Induction Of Filamentation Research Articles

Role of rec genes in SOS-induced inhibition of cell division in Escherichia coli

The inhibition of cell division induced by bleomycin (BM) and UV irradiation in the set of rec mutants of E. coli K12 was studied. Data presented in this work indicate that BM treatment requires mainly the RecBC pathway for the induction of cell filamentation. In the recB21 mutant cell filamentation is delayed and reduced compared to the wild type. Cell filamentation is BM-induced with similar kinetics in strains with a proficient RecBC recombination pathwa, ( rec +, recF143 and recN262), as well as is in the strain with a fully expressed RecF pathway ( recB21 recC22 sbcB15). Induction is completely abolished in the recB21 recF143 double mutant. On the other hand cell filamentation was induced similarly by UV irradiation in all strains with a functional recF gene and in the strain with a fully operative RecF pathway, but it was delayed in the recF143 and recB21 recF143 mutants.

Morphological changes induced by beta-lactam antibiotics in Mycobacterium avium-intracellulare complex

In vitro activity of seven beta-lactam antibiotics against strains of Mycobacterium avium-intracellulare was evaluated by the agar dilution method. The activity was influenced by the presence or absence of Tween 80 in Dubos medium, and cephazolin and cefotaxime were effective against most strains in the presence of Tween 80. beta-Lactam antibiotics at low concentrations induced long filamentous cells with branching. In contrast to the filaments induced by ampicillin, in which septation was rarely observed, filaments induced by cephazolin had many septa, suggesting that the mechanisms of filament induction were different from the drugs used. At high concentrations, ampicillin and cephazolin induced osmotically sensitive cells with bulging at polar end of the cells. Analysis of penicillin binding proteins (PBPs) of the organism showed that there were at least nine PBPs with molecular weights between 32,000 and 94,000 in the cytoplasmic membrane. Ampicillin showed the highest affinity for PBPs 1a or 1b, or both, and also PBPs 3a or 3b, or both. In contrast, there was very little specificity of binding of cephazolin for any of the PBPs.

Temperate phage induction and filament formation in [formula omitted] by furazolidone

Furazolidone a synthetic nitrofuran used in the treatment of cholera, was found to cause prophage induction and filament formation in Vibrio cholerae . Maximum induction of phage beta was obtained at a drug concentration of 0.5 μg/ml. Neither induction of prophage nor filamentation took place if the drug treatment was carried out in the presence of 2.5 μg/ml chloramphenicol, indicating a requirement for de novo protein synthesis. Our results strongly suggest the existence of “SOS” type functions in Vibrio cholerae .

Induction of filamentation by mutagens and carcinogens in a lon − of Escherichia coli

Induction of filamentation by mutagens and carcinogens in a lon − of Escherichia coli

Inhibitory effect of adenosine 3',5'-phosphate on cell division of Escherichia coli K-12 mutant derivatives.

Cell division of Escherichia coli K-12 strain PA3092 was inhibited by the addition of adenosine 3',5'-phosphate (cAMP), and the cellular morphology was changed from rods into filaments. Nucleoids in the filaments were regularly distributed and septum formation was perfectly inhibited. This inhibition of cell division by cAMP was reversed by the addition of guanosine 3',5'-monophosphate. To examine whether the inhibitory effect of cAMP on cell division in E. coli PA3092 was specific, its effect in several parental strains was investigated. Induction of cell filamentation by cAMP was observed in E. coli PA309 and P678, but not in E. coli W505, W1, Y10, or the wild-type strain. This result suggests that filamentation by cAMP in E. coli PA3092, PA309, and P678 was due to the mutagenesis by which E. coli P678 was derived from E. coli W595.

Tif-dependent induction of colicin E1, prophage lambda, and filamentation in Escherichia coli K-12.

To help understand how the tif-1 mutation of the recA gene of Escherichia coli confers adenine activability on the recA protein, we used the fact that cytidine plus guanosine inhibits induction of prophage lambda and cell filamentation in a tif-1 mutant, and that adenine reverses this inhibition. We varied the amount of adenine in agar plates containing a fixed amount of cytidine and scored for survivors of three different tif-dependent lethal induction processes. Much more adenine was required for cell killing when cytidine was present than when it was absent. Therefore adenine does not override cytidine inhibition, but instead appears to compete with it for a site of action which may be on the recA protein. The competition is not at the cell transport level. Our results lead to a model in which the tif form of the recA protein is an allosteric enzyme that binds both negative and positive modulators. By varying the adenine-cytidine ratio of the medium it is possible to control the degree of induction in a tif-1 cell. For the three different tif-dependent inductions studied here, least adenine was required for lambda induction and most for lethal filamentation, presumably reflecting requirements for different amounts of activated recA protein in each process. Varying the adenine-cytidine ratio revealed two stable intermediate stages in lambda induction, as well as a stage of colicin E1 induction in which the cells produced colicin without cell death. The rate of filament formation could be similarly controlled. Experiments with tif (ColE1, lambda) gave evidence of a competition between colicin repressor and lambda repressor for activated recA protein.

