Isolation and genetic analysis of Azospirillum brasilense Nif− mutants

1983 ◽  
Vol 29 (8) ◽  
pp. 968-972 ◽  
Author(s):  
P. Jara ◽  
B. Quiviger ◽  
P. Laurent ◽  
C. Elmerich

After ethylmethane sulfonate mutagenesis of Azospirillum brasilense strain 7000, mutants devoid of nitrogenase activity were isolated. Partial diploids were constructed by introducing plasmids pAB35 and pAB36 into the Nif− mutants. The two plasmids were derivatives of the broad host-range plasmid vector pRK290. Plasmid pAB35 contained a 6.7 kilobase pairs (kb) EcoRI fragment which carried the nifHDK gene cluster cloned from strain 7000. Plasmid pAB36 contained the same fragment from which a 2.6-kb PstI fragment that likely covers nifK, and a part of nifD was deleted. The restoration of a Nif+ phenotype by pAB35, but not by pAB36, was observed in the case of mutant 7571, which might be impaired in a structural gene for the nitrogenase complex.

2002 ◽  
Vol 211 (1) ◽  
pp. 91-95 ◽  
Author(s):  
Eza Kalyaeva ◽  
Irina Bass ◽  
Gennady Kholodii ◽  
Vadim Nikiforov

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.


1991 ◽  
Vol 173 (11) ◽  
pp. 3463-3477 ◽  
Author(s):  
P Goncharoff ◽  
S Saadi ◽  
C H Chang ◽  
L H Saltman ◽  
D H Figurski

Plasmid ◽  
1989 ◽  
Vol 21 (2) ◽  
pp. 99-112 ◽  
Author(s):  
Thomas J. Schmidhauser ◽  
David H. Bechhofer ◽  
David H. Figurski ◽  
Donald R. Helinski

Plasmid ◽  
1983 ◽  
Vol 9 (3) ◽  
pp. 325-330 ◽  
Author(s):  
Thomas J. Schmidhauser ◽  
Marcin Filutowicz ◽  
Donald R. Helinski

Gene ◽  
1985 ◽  
Vol 34 (2-3) ◽  
pp. 219-226 ◽  
Author(s):  
Francis E. Nano ◽  
W.D. Shepherd ◽  
M.M. Watkins ◽  
S.A. Kuhl ◽  
S. Kaplan

1995 ◽  
Vol 41 (7) ◽  
pp. 624-628 ◽  
Author(s):  
Yuwen Hong ◽  
J. J. Pasternak ◽  
Bernard R. Glick

When the broad host range plasmid vector pGSS15 was used to genetically transform the plant growth promoting rhizobacterium Pseudomonas putida GR12-2, the transformants were physiologically debilitated. It was postulated that the expression of the β-lactamase gene of pGSS15 caused a metabolic load resulting in the impaired functioning of the bacterium. To test this hypothesis, derivatives of pGSS15 that either lack the β-lactamase gene (pYH122) or in which a β-glucosidase gene was substituted for the β-lactamase gene (pYH124) were constructed and examined to see whether their presence also impaired the functioning of P. putida GR12-2. On the basis of growth rates, siderophore production, and the ability to stimulate canola root elongation in sterile growth pouches, neither of the newly constructed plasmids debilitated P. putida GR12-2. In addition, P. putida GR12-2 transformed with pYH124 facilitated the proliferation of the bacterium in minimal medium containing cellobiose at low temperature. This latter trait may enable P. putida GR12-2 to persist in the soil in competition with other microorganisms.Key words: plant growth promoting rhizobacteria, PGPR, bacterial fertilizer, soil bacteria, metabolic load, β-glucosidase


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