PMID- 191634
OWN - NLM
STAT- MEDLINE
DCOM- 19770527
LR  - 20200724
IS  - 0022-538X (Print)
IS  - 1098-5514 (Electronic)
IS  - 0022-538X (Linking)
VI  - 21
IP  - 3
DP  - 1977 Mar
TI  - Distinguishable transformation-defective phenotypes among temperature-sensitive 
      mutants of Rous sarcoma virus.
PG  - 1042-55
AB  - Eight transformation-defective, temperature-sensitive (ts) mutants of the Prague 
      strain of Rous sarcoma virus, subgroup A, have been isolated after mutagenesis 
      with 5-bromodeoxyuridine followed by selection on the basis of focus tests. Five 
      of these mutants, ts GI201, GI202, GI203, GI204, and GI205, exhibit properties 
      like most previously reported isolates in that they show a temperature-sensitive 
      response to each of a variety of transformation-specific parameters tested. 
      Interestingly, GI201, in addition to the temperature-sensitive defect, carries a 
      lesion that was observed as a nonconditional loss of expression of plasminogen 
      activator protease. Three mutants, ts GI251, GI252, and GI253 have been 
      disignated partial transformation-defective (PTD) mutants since they behave as ts 
      mutants according to some tests for transformation and as wild type according to 
      others. These three mutants fail to form foci at the nonpermissive temperature 
      (41 degrees C) and art nontumorigenic in 3-week-old chickens (body temperature, 
      42 degrees C). The agglutinability by concanavalin A of cells infected with these 
      mutants shows a definite temperature sensitivity, as do the rate of 
      2-deoxyglucose uptake and the disappearance of the 250, 000-dalton normal cell 
      glycoprotein (large, external, transformation sensitive [LETS]). Although the PTD 
      mutant-infected cells, unlike cells infected with other transformation mutants, 
      exhibit a cell-bound plasminogen activator protease at the nonpermissive 
      temperature, this activator is not detectable as a free protease in the medium, 
      as it is with wild-type, virus-infected cells. The PTD mutants behave like the 
      wild-type parent in their ability to induce transformed growth properties in the 
      infected cells, i.e., growth beyond normal cell saturation density with or 
      without serum-supplemented medium and growth leading to colony formation in 
      soft-agar- or methyl cellulose-containing suspension media.
FAU - Becker, D
AU  - Becker D
FAU - Kurth, R
AU  - Kurth R
FAU - Critchley, D
AU  - Critchley D
FAU - Friis, R
AU  - Friis R
FAU - Bauer, H
AU  - Bauer H
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Virol
JT  - Journal of virology
JID - 0113724
RN  - 0 (Glycoproteins)
RN  - 0 (Mutagens)
RN  - 11028-71-0 (Concanavalin A)
RN  - 9G2MP84A8W (Deoxyglucose)
RN  - EC 3.4.21.- (Plasminogen Activators)
RN  - G34N38R2N1 (Bromodeoxyuridine)
SB  - IM
MH  - Agglutination
MH  - Avian Sarcoma Viruses/*growth & development
MH  - Bromodeoxyuridine
MH  - *Cell Transformation, Neoplastic
MH  - Concanavalin A/pharmacology
MH  - Culture Techniques
MH  - Deoxyglucose/metabolism
MH  - Glycoproteins/biosynthesis
MH  - Mutagens
MH  - *Mutation
MH  - Phenotype
MH  - Plasminogen Activators/metabolism
MH  - Temperature
PMC - PMC515644
EDAT- 1977/03/01 00:00
MHDA- 1977/03/01 00:01
PMCR- 1977/03/01
CRDT- 1977/03/01 00:00
PHST- 1977/03/01 00:00 [pubmed]
PHST- 1977/03/01 00:01 [medline]
PHST- 1977/03/01 00:00 [entrez]
PHST- 1977/03/01 00:00 [pmc-release]
AID - 10.1128/JVI.21.3.1042-1055.1977 [doi]
PST - ppublish
SO  - J Virol. 1977 Mar;21(3):1042-55. doi: 10.1128/JVI.21.3.1042-1055.1977.