Strain-specific difference that affects the inhibition of division of Escherichia coli filaments by chloramphenicol

Walker, James R.; Kovarik, A

doi:10.1128/jb.123.2.752-754.1975

Cited by 4 publications

(1 citation statement)

References 12 publications

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“…7), whereas ftsE strains divide at the permissive tempers,ture even in the presence of chloramphenicol (28). This requirement for new protein synthesis for division of cell division mutants as determined by chloramphenicol treatment may depend on the strain that harbors the cell division lesion (34). Strain JS10 is sensitive to low amounts ofdeoxycholate, whereas ftsE strains are no more sensitive to this detergent than their parent strain.…”

Section: Discussion Mutants Previously Described By Ricard Andmentioning

confidence: 99%

Low-temperature conditional cell division mutants of Escherichia coli

Sturgeon¹,

Ingram²

1978

J Bacteriol

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Fifteen low-temperature conditional division mutants of Escherichia coli K-12 were isolated. They grew normally at 390C but formed filaments at 300C. All exhibited a coordinated burst of cell division when the filaments were shifted to the permissive temperature (390C). None of the various agents that stimulate cell division in other mutant systems (salt, sucrose, ethanol, and chloramphenicol) was very effective in restoring colony-forming ability at 250C or in stimulating cell division in broth. One of these mutants, strain JS10, was found to have an altered cell envelope as evidenced by increased sensitivity to deoxycholate and antibiotics, as well as leakage of ribonuclease I, a periplasmic enzyme. This mutant had normal rates of DNA synthesis, RNA synthesis, and phospholipid synthesis at both the nonpermissive and permissive temperatures. However, strain JS10 required new protein synthesis in the apparent absence of new RNA synthesis for division of filaments at the permissive temperature. The division lesion in strain JS10 is cotransducible with maU, aroB, and glpD and maps within min 72 to 75 on the E. coli chromosome. ily applicable to "cold-sensitive mutants" (36). Thus, it seemed possible that the isolation and characterization of low-temperature conditional cell division mutants might reveal new and different loci involved in the cell division process. This paper descibes the physiology and genetic lesion in a UV-induced "cold-sensitive" mutant of E. coli K-12. MATERIALS AND MEIODS Bacterial strains. The bacterial strains and their genotypes are listed in Table 1. Genetic designations, map positions of amino acids, sugars, and antibiotics are in accordance with the revised linkage map of Bachmann et al. (4). Bacteriophage Plvir was part of the alive strain kit obtained from Cold Sprmg Harbor Laboratory, Cold Spring Harbor, N.Y. Strains JS20, JS101, and JS21 are maLA derivatives of strains x462, JS10, and LW3, repectively. The malA lesion was introduced into these three strains by 2-aminopurine mutagenesis (24) and subsequent selection of Mal7 colonies on MacConkey agar supplemented with 0.2% maltose. The glpD lesion was introduced into a X462 malA strain in an analagous fashion. Media. Dix and Helmatetter minimal medium (5) and Luria (L) broth (19) were used for isolation, enrichment, and subsequent experiments involving the low-temperature conditional cell division mutants.

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Section: Discussion Mutants Previously Described By Ricard Andmentioning

confidence: 99%

Low-temperature conditional cell division mutants of Escherichia coli

Sturgeon¹,

Ingram²

1978

J Bacteriol

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Fluoride‐induced filaments of Erwinia carotovora

Gashe

Grula

1983

J of Basic Microbiology

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Sodium fluoride induces filamentous growth ofErwinia carotovora whenit is grown in liquidmedia containing aspartic acid only as the sole source of nitrogen. It is proposed that a stable complex of F--MgZ+ -enzyme and POi,resulting in Mge+ deficiency and consequent inability of E. cardouora cells to oxidize aspartic acid normally, is responsible for the formation of filaments in the presence of fluoride ions. ion to bring about division inhibition in any bacterium has not been reported. Fluoride is capable of inducing very long filaments in E. carotovora under certain conditions without being extremely toxic for growth. The observations reported here are related to the mechanism of control of cell division in E . carotovora and, we believe they could contribute to a better understanding of this mechanism. Mater~a~s and methodsThe test organism'used is Erwinia carotovora. Conditions for handling of culture, preparation for inoculation and incubation have been described elsewhere (GASHE 1977). Growth media used were: glucose-aspartic acid medium (GA) glucose-aspartic acid medium containing sodium fluoride (GAF), and aspartic acid medium. Unless otherwise specified all media had a final pH of 6.8. Whenever filamentous cells (division inhibited) were to be obtained, sodium fluoride (NaF) a t final medium concentration of 16 mm was added a t 0 hrs into GA or aspartic acid medium.14C-~ Aspartic acid (0.02 pc/ml of medium) was added after 12 hr of growth int,o the GA and GAF media to study the labelling patterns in control (short) and filamentous (division inhibited) cells.The procedures of BENNET and W~LLIAYS (1957) for digestion of normal and filamentous cells and that of NORRIS and RIBBONS (1971) for quantitation of phosphate were utilized.The PARK and HANCOCK system (1960) was used to determine the distribution of phosphate and aspartic acid-carbon (uniformly labelled) in the different cellular components.Keto acids were extracted (SHERMA and ZWEIG 1971), quantitated (HAIDLE and KNIGHT 1960) and their hydrazone derivatives were chromatographed (ISHERWWD and NAVIS 1956) using various procedures. A small fraction of the keto acids was also converted to amino acids (KUN and HER-NANDEZ 1956). ResultsConcentrations of 0.04 to 70 mM sodium fluoride in aspartic acid-containing media result in the formation of filaments (90% biomass-consists of filament 50-100 micrometers long). Average length of filaments is a function of the concentration of F--ion, aspartic acid, and inorganic phosphate (Fig. 1).

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