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A Baros

Publications and source records attributed to A Baros.

4 recordsLinked to original sources
PubMed1976

Transcriptional control of T4 coliphage-specific genes 30, 42, 43, rIIA, rIIB, and e.

Escherichia coli B/r (suo) was infected, at 30 degrees C, with T4Dam+, T4DamB24-amN82 (I-, 44-, DNA-negative phenotype), and T4DamN134amBL292 (33-, 55-, maturation-defective phenotype). A genetic ('transformation') assay was used to monitor transcription of genes 30 (polynucleotide ligase), 42 (deoxycytidylate hydroxymethylase), 43 (DNA polymerase), rIIA, rIIB, and e (endolysin). The principal results are: (I) All of the genes studied were transcribed exlusively from the so-called l-strand of phage DNA. (2) DNA synthesis and the maturation-defective proteins were required to turn-off transcription of genes 42, rIIA, tIIB, and 43. Experiments performed with chloramphenicol suggested that all phage-specific proteins required to turn-off transcription of these genes were not present until 6 to 8 min post infection (p.i.). (3) During a normal developmental programme, gene 30 was transcribed throughout the eclipse. DNA-negative and maturation-defective conditions had no obvious effect on transcription of this gene. (4) During a normal lytic event, two discrete waves of gene e transcription were observed. The late wave was dependent upon DNA-synthesis and presence of functional maturation-defective proteins. The early wave was unaffected by DNA-negative or maturation-defective conditions. Experiments with chloramphenicol indicated that, if any virus-specific proteins are involved with regulation of early e transcription, such proteins are present by 3 min p.i. The data are interpreted to mean that early gene transcription is regulated by a minimum of two mechanisms. One of these mechanisms is fully operational by the 3rd min and, among the genes studied, controlled early e transcription. A second mechanism becomes operational between 6 and 8 min p.i. and controls transcription of genes 42, 43, rIIA, and rIIB.

Animals↗
PubMed1976

Control of synthesis of mRNA's for T4 bacteriophage-specific dihydrofolate reductase and deoxycytidylate hydroxymethylase.

A 30 degrees C, functional messengers for dCMP hydroxymethylase first appeared 3 to 6 min postinfection and reached their maximum levels at 12 min. Chloramphenicol, added before the phage, reduced the rate of mRNA accumulation. When the antibiotic was added 6 min postinfection, mRNA levels increased at their normal rate but there was no obvious repression of messenger accumulation. Delaying the addition of drug until 8 or 12 min had progressively less effect on the pattern of hydroxymethylase mRNA metabolism. When chloramphenicol was present from preinfection times or from 6 min postinfection, all hydroxymethylase mRNA's synthesized were stable; at later times, however, the ability of the drug to stabilize mRNA decreased with its ability to delay the turnoff of mRNA production. An overaccumulation of hydroxymethylase mRNA was also seen when phage-specific DNA synthesis was inhibited either by mutational lesion in an essential viral gene or by 5-fluorodeoxyuridine. By min 20 of a DNA-negative program, hydroxymethylase mRNA synthesis was repressed to the point where it no longer compensated for decay. However, a finite level of hydroxymethylase mRNA synthesis was maintained at later times of a DNA-negative infection. Such results indicate that replication of the phage chromosome is necessary but not sufficient for a complete turnoff of hydroxymethylase mRNA production. Functions controlled by the maturation-defective proteins (the products of genes 55 and 33) played only a minor role in the regulation of hydroxymethylase mRNA, metabolism. Thus, we favor the hypothesis that a complete turnoff of hydroxymethylase messenger production requires one or more new proteins as well as an interval of DNA replication. The absence of DNA synthesis had no particular effect upon dihydrofolate reductase messenger production. The preinfection addition of chloramphenicol likewise had little effect on dihydrofolate reductase messenger metabolism. These latter data imply that prior synthesis of a phage-coded protein synthesis may not be required for the turnoff of reductase messenger production.

Chloramphenicol↗