Normal Cellular Components Research Articles

Interference of cellular ferric ions with DNA extraction and the application to methods of DNA determination

Iron present in biological samples prevents the extraction of DNA by hot acid hydrolysis as used in both the Schneider and Ogur-Rosen procedures [Schneider, W. C. (1945) J. Biol. Chem. 161, 293–303; Ogur, M., and Rosen, G. (1950) Arch. Biochem. 25, 262–276.] for DNA determination. Purified DNA, which is normally hot acid hydrolyzable, is rendered nonhydrolyzable by the presence of trace (0.1 m m) quantities of iron (III). Addition of a metal ion chelator, such as EDTA, to samples before hot acid treatment of DNA overcomes the inhibitory effect of iron, and, since iron is a normal cellular component, it is recommended as a general procedure for DNA determination.

Specific serological relationships among partially purified DNA polymerases of avian leukosis-sarcoma viruses, reticuloendotheliosis viruses, and avian cells.

Specific serological relationships were found among the partially purified DNA polymerases of the two groups of avian viruses whose virions contain RNA and a DNA polymerase-the avian leukosis-sarcoma viruses and the reticuloendotheliosis viruses-and three avian species which are natural hosts for these viruses: chickens, turkeys, and Pekin ducks. No relationships were found to DNA polymerases of HeLa cells or Escherichia coli. These results are consistent with the hypothesis that RNA viruses with a DNA polymerase originated from normal cellular components.

Membrane alterations which accompany MuMTV maturation: I. Studies by freeze-cleave techniques

As part of a study of the assembly of viral envelope at the surface of cells producing the mouse mammary tumor virus (MuMTV), freeze-cleave replicas were obtained of virus producing regions of mammary tumors. Free virions in the acinar space appeared identical to separately prepared, purified virus as reported earlier, with A (convex) and B (concave) fracture surfaces exposed. The A face of microvilli in the tumor was covered with intramembranous particles (IMP), while the B face was generally devoid of IMP. The A face of microvilli with virus in them was covered with IMP except in the region of virus maturation. There was no observable difference between the B surfaces of microvilli and adjacent maturing virus. Our results suggest that while new virus proteins and antigens are added to the cell membrane, converting it to a viral envelope, some normal cellular membrane components are displaced or absent from the region of virus maturation. Some possible mechanisms for this process are discussed.

Ultrastructure of a cytoplasmic polyhedrosis virus affecting the monarch butterfly, Danaus plexippus: I. Development of virus and normal polyhedra in the larva

An account is given of the replication cycle of the virus and the development of normal polyhedra, as contrasted with a cubic mutation, in a cytoplasmic polyhedrosis affecting the larvae of Danaus plexippus, the monarch butterfly. The polyhedra are somewhat unusual being almost spherical and varying in size from very small to 5 μ in diameter. Two general lattice patterns were observed in the polyhedra, a dot pattern and a line pattern which are two views of the same crystal lattice. In the early stages of the disease a virogenic stroma forms in the cytoplasm in which the virus particles appear to develop. At a later stage what has been termed a crystallogenic matrix is produced which surrounds the developing polyhedra. Both contain virus particles but no normal cellular components. The crystallogenic matrix has many complete virus particles in it while the virogenic stroma has few complete, but many incomplete, particles present. The virus particle itself consists of a central electron-opaque core surrounded by a less dense capsid. The particle measures about 670 A in diameter, and the core, which may be hexagonal or pentagonal, measures about 350 A. There are 12 projections on the surface of the capsid measuring about 170 A in length, in section often six projections are visible forming a six-pointed star. An unusual feature is the presence of a “tail” extending from a vertex of the hexagon; the length of the tail is almost that of the diameter of the virus particle and is much longer than the regular projections. There is circumstantial evidence that the virus is transovarially transmitted.

Fine structure of cellular inclusions in measles virus infections.

Cells which are infected with measles virus have been known for some time to contain inclusion material that is distinguishable from normal cellular components by application of traditional staining methods and observation in the light microscope. The fine structure of the inclusion material contained in HeLa cells infected with Edmonston strain of measles virus has been examined in the electron microscope. Two steps have been found necessary in this study: (1) the recognition by phase-contrast microscopy of the living cell of bodies that are defined as inclusion material when the cells are classically stained; and (2) the recognition in the electron microscope of inclusion-body material that had previously been identified in the living cell. The fine structure of the nuclear and cytoplasmic inclusion material in osmium-treated cells was found to consist mainly of randomly arrayed filaments of low electron density. Dense, highly ordered arrays of filaments were found near the center of the nuclear inclusions, sometimes as a two-dimensional, nearly orthogonal arrangement. If the size of the measles virus is taken to be around 100 mmicro in diameter, the strands seen in the inclusions cannot be fully formed virus.

Interaction of tumor agents and normal cellular components in amphibia.

Annals of the New York Academy of SciencesVolume 54, Issue 6 p. 1110-1125 INTERACTION OF TUMOR AGENTS AND NORMAL CELLULAR COMPONENTS IN AMPHIBIA S. Meryl Rose, S. Meryl Rose Department of Zoology, University of Illinois, Urbana, IllinoisSearch for more papers by this author S. Meryl Rose, S. Meryl Rose Department of Zoology, University of Illinois, Urbana, IllinoisSearch for more papers by this author First published: July 1952 https://doi.org/10.1111/j.1749-6632.1952.tb39982.xCitations: 12 This work has been aided by a grant from the American Cancer Society on the recommendation of the Committee on Growth of the National Research Council. AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Citing Literature Volume54, Issue6Viruses as Causative Agents in CancerJuly 1952Pages 1110-1125 RelatedInformation