Induction of protein synthesis in Escherichia coli following UV-or γ-irradiation, mitomycin C treatment or tif expression View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1977-01

AUTHORS

Stephen C. West, Peter T. Emmerson

ABSTRACT

The rate of synthesis of total cellular proteins has been studied by pulse labelling cells at various periods after irradiation with UV or gamma-rays, after treatment with mitomycin C (MMC) or after expression of the temperature sensitive mutation tif. Subsequent gel electrophoresis and autoradiography reveals changes in the rate of synthesis of several proteins. The most striking change is in a protein of molecular weight 40,000, protein X, which has been previously most extensively studied in cells treated with nalidixic acid (Gudas, 1976). Synthesis of large quantities of protein X is induced by UV, gamma-rays, MMC treatment or tif expression in rec+ but not recA cells. A feature of recA cells is that they break down their DNA excessively after irradiation or MMC treatment. However, if protein synthesis following irradiation is prohibited by chloramphenicol, post-irradiation degradation becomes excessive in recA+ cells. This inverse relationship between DNA degradation and new protein synthesis consistent with the hypothesis that an induced protein such as X is responsible for controlling DNA degradation following irradiation. Protein X is not induced in a lexB mutant following MMC treatment. In this respect the lexB mutant behaves like lexA and recA mutants in that the ability to induce protein X can be correlated with excessive DNA degradation. Studies on the induction of proteins in inf, tif and tif sfi mutants fail to reveal any correlation between induction of protein X and either the induction of prophage lambda or septation. More... »

PAGES

57-67

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/bf00446913

DOI

http://dx.doi.org/10.1007/bf00446913

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1041508194

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/325368


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