scholarly journals Discriminatory function of ribonuclease H in the selective initiation of plasmid DNA replication

1982 ◽  
Vol 10 (3) ◽  
pp. 833-853 ◽  
Author(s):  
Günter Hillenbrand ◽  
Walter L. Staudenbauer
1995 ◽  
Vol 42 (2) ◽  
pp. 233-239 ◽  
Author(s):  
A Szalewska-Pałasz ◽  
G Wegrzyn

Replication of lambda plasmid DNA is halted in amino acid-starved wild type (stringent) strains whereas it proceeds in relA (relaxed) mutants. The only transcription which could be important in lambda plasmid DNA replication in amino acid-starved Escherichia coli cells is that starting from the pR promoter. Using a fusion which consists of the lacZ gene under the control of bacteriophage lambda pR promoter we found that transcription starting from this promoter was inhibited during the stringent, but not the relaxed, response in E. coli. We confirmed our conclusion by estimating the relative level of the pR transcript by RNA-DNA hybridization. We propose that decreased transcription from the pR promoter which serves as transcriptional activation of ori lambda is responsible for inhibition of lambda plasmid replication during the stringent response. The results presented in this paper, combined with our recent findings (published elsewhere), indicate that the transcriptional activation of ori lambda may be a main regulatory process controlling lambda DNA replication not only during the relaxed response but also in normal growth conditions.


1982 ◽  
Vol 152 (3) ◽  
pp. 1078-1090
Author(s):  
R Meyer ◽  
M Hinds

By cloning fragments of plasmid DNA, we have shown that RK2 expresses incompatibility by more than one mechanism. One previously identified (R. J. Meyer, Mol. Gen, Genet. 177:155--161, 1979; Thomas et al., Mol. Gen. Genet. 181:1--7, 1981) determinant for incompatibility is linked to the origin of plasmid DNA replication. When cloned into a plasmid vector, this determinant prevents the stable inheritance of a coresident RK2. However, susceptibility to this mechanism of incompatibility requires an active RK2 replicon and is abolished if another replicator is provided. We have also cloned a second incompatibility determinant, encoded within the 54.1- to 56.4-kilobase region of RK2 DNA, which we call IncP-1(II). An RK2 derivative remains sensitive to IncP-1(II), even when it is not replicating by means of the RK2 replicon. The 54.1- to 56.4-kilobase DNA does not confer susceptibility to the IncP-1(II) mechanism, nor does it encode a detectable system for efficient plasmid partitioning. The incompatibility may be related to the expression of genes mapping in the 54.1- to 56.4-kilobase region, which are required for plasmid maintenance and suppression of plasmid-encoded killing functions.


1979 ◽  
Vol 43 (0) ◽  
pp. 91-97 ◽  
Author(s):  
R. Kolter ◽  
M. Inuzuka ◽  
D. Figurski ◽  
C. Thomas ◽  
D. Stalker ◽  
...  

1986 ◽  
Vol 5 (3) ◽  
pp. 631-637 ◽  
Author(s):  
H. te Riele ◽  
B. Michel ◽  
S.D. Ehrlich
Keyword(s):  

Author(s):  
Marcelo E. Tolmasky ◽  
Luis A. Actis ◽  
Jorge H. Crosa
Keyword(s):  

1972 ◽  
Vol 237 (70) ◽  
pp. 29-31 ◽  
Author(s):  
DON B. CLEWELL ◽  
BRUCE EVENCHIK ◽  
JOSEPH W. CRANSTON

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