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A R Bräutigam

Publications and source records attributed to A R Bräutigam.

4 recordsLinked to original sources
PubMed1974

Transcription unit mapping in bacteriophage T7. II. Proportionality of number of gene copies, mRNA, and gene product.

The effect of UV irradiation of bacteriophage T7 on in vivo early RNA synthesis has been studied by direct quantitation of the gene-specific RNA transcripts. The results show that the early region of phage T7 is transcribed from left to right as a single unit. Furthermore, gene inactivation, the UV sensitivity of synthesis of gene-specific RNA, and the UV sensitivity of synthesis of the corresponding proteins all follow pseudo first-order kinetics in multiply infected cells, demonstrating a random statistical correlation between both transcriptional sampling of gene copies and translational sampling of the resultant RNA transcripts. In addition, these simple kinetics imply an absence of positive feedback mechanisms compensating for the differential decline of individual early gene products in cells multiply infected with phage T7.

Coliphages↗
PubMed1973

Transcription unit mapping in bacteriophage T7. I. In vivo transcription by Escherichia coli RNA polymerase.

Premature termination of transcription at UV lesions in DNA permits a study of the sequential order of transcription by E. coli RNA polymerase of the genes in the early region of T7. This analysis is extended to the transcription by E. coli polymerase of the late region of T7 by deleting the early terminator. The results demonstrate the existence of a single large transcription unit spanning the early region, with a promotor located at the left end of the T7 genome. Furthermore, there are no initiation sites for E. coli RNA polymerase in the late region. When E. coli polymerase transcribes the late region, it does so exclusively by initiation at the early promotor.

Amino Acids↗
PubMed1969

Control of gene function in bacteriophage T4. I. Ribonucleic acid and deoxyribonucleic acid metabolism in T4rII-infected lambda-lysogenic hosts.

Deoxyribonucleic acid (DNA) synthesis in T4rII-infected, lambda-lysogenic strains of Escherichia coli proceeds with one-half the rate of T4 wild-infected bacteria and stops 16 min after infection at 37 C. The rates of ribonucleic acid (RNA) synthesis, however, are the same with T4rII and T4 wild. The turnover of pulse-labeled RNA is slow in K strains (half-lives 10 to 20 min) as compared with B strains (half-lives 2.5 to 6 min). Lambda-lysogeny increases the apparent messenger (m) RNA half-lives in pulse-chase experiments. The shutoff of host RNA synthesis in T4rII infected K(lambda) is incomplete. Moreover, the preferential transcription of T4 DNA ceases 13 min after infection, and transcription of host and prophage lambda DNA is resumed. The T4 RNA synthesized in rII-infected K(lambda) contains no late T4 mRNA. The early portion of the T4 genome, however, is transcribed completely. The T4-induced early modification of bacterial RNA polymerase does occur. Resumption of host DNA transcription at 13 min after infection is not associated with a reversal of the above polymerase modification. It is concluded that in lambdalysogenic bacteria T4rII infections are abortive because RNA polymerase is prevented from transcribing late T4 genes.

Centrifugation, Density Gradient↗