Biomedical subjects
Publications and source records attributed to M B Yarmolinsky.
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P1 bacteriophage carries at least two replicons: a plasmid replicon and a viral lytic replicon. Since the isolated plasmid replicon can maintain itself stably at the low copy number characteristic of intact P1 prophage, it has been assumed that this replicon is responsible for driving prophage replication. We provide evidence that when replication from the plasmid replicon is prevented, prophage replication continues, albeit at a reduced rate. The residual plasmid replication is due to incomplete repression of the lytic replicon by the c1 immunity repressor. Incomplete repression was particularly evident in lysogens of the thermoinducible P1 c1.100 prophage, whose replication at 32 degrees C remained almost unaffected when use of the plasmid replicon was prevented. Moreover, the average plasmid copy number of P1 in a P1 c1.100 lysogen was elevated with respect to the copy number of P1 c1+. The capacity of the lytic replicon to act as an auxiliary in plasmid maintenance may contribute to the extraordinary stability of P1 plasmid prophage.
Nonparticipation of the bacterial dnaA gene in plasmid replication has been assumed to be the general rule. In conditional dnaA mutants of Escherichia coli, only plasmid pSC101 has been shown to have a dnaA requirement. Experiments with dnaA null mutants of E. coli, presented here, show that dnaA plays a critical and direct role in the replication of miniplasmids derived from P1 and F as it does in the initiation of bacterial replication. Evidence is also presented for the existence of a dnaA-independent secondary replicon of P1 that is able to drive bacterial chromosome replication but is inadequate to support the maintenance of P1 as a plasmid in E. coli.
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UV-damaged bacteriophage P1 causes an SOS response in infected bacteria that can be measured colorimetrically with the aid of a lambda pL-lacZ fusion strain of Escherichia coli. This response is blocked by a P1 prophage. Evidence is offered that the blockage is caused by the concerted action of the incompatibility determinant incA and the immunity (c1 and c4) repressors of the prophage. We suggest that indirect induction of lambda by damaged P1 is caused by the abortive initiation of replication in either of two modes, one under incA control, the other under c1 control and indirectly (via ant, the determinant of a repression antagonist) under c4 control.
Simple, rapid colorimetric tests for lysogenic induction (the derepression of a latent bacterial virus) are described. A quantitative test and a more rapid semiquantitative test are based on the assay of the beta-galactosidase synthesized from lacZ gene fused to an operon under lambda repressor control. These biochemical "inductests" are suitable for screening programs designed to detect agents that damage DNA and that are of potential interest in carcinogenesis and cancer chemotherapy.
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The segregation of a bacterial plasmid, the sex factor F', has been investigated in a cell-division mutant of Escherichia coli which produces small anucleate cells (minicells). Significant amounts of isotopically labeled DNA segregate into minicells dependent upon the presence of F'. Minicells containing F'Gal or F'(lambda) are shown to donate the plasmid in conjugation. These results demonstrate that the sex factor may be dissociated from the bacterial chromosome and that this separation does not prevent its subsequent transfer.
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An upper limit for beta-galactosidase transfer between mating F(+) and F(-)Escherichia coli has been determined by a new technique which relies on selective lysis of the donor strain by heat induction of a thermo-inducible strain of lambda, accompanied by chymotryptic digestion of the released beta-galactosidase. No significant transfer of beta-galactosidase during mating between F(+) and F(-) cells has been observed: 0.05 +/- 0.05% of the enzyme originally present in the male cells is found in the female cells after 1 hr of mating at 37 C.