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J Maniloff

Publications and source records attributed to J Maniloff.

At least 55 records · Page 3Linked to original sources
PubMed1980

Phylogenetic analysis of the mycoplasmas.

The phylogenetic relationships between the mycoplasmas and bacteria have been established from a comparative analysis of their 16S rRNA oligonucleotide catalogs. The genera Mycoplasma, Spiroplasma, and Acholeplasma arose by degenerative evolution, as a deep branch of the subline of clostridial ancestry that led to Bacillus and Lactobacillus. Thermoplasma has no specific relationship to the other mycoplasmas; it belongs with the archaebacteria.

Acholeplasma↗
PubMed1980

Virus and host cell DNA syntheses during infection of Acholeplasma laidlawii by MVL3, a nonlytic cytocidal mycoplasmavirus.

The replication of mycoplasmavirus MVL3 in Acholeplasma laidlawii K2 host cells was studied by analysis of infected-cell lysates using sedimentation in sucrose gradients and DNA-DNA hybridization. Viral DNA replication was found to involve intermediates sedimenting faster than free viral DNA, which is a linear, double-stranded molecule of about 26 x 10(6) daltons. After the shutdown of cellular DNA synthesis, viral DNA synthesis continued for many hours. The fate of cellular and parental viral DNAs was examined.

Acholeplasma laidlawii↗
PubMed1980

Adsorption, capping, and release of a complex bacteriophage by mycoplasma cells.

By electron microscopic studies, the adsorption and release of nonlytic, cytocidal mycoplasma virus MVL3, which infects ACholeplasma laidlawii cells, have been examined. The MVL3 virion has a polyhedral head, collar, short tail, and tail fibers and contains linear double-stranded DNA. Adsorbed MVL3 virus showed a temperature-dependent clustering or capping on the mycoplasma cell membrane. During infection, a number of virus-cell membrane-related structures were observed, suggesting a general model in which MVL3-infected cells release progeny virions in membrane vesicles. These vesicles must then break down to release MVL3 particles.

Absorption↗
PubMed1980

Ultraviolet, photodynamic and thermal inactivation of mycoplasmaviruses.

The ultraviolet light, photodynamic, and thermal inactivation parameters have been measured for the three groups of mycoplasmaviruses. The differences in these parameters for the three virus groups reflect differences in virion structure and in genome size and structure.

Acholeplasma laidlawii↗
PubMed1979

Gliding mycoplasmas are inhibited by cytochalasin B and contain a polymerizable protein fraction.

Studies are presented on the effect of cytochalasin B (CB) on the growth of five Mycoplasma species, three Acholeplasma species, and one Spiroplasma species. The three gliding mycoplasma species (M gallisepticum, M pneumoniae and M pulmonis are the only mycoplasmas inhibited by CB. These are the only prokaryotes reported to be inhibited by CB. This suggested that these three mycoplasmas might have some sort of cytoskeletal structure. A protein fraction has been isolated from M gallisepticum which polymerizes in 0.6 M KCl and depolymerizes when KCl is removed. This fraction contains a major 58,000-dalton protein, a 46,000-dalton protein, and a minor 87,000-dalton protein.

Bacterial Proteins↗
PubMed1979

Physical characterization of the superhelical DNA genome of an enveloped mycoplasmavirus.

Mycoplasmavirus MVL2 is a nonlytic enveloped virion containing DNA. This DNA has been shown to be a double-stranded circular superhelical molecule of 11.8 kilobase pairs (7.8 X 10(6) daltons). The superhelix density is greater than that of phi X174 RFI but less than that of PM2 phage DNA. A physical map of the MVL2 genome has been obtained using restriction endonucleases.

Acholeplasma laidlawii↗
PubMed1979

Structural and biological properties of mycoplasmavirus MVL3: an unusual virus-procaryote interaction.

The kinetics of adsorption and growth of mycoplasmavirus MVL3 in Acholeplasma laidlawii 1305/68 host cells have been studied with one-step growth, premature lysis, and single-burst experiments. The virus was found to kill infected host cells. Virus release starts 90 min after infection and continues for about 10 to 15 h. Hence, virus production is unlike the classical lytic bacteriophages and instead resembles nonlytic cytocidal animal viruses. Structural details of the virus are described, and the molecular weight of the viral linear DNA has beenfound to be 26 x 10(6).

Acholeplasma laidlawii↗
PubMed1978

Photodynamic inactivation and its repair in mycoplasmas.

Photodynamic inactivation is the loss in viability observed when organic dye-treated cells are exposed to visible light and molecular oxygen. The photodynamic inactivation of mycoplasmas, the smallest free living cells, has been studied. Depending on the extent of inactivation in Acholeplasma laidlawii, photodynamic induced damage can be repaired if the irradiated cells are incubated in the dark in buffer. Analysis of the DNA of these cells shows that photodynamic inactivation induces single strand breaks which can be repaired during liquid holding. To examine possible damage to the cell membrane, glucose uptake was studied as a permeability measure. Neither acriflavine nor photodynamic inactivation had any measurable effect on membrane permeability.

Acholeplasma laidlawii↗
PubMed1978

Effect of acriflavine on ultraviolet inactivation of Acholeplasma laidlawii.

An increased sensitivity to inactivation was observed when ultraviolet light-irradiated Acholeplasma laidlawii cells were plated on medium containing either acriflavine or chloramphenicol. Chloramphenicol reduced liquid holding recovery (dark repair) to about 10% of that in untreated irradiated cells. In acriflavine treated cells no dark repair could be observed and there was a progressive degradation of cell DNA during holding. While the primary effect of acriflavine may be to inhibit excision repair, since ultraviolet-irradiated Mycoplasma gallisepticum (cells which lack an excision repair mechanism) show a slight increase in inactivation when plated on medium containing acriflavine the dye must also have some other effects on ultraviolet repair processes. Acriflavine treatment of A. laidlawii cells before ultraviolet irradiation has a protective effect, as seen by an increased cell survival.

Acholeplasma laidlawii↗
PubMed1978

Inhibition of mycoplasma cell division by cytochalasin B.

Mycoplasma gallisepticum has subcellular organelles which may function as a primitive "mitotic-like" apparatus. To investigate these further, we have studied the effects of cytochalasin B (CB) on M. gallisepticum. We found that CB inhibits cell division; this is the only procaryote thus far reported to be inhibited by CB. CB does not inhibit glucose or macromolecule precursor uptake. It stops cellular DNA synthesis, however, although RNA and protein synthesis continue (at a reduced rate). CB removal results in a resumption of DNA synthesis, followed by cell division. There appears to be some degree of cell synchrony in this first division after CB removal. These results, together with morphological data, indicate that CB blocks at two points in the cell cycle: at the time "mitotic-like" structures are formed and at the time of cell division. It is suggested that the CB blocks may result from a disruption of actin-like protein structures required at these points in the cell cycle.

Bacterial Proteins↗
PubMed1978

Properties of a persistent viral infection: possible lysogeny by an enveloped nonlytic mycoplasmavirus.

MVL2, an enveloped double-stranded DNA mycoplasmavirus, causes a nonlytic infection of Acholeplasma laidlawii leading to the establishment of a persistent infection. Persistently infected clones were found to be resistant to superinfection by homologous virus, but could be infected by heterologous virus. Cells in a persistently infected culture had the potential to produce virus and transmitted this potential as a stable heritable trait. Mitomycin C and UV light induced an increase in infectious centers in persistently infected cultures.

Acholeplasma laidlawii↗