ライフサイエンスコーパス: SOS induction

1 side-effect of growth with an amplification (SOS induction).

2 oximately 1-2% in the presence or absence of SOS induction).

3 f RecA, thereby preventing LexA cleavage and SOS induction.

4 ncluded that ATP hydrolysis is essential for SOS induction.

5 and severe cell filamentation, indicative of SOS induction.

6 important for recombination, DNA repair, and SOS induction.

7 in understanding the detailed mechanisms of SOS induction.

8 hyperrecombination phenotype, and increased SOS induction.

9 hat the role of RecF in mutation is to allow SOS induction.

10 n C, in addition to the RecA-LexA pathway of SOS induction.

11 ccur when UvrA and UvrB are increased during SOS induction.

12 rC and uvrD, both of which result in partial SOS induction.

13 dependent and uvrA-independent components of SOS induction.

14 ensitivity, and a lack of ability to support SOS induction.

15 We found that, without SOS induction, all alpha-dN lesions except alpha-dA stro

16 ction resolvase to survive rapid growth, but SOS induction, although elevated, is not required.

17 topoisomerase I cleavage complex can lead to SOS induction and cell death in Escherichia coli.

18 ing HAP leads to increased recombination and SOS induction and even cell death.

19 SOS induction and filamentation commenced after an appar

20 phenotype, which includes reduced viability, SOS induction and filamentation, and abnormal nucleoid m

21 titive relationship between the processes of SOS induction and genetic recombination.

22 single-stranded DNA that, if left, leads to SOS induction and PolIV-dependent mutagenesis.

23 in this work, recA(Q300R), is proficient in SOS induction and repair of UV-induced DNA damage, but i

24 C, such strains grow but have RecA-dependent SOS induction and show constitutive RecBCD-dependent DNA

25 To correlate the level of SOS induction and the up-regulation of genes involved in

26 hemical roles for recombinational processes, SOS induction, and mutagenic lesion bypass.

27 with RecA in double-strand-break repair and SOS induction, and RuvABC Holliday-junction resolvase.

28 in the absence of Fis and the other assessed SOS induction as a readout of increased DNA cleavage.

29 romosome and DpiA-targeted plasmids-reversed SOS induction as well as plasmid destabilization by DpiA

30 esponse is manifested in cells deficient for SOS induction, as well as for all four of the 'non-repli

31 investigated the use of the Escherichia coli SOS induction assay as a screen for yeast and human gene

32 The SOS induction assay was then extended to the isolation o

33 ed repair of CPDs occurred in the absence of SOS induction but was undetectable when the response was

34 s and reduces the level of recombination and SOS induction, but it increases the level of mutagenesis

35 in do not mediate DNA damage, as measured by SOS induction, but nevertheless partially restrict M.Hpa

36 merase transcription occur in the absence of SOS induction by exogenous agents and indicate that cell

37 , the only proteins known to be required for SOS induction by nalidixic acid are RecA and RecBC.

38 genes were found to cause partial defects in SOS induction by one or both pathways, providing possibl

39 k reversal function of RuvAB is required for SOS induction by the covalent complex formed by topoisom

40 are converted into double-strand breaks for SOS induction by the RecBCD pathway.

41 SOS induction caused little change in the efficiency of

42 ecQ, implying that neither recombination nor SOS induction causes hyper-TLD in recB cells, and RecQ i

43 high levels of chromosomal fragmentation and SOS induction, characteristic of the DeltaseqA mutants.

44 very high efficiency under damage-response (SOS induction) conditions.

45 In addition, SOS induction could lead to markedly elevated bypass eff

46 Escherichia coli RecA protein is involved in SOS induction, DNA repair, and homologous recombination.

47 Thus, SOS induction does not require ATP hydrolysis by the Rec

48 ecN contributes to maintaining low levels of SOS induction during double-strand break repair.

49 mutants that were substantially reduced for SOS induction following nalidixic acid but not UV treatm

50 products that are specifically necessary for SOS induction following nalidixic acid treatment.

51 SOS induction following topoisomerase I complex accumula

52 Furthermore, although spontaneous SOS induction has been observed to occur in only a small

53 for SOS, dut mutants are not rescued by full SOS induction if RecA is not available, suggesting that

54 and breaks but does not require or result in SOS induction in B. subtilis.

55 how that double-strand breaks provoke global SOS induction in E. coli but not in B. subtilis.

56 cellular events of genetic recombination and SOS induction in Escherichia coli, RecA protein promotes

57 essential for recombination, DNA repair and SOS induction in Escherichia coli.

58 Genetic analyses have shown that SOS induction in response to double-stranded DNA (dsDNA)

59 ks induced by ionizing radiation resulted in SOS induction in virtually every cell.

60 R, the recA E38K/K72R double mutant promotes SOS induction in vivo after UV treatment.

61 equirement of ATP binding and hydrolysis for SOS induction in vivo is tested here through the study o

62 Strains with this mutation do not undergo SOS induction in vivo.

63 that ATP hydrolysis will not be required for SOS induction in vivo.

64 All isolated mutants show varying degree of SOS induction, indicating elevated levels of chromosomal

65 In vitro reactions modelling SOS induction minimally require ssDNA and non-hydrolyzab

66 rther increase in mutagenesis, implying that SOS induction of DinB, although necessary, is insufficie

67 d in the cells by irradiation with UV light (SOS induction) prior to transformation.

68 Mutant topoisomerases identified by SOS induction screening demonstrated that accumulation o

69 entral role in recombination, DNA repair and SOS induction through forming a RecA-DNA helical filamen

70 Thus, we found that the contribution of SOS induction to double-strand break repair differs subs

71 resistance, conjugational recombination, and SOS induction to recA(-) cells.

72 the damage-inducible dinA gene and exhibits SOS induction under the control of Lex A repressor.

73 it increased mutagenesis, recombination, and SOS induction upon HAP exposure.

74 or E. coli mutants specifically deficient in SOS induction upon nalidixic acid treatment by using a d

75 If SOS induction was blocked by lexA3 (Ind-), filaments did

76 E. coli strains incapable of SOS induction were sensitive to ionizing radiation.