Different distribution of pattern of 100-Å filaments in resting and locomotive leukaemia cells

Two types of filaments have been described in the cytoplasm of non-muscular cells—microfilaments (40–70 A in diameter) and 100-A filaments (90–110 A). Microfilaments have been found in almost every type of animal cell1, and they are known to be actin-like2 and believed to have a role in many contractile processes1,3. In contrast, the 100- A filaments have been observed only in a limited number of cell types, such as tissue culture cells2,4, smooth5 and skeletal6 muscle cells, nerve cells7,8 and tumour cells9,10, and are thought not to be actin-like2,3,10,11. The function of 100- A filaments is not clear although they have been suggested to act in the intracellular transport of organelles in fibroblasts4, the axoplasmatic transport in nerve cells12,13 and the spreading of cells3, or to serve as a cytoskeleton14. Induction of 100-A filaments by colcemide6 and cytochalasin B and colcemide15,16 has also been demonstrated. A clue to their function may lie in the demonstration, reported here, that the distribution of the 100-A filaments differs in resting and locomotive cells.

Relative morphological effects induced by cefoxitin and other beta-lactam antibiotics in vitro.

Cefoxitin, a new semisynthetic cephamycin antibiotic, induced filament formation at subinhibitory concentrations with a beta-lactamaseless strain of Enterobacter cloacae (HSC 18410 M66). The extent of filament induction by cefoxitin was similar to that seen with cephalothin, cefazolin, and benzylpenicillin. Filament induction by cefoxitin was markedly less than that seen with cephalexin, carbenicillin, ticarcillin, cephradine, and cephapirin. Antibiotics which failed to induce filaments at any level tested included cephaloridine, cephacetrile, cephalosporin C, the cephamycins, 6-aminopenicillanic acid, 7-aminocephalosporanic acid, A16884, A16886, and FL-1060. Those antimicrobial agents tested which lacked an aromatic substituent in the 7-position (for cephems) or in the 6-position (for penams) did not induce filaments. These observations suggest a possible relationship between filament induction of the test organism and the molecular nature of constituents in the 7- or 6-position of beta-lactams.

The development of the female Drosophila reproductive system.

AbstractLight and electron microscopical studies allow a descriptive account to be given of the preadult development of the ovary of Drosophila melanogaster. The lineage of the cell groups which contribute to the tissues of the adult ovary has been determined. The earliest morphologically detectable event in the differeentiation of each ovariole is the formation during the larval period of its terminal filament. Oogonia play no role in the induction of terminal filaments. The developmental events which transform a spherical mass of ovarian cells into a collection of multicellular cylinders is described. The importance in morphogenesis of acellular membranes secreted at the interface separting cells of different prospective significances is stressed. Such membranes may serve to regulate the future migration of cell populations or as sites of attachment for monolayers of cells which later fuse to form multinucleated muscle sheaths. The transformation of oogonia to cystoblasts coincides with and presumably depends upon the same hormonal stimulus which causes metamorphosis. The first oocytes to undergo crossing over do so between 24 and 36 hours after puparium formation.

TEMPERATURE LIMITS, GENEALOGICAL ORIGIN, DEVELOPMENTAL COURSE, AND ULTIMATE FATE OF HEAT-INDUCED FILAMENTS IN ESCHERICHIA COLI MICROCULTURES.

Hoffman, Heiner (New York University, New York, N.Y.) and Michael E. Frank. Temperature limits, genealogical origin, developmental course, and ultimate fate of heat-induced filaments in Escherichia coli microcultures. J. Bacteriol. 85:1221-1234. 1963.-The heat induction of filaments in microcultures of Escherichia coli occurred through a wide range of temperature, with 43.5 C being the upper limit at which all cells continued to grow. The lower temperature limit was not determined, but filaments were obtained at room temperature in overnight cultivations. The evidence from genealogical histories, growth rates, and cell and filament lengths strongly suggested that the filaments are collections of morphologically undifferentiated, but quasi-independent cell units which continue to grow and multiply while retaining the capacity eventually to break off completely as normal, nonfilamented cells. Filaments which failed to give off a daughter by the end of the second generation after their inception lyse explosively. The evidence obtained contradicts the hypothesis that the mother cell of a clonal microcolony becomes a filament and eventually lyses, although the cell length patterns upon which this hypothesis is based were reproduced. A high degree of synchronization of division was obtained and maintained through the entire period of incubation, which in some cultivations extended into the tenth generation.

Studies on the mode of action of novobiocin.

Novobiocin (Streptonivicin) is a new broadtherapy antibiotic recently announced by Smith et al. (1956). Chemically it is an acid containing a nine carbon sugar attached glycosidically to the seven position of 3 [4 hydroxy 3 (3 methyl 2 butenyl) benzamido] 4,7 dihydroxy 8 methyl coumarin (Hoeksema et al., 1956; Hinman et al., 1956). Some in vitro studies are presented here which may have some bearing on the mode of action of this antibiotic. These include the effect of MgSO4 and other metals on antibiotic activity, the induction of filamentation, and the effect of the antibiotic on the synthesis of nucleic acid.

Filament induction in Escherichia coli by ricinoleic acid.

SummarySodium ricinoleate interferes with cell division in E. coli causing the organisms to develop as filaments. The effect appears to be specific and dependent upon the 9:10 unsaturation and the 12-hydroxy group as well as the cis-configuration around the double bond, present in this fatty acid. A variety of metabolites, as well as other organic and inorganic compounds, were tested for an ability to induce cell division in filamentous forms of the organisms. Of the substances evaluated, only inorganic phosphate consistently and rapidly caused such an effect.