A cluster of mutations determining erythromycin resistance in Bacillus subtilis.
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The structural and functional organization of F-factor reviewed and the physical map of F DNA, supplemented with a list of genetic markers, is presented. The DNA transfer during the conjugation is considered and especial attention is given to F-gene functions involved in this process. The special sequences of F DNA, homologous to resident insertion sequences in bacterial DNA are described and its participation in plasmido-chromosomal recombinant events both dependent and independent on recA function is discussed. The mechanism for chromosome mobilization by F-Factor are reviewed. A possibility of chromosome transfer without F DNA insertion is considered. In a latter case it proposed that spontaneous single-strand breaks may serve as the origins for initiation of chromosomal transfer.
A sudden induction of the imbalance between the rates of DNA and protein synthesis in the cell (by nalidixic acid or by thymine starvation) results in the stabilization of breaks in DNA chains in vivo. Such "imbalance induced breaks" represent gaps in DNA chains formed with the participation of exonuclease V. Stabilization of the "imbalance induced breaks" is accompanied by DNA degradation and cell death. Restoration of the imbalance between the rates of DNA and protein syntheses by balanced inhibition completely prevents the stabilization of breaks in cells with competent repair systems. Balanced inhibition of intracellular DNA and protein synthesis decreases the rate of repair and permits to see the sequence of induction (stabilization) and disappearance (repair) of breaks in DNA chains in vivo. Repair of breaks occuring on the background of balanced inhition of DNA and protein synthesis decreases the extent of DNA degradation and completely prevents death of E. coli cells with completely functional repair systems.
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