These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: Evidence for the control by exrA and polA genes of two branches of the uvr gene-dependent excision repair pathway in Escherichia coli K-12.
    Author: Youngs DA, Smith KC.
    Journal: J Bacteriol; 1973 Oct; 116(1):175-82. PubMed ID: 4583206.
    Abstract:
    A polA1 exrA strain of Escherichia coli K-12 was found to be more sensitive to ultraviolet radiation than the closely related polA1 or exrA strains, but not as sensitive as either the exrA uvrB or recA strains. The exrA and polA1 mutations both resulted in a deficiency in the repair of single-strand breaks arising in the deoxyribonucleic acid as a result of the excision repair process (incision breaks). These deficiencies were at least partially independent since the double mutant, polA1 exrA, was more deficient than a strain containing either the polA1 or exrA mutation alone. These results suggest that the polA1 and exrA mutations result in defects in two different branches of the uvr gene-dependent excision repair process. The repair of incision breaks was still observed in the polA1 exrA strain after low exposures of ultraviolet radiation, suggesting the existence of a third branch of the excision repair process which is dependent on neither the polA nor exrA genes. The polA1 and polA1 uvrA strains were not deficient in post-replicational repair. The exrA strain was partially deficient in post-replicational repair, but the polA1 exrA strain was no more deficient than the exrA strain in this repair process. Thus, the increased ultraviolet irradiation sensitivity of the polA1 exrA strain relative to the polA1 and exrA strains appears to be related to the effect of the polA1 and exrA mutations on different branches of the uvr gene-dependent excision repair process as well as to the effect of the exrA mutation on the post-replicational repair process.
    [Abstract] [Full Text] [Related] [New Search]