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Functions that protect Escherichia coli from DNA-protein crosslinks.

Publication ,  Journal Article
Krasich, R; Wu, SY; Kuo, HK; Kreuzer, KN
Published in: DNA Repair (Amst)
April 2015

Pathways for tolerating and repairing DNA-protein crosslinks (DPCs) are poorly defined. We used transposon mutagenesis and candidate gene approaches to identify DPC-hypersensitive Escherichia coli mutants. DPCs were induced by azacytidine (aza-C) treatment in cells overexpressing cytosine methyltransferase; hypersensitivity was verified to depend on methyltransferase expression. We isolated hypersensitive mutants that were uncovered in previous studies (recA, recBC, recG, and uvrD), hypersensitive mutants that apparently activate phage Mu Gam expression, and novel hypersensitive mutants in genes involved in DNA metabolism, cell division, and tRNA modification (dinG, ftsK, xerD, dnaJ, hflC, miaA, mnmE, mnmG, and ssrA). Inactivation of SbcCD, which can cleave DNA at protein-DNA complexes, did not cause hypersensitivity. We previously showed that tmRNA pathway defects cause aza-C hypersensitivity, implying that DPCs block coupled transcription/translation complexes. Here, we show that mutants in tRNA modification functions miaA, mnmE and mnmG cause defects in aza-C-induced tmRNA tagging, explaining their hypersensitivity. In order for tmRNA to access a stalled ribosome, the mRNA must be cleaved or released from RNA polymerase. Mutational inactivation of functions involved in mRNA processing and RNA polymerase elongation/release (RNase II, RNaseD, RNase PH, RNase LS, Rep, HepA, GreA, GreB) did not cause aza-C hypersensitivity; the mechanism of tmRNA access remains unclear.

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Published In

DNA Repair (Amst)

DOI

EISSN

1568-7856

Publication Date

April 2015

Volume

28

Start / End Page

48 / 59

Location

Netherlands

Related Subject Headings

  • Transcription, Genetic
  • RNA, Bacterial
  • Escherichia coli Proteins
  • Escherichia coli
  • Developmental Biology
  • DNA Repair
  • DNA Damage
  • Azacitidine
  • 3101 Biochemistry and cell biology
  • 0601 Biochemistry and Cell Biology
 

Citation

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Krasich, R., Wu, S. Y., Kuo, H. K., & Kreuzer, K. N. (2015). Functions that protect Escherichia coli from DNA-protein crosslinks. DNA Repair (Amst), 28, 48–59. https://doi.org/10.1016/j.dnarep.2015.01.016
Krasich, Rachel, Sunny Yang Wu, H Kenny Kuo, and Kenneth N. Kreuzer. “Functions that protect Escherichia coli from DNA-protein crosslinks.DNA Repair (Amst) 28 (April 2015): 48–59. https://doi.org/10.1016/j.dnarep.2015.01.016.
Krasich R, Wu SY, Kuo HK, Kreuzer KN. Functions that protect Escherichia coli from DNA-protein crosslinks. DNA Repair (Amst). 2015 Apr;28:48–59.
Krasich, Rachel, et al. “Functions that protect Escherichia coli from DNA-protein crosslinks.DNA Repair (Amst), vol. 28, Apr. 2015, pp. 48–59. Pubmed, doi:10.1016/j.dnarep.2015.01.016.
Krasich R, Wu SY, Kuo HK, Kreuzer KN. Functions that protect Escherichia coli from DNA-protein crosslinks. DNA Repair (Amst). 2015 Apr;28:48–59.
Journal cover image

Published In

DNA Repair (Amst)

DOI

EISSN

1568-7856

Publication Date

April 2015

Volume

28

Start / End Page

48 / 59

Location

Netherlands

Related Subject Headings

  • Transcription, Genetic
  • RNA, Bacterial
  • Escherichia coli Proteins
  • Escherichia coli
  • Developmental Biology
  • DNA Repair
  • DNA Damage
  • Azacitidine
  • 3101 Biochemistry and cell biology
  • 0601 Biochemistry and Cell Biology