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The Role of Inducible DNA Repair in W-Reactivation and Related Phenomena

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Progress in Molecular and Subcellular Biology

Part of the book series: Progress in Molecular and Subcellular Biology ((PMSB,volume 8))

Abstract

Damage to cellular DNA or inhibition of DNA replication induces an array of coordinately controlled functions (“SOS” responses) in Escherichia coli including derepression of repair enzymes and mutagenesis. Most of the UV-induced photoproducts in the DNA of bacteria and their viruses are repaired by “error-proof” repair mechanisms such as photoreactivation, “short-patch” excision repair, and recombinational repair. Single-strand gaps resulting from replication of DNA which contains pyrimidine dimers, can be repaired by ultraviolet (UV)-inducible, recA + lexA +-dependent “error-prone” repair (“SOS” repair) which leads to mutations in the bacteria and its phages. Other UV-induced, recA + lexA +-dependent functions, such as prophage induction, filamentous growth, and W-reactivation, are coordinately regulated with the error-prone repair functions. An increasing amount of experimental evidence suggests that misincorporation of bases could result from an inducible factor which affects the proofreading activities of DNA polymerase, allowing it to fill postreplication daughter strand gaps across from noncoding UV photoproducts. Mutagenic W-reactivation illustrates the role of UV-inducible, recA + lexA +-dependent functions in the error-prone DNA repair of bacteria and their viruses.

The views of the author do not purport to reflect the positions of the Department of the Army or the Department of Defense

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Authors
  1. Gregory B. Knudson
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  1. Division of Communicable Diseases and Immunology, Walter Reed Army Institute of Research, Washington, D.C., 20307, USA

    Fred E. Hahn Ph.D.

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© 1983 Springer-Verlag Berlin Heidelberg

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Knudson, G.B. (1983). The Role of Inducible DNA Repair in W-Reactivation and Related Phenomena. In: Hahn, F.E., Kopecko, D.J., Müller, W.E.G. (eds) Progress in Molecular and Subcellular Biology. Progress in Molecular and Subcellular Biology, vol 8. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-69228-4_2

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