecting fibrinogen and thrombin into the cisterna magna of vagotomized rats (fibrin-induced pulmonary edema). Before the intrathecal injections, rats were pretreated with intravenous injection of one of the following vasodilators: phentolamine, isoproterenol, nifedipine, diltiazem, isosorbide dinitrate, or substance P. Each vasodilator reduced the incidence of fibrin-induced pulmonary edema and lung-water ratio dose-dependently except nifedipine and diltiazem. There was a uniform relationship between the lung-water ratio and the prefibrin mean arterial pressure obtained under administration of different doses of the each drug. A similar relationship was obtained even if the drug used was different. Treatment with nifedipine or diltiazem, however, diminished the blood pressure but provided less protection against the development of pulmonary edema. The blood volume in edema-positive lungs was minimally different from that in edema-negative lungs. These results suggest that the neurogenic pulmonary edema may be effectively prevented by most vasodilators except Ca++-blockers.