ライフサイエンスコーパス: alcaligin

1 tions, B. pertussis produces the siderophore alcaligin.

2 tion blunted the transcriptional response to alcaligin.

3 ron is through production of the siderophore alcaligin.

4 produce the native dihydroxamate siderophore alcaligin.

5 se activity required for the biosynthesis of alcaligin.

6 ssed in vivo, showing early induction of the alcaligin and enterobactin siderophore systems, and dela

7 ed by the inability to produce and transport alcaligin and express the two iron-repressed proteins.

8 tition studies established the importance of alcaligin and haem utilization for B. pertussis in vivo

9 on mutant BRM17 was unable to utilize ferric alcaligin, and in complementation analyses ferric alcali

10 red for the uptake and utilization of ferric alcaligin as an iron source.

11 on iron-restricted medium containing ferric alcaligin as the sole iron source.

12 he siderophore, the mutant failed to produce alcaligin as well as two known iron-regulated proteins,

13 is involved in the regulation of Bordetella alcaligin biosynthesis and transport genes and is requir

14 Concordantly, the alcaligin biosynthesis defect of BRM3 was functionally c

15 ussis DNA fragment mapping downstream of the alcaligin biosynthesis genes alcABC restored both sidero

16 tronic transcriptional organization of these alcaligin biosynthesis genes.

17 ) genomic DNA fragment that complements a Bb alcaligin biosynthesis mutant, and reported the identifi

18 e transcriptional start site of the putative alcaligin biosynthesis operon containing alcABC to a pro

19 regulated proteins, one of which is the AlcC alcaligin biosynthesis protein.

20 fauA genes, encodes activities required for alcaligin biosynthesis, the export of the siderophore fr

21 ne into alcA, one of the genes essential for alcaligin biosynthesis.

22 hore from the cell, the uptake of the ferric alcaligin complex across the outer membrane, and the tra

23 itive to inducer, occurring at extremely low alcaligin concentrations.

24 ression patterns of the Bordetella pertussis alcaligin, enterobactin and haem iron acquisition system

25 uding the known outer membrane receptors for alcaligin, enterobactin and haem, supporting the hypothe

26 structurally distinct siderophores including alcaligin, enterobactin, ferrichrome, and desferrioxamin

27 ll-associated alcaligin, implicating AlcS in alcaligin export.

28 nditions, in iron source utilization, and in alcaligin export.

29 hese transcription studies indicate that the alcaligin exporter activity of AlcS is required to maint

30 Bcr), was reported to be encoded within the alcaligin gene cluster.

31 transcriptional regulator encoded within the alcaligin gene cluster.

32 tants had elevated levels of cell-associated alcaligin, implicating AlcS in alcaligin export.

33 Putrescine is an essential precursor of alcaligin in Bordetella spp.

34 and Bvg(-) phase-locked mutants both produce alcaligin in response to iron starvation.

35 es under conditions in which the presence of alcaligin in the environment is perceived.

36 esidue 103 affects a critical determinant of alcaligin inducer dependence of AlcR-mediated transcript

37 s established the critical roles of AlcR and alcaligin inducer in positive regulation of alcaligin si

38 -dependent transcriptional responsiveness to alcaligin inducer; conversely, AlcS overproduction blunt

39 quired to maintain appropriate intracellular alcaligin levels for normal inducer sensing and responsi

40 Although the levels of extracellular alcaligin measured in alcS strain culture fluids were se

41 Alcaligin-mediated iron acquisition by B. pertussis may

42 A nonrevertible alcaligin mutant derived from the virulent strain 4609,

43 In contrast, we report that alcaligin production by RB50 does not require Bvg phenot

44 This suppression and the alcaligin production defect were reversed by trans compl

45 tingly, a deltaalcA mutation that eliminated alcaligin production suppressed the growth defects of al

46 t carried multiple genes required to restore alcaligin production to these siderophore-deficient muta

47 Alcaligin production was fully restored to group III mut

48 phenotype of alcS mutants is associated with alcaligin production.

49 del, inactivation of the B. pertussis ferric alcaligin receptor protein was found to have a profound

50 iseptica B013N alcR partially suppressed the alcaligin requirement for transcriptional activation.

51 s and genetic complementation confirmed that alcaligin-responsive transcriptional activation of Borde

52 m genes by an autogenous mechanism involving alcaligin sensing.

53 ositive autogenous control circuit involving alcaligin siderophore as the inducer for AlcR-mediated t

54 AlcR-mediated transcriptional activation of alcaligin siderophore biosynthesis and transport genes c

55 alcaligin inducer in positive regulation of alcaligin siderophore biosynthesis and transport genes i

56 alcA, alcB, and alcC, which are involved in alcaligin siderophore biosynthesis in response to iron s

57 rnithine decarboxylase activity required for alcaligin siderophore biosynthesis.

58 ired for transport and utilization of ferric alcaligin siderophore complexes by Bordetella species.

59 The alcaligin siderophore gene cluster, consisting of the al

60 A previous study found that alcaligin siderophore production by Bordetella bronchise

61 ene defined by these mutations that abrogate alcaligin siderophore production.

62 ur and iron mediate repression of Bordetella alcaligin siderophore system (alc) genes under iron-repl

63 hogen that can acquire iron using its native alcaligin siderophore system, but can also use the catec

64 wild-type fauA gene in trans regained ferric alcaligin siderophore transport and utilization function

65 h 2 mM ascorbate reductant was inhibitory to alcaligin siderophore-dependent growth at pH 7.6, but ha

66 s conditions is dependent on the presence of alcaligin siderophore.

67 nonrevertible defects in genes required for alcaligin synthesis may be candidates for evaluation as

68 iveness necessary for positive regulation of alcaligin system gene expression.

69 brane, and the transcriptional activation of alcaligin system genes by an autogenous mechanism involv

70 ive transcriptional activation of Bordetella alcaligin system genes is dependent on AlcR, a Fur-regul

71 erichia coli suggested the presence of three alcaligin system genes, namely, alcA, alcB, and alcC.

72 transcription of additional, uncharacterized alcaligin system genes.

73 mammals, produce and utilize the siderophore alcaligin to acquire iron in response to iron starvation

74 calized putative Bordetella pertussis ferric alcaligin transport genes and Fur-binding sequences to a

75 , suggesting that the contribution of ferric alcaligin transport to the ecological fitness of B. pert

76 rric alcaligin utilization and (55)Fe-ferric alcaligin uptake and no longer produced a 79-kDa iron-re

77 A deletion mutation, was defective in ferric alcaligin utilization and (55)Fe-ferric alcaligin uptake

78 igin, and in complementation analyses ferric alcaligin utilization was restored to this mutant by sup