Transient repression of catabolite-sensitive enzyme synthesis elicited by 2,4-dinitrophenol.

Transient inhibition of catabolic enzyme synthesis in Escherichia coli occurred when a low concentration of 2,4-dinitrophenol (DNP) was simultaneously added with inducer. Using mutant strains defective for gamma-gene product or constitutive for lac enzymes, it was found that the inhibition is not due to the exclusion of inducer by uncoupling. The addition of cyclic adenosine 3',5'-monophosphate overcame repression. The components of the lac operon coordinately responded to DNP inhibition. From deoxyribonucleic acid-ribonucleic acid hybridization experiments, it was found that the inhibition of beta-galactosidase induction occurred at the level of messenger ribonucleic acid synthesis specific for the lac operon. It seems probable that DNP represses induction in a similar manner to that of transient repression observed upon the addition of glucose. Furthermore, it was found that transient repression disappeared if cells were preincubated with DNP before induction. This indicates that new contact of cells with DNP is obligatory for transient repression. From these results, it is suggested that the cell membrane may be responsible for regulation of catabolite-sensitive enzyme synthesis.     

Degradation of 2,4-dinitrophenol and selected nitroaromatic compounds by Sphingomonas sp. UG30

Sphingomonas strain UG30 mineralizes both p-nitrophenol (PNP) and pentachlorophenol (PCP). Our current studies showed that UG30 oxidatively metabolized certain other p-substituted nitrophenols, i.e., p-nitrocatechol, 2,4-dinitrophenol (2,4-DNP), and 4,6-dinitrocresol with liberation of nitrite. 2,6-DNP, o- or m-nitrophenol, picric acid, or the herbicide dinoseb were not metabolized. Studies using 14C-labelled 2,4-DNP indicated that in glucose-glutamate broth cultures of UG30, greater than 90% of 103 microM 2,4-DNP was transformed to other compounds, while 8-19% of the 2,4-DNP was mineralized within 5 days. A significant portion (20-50%) of the 2,4-DNP was metabolized to highly polar metabolite(s) with one major unidentified metabolite accumulating from 5 to 25% of the initial radioactivity. The amounts of 2,4-DNP mineralized and converted to polar metabolites was affected by glutamate concentration in the medium. Nitrophenolic compounds metabolized by UG30 were also suitable substrates for the UG30 PCP-4-monooxygenase (pcpB gene expressed in Escherichia coli) which is likely central to degradation of these compounds. The wide substrate range of UG30 could render this strain useful in bioremediation of some chemically contaminated soils.     

Induction of tension wood by 2,4-dinitrophenol and auxins

Summary The effect of DNP and auxins on the development of the secondary xylem in erect stems ofAcer rubrum was studied. DNP affected the development of the secondary xylem only locally in the treated internode. Tension wood is formed in the stem below the DNP treatment site whereas above the application site the development of tracheary elements is altered. InAcer rubrum seedlings that were treated with auxin, especially at low concentrations, a thick ring of tension wood is developed in the erect stem below the treatment site. Previous suggestions that the formation of tension wood in arborescent angiosperms is a developmental response to auxin deficiency are discussed in terms of the induction of tension wood inAcer rubrum by DNP and auxins.The following abbreviations will be used TIBA (2,3,5-tri-iodobenzoic acid) - IAA (indole-3-acetic acid) - GA (gibberellic acid) - NAA (naphthaleneacetic acid) - 2,4-D (2,4-dichlorophenoxyacetic acid) - DNP (2,4-dinitrophenol) This material was included in a doctoral thesis submitted by P. R.Morey to the graduate school of Yale University, New Haven.     

Degradation of 2-sec-butyl-4,6-dinitrophenol (dinoseb) by Clostridium bifermentans KMR-1.

A strain of Clostridium bifermentans, KMR-1, degraded 2-sec-butyl-4,6-dinitrophenol (dinoseb) to a level below the limit of detection by high-performance liquid chromatography (0.5 mg/liter) within 96 h, with no accumulation of aromatic intermediates. KMR-1 could not utilize dinoseb as a sole carbon or energy source, and degradation occurred via cometabolism in the presence of a fermentable carbon source. KMR-1 mineralized some dinoseb in anaerobic cultures, evolving 7.2% of the radioactive label in U-ring 14C-labeled dinoseb as 14CO2. The remaining anaerobic degradation products were incubated with aerobic soil bacteria, and 35.4% of this residual radioactive label was evolved as 14CO2. During this mineralization experiment, 38.9% of the initial label was evolved as 14CO2 after both anaerobic and aerobic phases. This is the first demonstration of dinoseb degradation by a pure microbial culture.     

Alterations in the survival of X-irradiated cells by 2,4-dinitrophenol depending on ATP deprivation.

The dose-survival curve of cultured melanoma cells was changed by post-irradiation treatment with 2,4-dinitrophenol (DNP). The parameters of the curves were Do = 147 R and n = 5 . 6 for untreated cells and Do = 143 R, n = 7 . 9 and Do = 142 R, n = 2 . 0 for the cells treated with 10(-5) M DNP and 5 x 10(-5) M DNP in phosphate-buffered saline, respectively. The content of ATP in the cell decreased to 5% of the control level after treatment with either concentration of DNP. The recovery of ATP content was rapid and complete after 2 hours' incubation in culture medium after the removal of 10(-5) M DNP, but was retarded and incomplete after 4 hours with 5 x 10(-5) M DNP. Thus prolonged ATP deprivation with a high concentration of DNP results in an inhibition of recovery and a reduction in the n-value.