PubMed Health⌕ Search

Biomedical subjects

M L Breitman

Publications and source records attributed to M L Breitman.

79 records · Page 5Linked to original sources
PubMed1980

Growth-related alterations induced in chick embryo fibroblasts by src-gene deletion mutants of the Schmidt-Ruppin strain of Rous sarcoma virus.

Certain tdSRD viruses induce multilayered cell foci, agar colony formation, and increased density of cellular populations in line-15 chick embryo fibroblasts. These alterations in cellular growth properties are distinct from oncogenic transformation. Available evidence favors the idea that transformation-defective focus formation is caused by one or more of the replicative viral genes, but which of the three-gag, pol, or env-is involved, remains to be determined.

Animals↗
PubMed1980

Genetic variation and host markers in the src gene of recovered avian sarcoma viruses.

The src genes of three recovered avian sarcoma viruses were compared by RNase T1 oligonucleotide fingerprinting and tryptic peptide analysis. In all three recovered avian sarcoma viruses the oligonucleotide composition of src was different and also distinct from that of the parental Schmidt-Ruppin strain of Rous sarcoma virus. This evidence for genetic variation src was strengthened by two dimensional peptide maps of the src gene products pp60src, translated in a reticulocyte lysate system in vitro. Numerous differences between the peptide patterns of the pp60src proteins produced by the parental and the recovered viruses were detected. No two src proteins were identical, while the tryptic peptide maps of the internal gag proteins synthesized by these viruses were indistinguishable. The src proteins of recovered avian sarcoma viruses also contained peptides that were absent from the src protein of parental Schmidt-Ruppin D virus but were found in the endogenous src protein of normal cells. We conclude that there is considerable genetic variation in the src gene of recovered avian sarcoma viruses and that these recovered src genes contain host cell-derived markers.

Animals↗
PubMed1978

Proviruses of avian sarcoma virus are terminally redundant, co-extensive with unintegrated linear DNA and integrated at many sites.

We have analyzed the DNA from 15 clones of avian sarcoma virus (ASV)-transformed rat cells with restriction endonucleases and molecular hybridization techniques to determine the location and structure of proviral DNA. All twenty units of proviral DNA identified in these 15 clones appear to be inserted at different sites in host DNA. In each of the ten cases that could be sufficiently well mapped, entirely different regions of cellular DNA were involved. Thus ASV DNA can be accommodated at many positions in cellular DNA, but the existence of preferred sites has not been excluded. Six of the 15 clones carry only one normal provirus, two contain two normal proviruses, and seven harbor either one or two proviruses that appear anomalous in physical mapping tests. Both ends of at least 18 proviruses, however, were found to contain sequences specific to both the 3' and 5' termini of viral RNA. The organization of these terminally redundant sequences appeared identical to that of the 300 base pair (bp) repeats found at the ends of unintegrated linear DNA (Shank et al., 1978). Proviral DNA is therefore co-extensive, or nearly co-extensive, with unintegrated linear DNA and has a structure we denote as CELL DNA-3'5'----------3'5'-CELL DNA. Three of the four anomalous proviruses which were fully analyzed were deletion mutants lacking 25--65% of the genetic content of ASV; the fourth provirus had a novel site for cleavage by Eco RI but was otherwise normal. Tests for the biological competence of proviral DNA, based upon rescue of transforming virus after fusion with chicken cells, were generally consistent with the physical mapping studies.

Avian Sarcoma Viruses↗