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. 2000 Feb;182(4):956–960. doi: 10.1128/jb.182.4.956-960.2000

FIG. 2.

FIG. 2

Growth-phase-dependent induction of Pu in a P. putida MAD2 derivative lacking ptsN. (A) P. putida MAD2 ptsN::Km cells from a stationary-phase culture were diluted to an A600 of ∼0.05 and regrown at 30°C in M9-caa medium with or without glucose as an extra C source as indicated. β-Galactosidase levels were followed soon after growth resumed in the fresh medium. (B) Same as above, but instead with P. putida MAD2 ptsN::Km cells transformed with plasmid pJM154, which harbors a copy of the ptsN gene under the control of a Plac promoter. Note that although Pu lacks inhibition by glucose in the ptsN mutant, it still retains its exponential silencing to the same degree as the wild-type strain. (C) Comparison of the intracellular levels of ς54 in P. putida MAD2 and P. putida MAD2 ptsN::Km cells in the different culture conditions described above. The loss of the ptsN gene did not grossly affect ς54 amounts as detected by Western blot with anti-ς54 polyclonal serum.