ライフサイエンスコーパス: tRNA(Ala)

1 a non-cognate tRNA replaced with the stem of tRNAAla.

2 utants forming substantial amounts of alanyl-tRNAAla.

3 lity of the molecule for formation of alanyl-tRNAAla.

4 could significantly amplify cellular alanyl-tRNAAla.

5 ans C-Ala specifically targets the D-loop of tRNA(Ala).

6 AlaRSs), which remove serine from mischarged tRNA(Ala).

7 f both aminoacylation and editing domains to tRNA(Ala).

8 nome-encoded editing proteins that clear Ser-tRNA(Ala).

9 gh clearance of mischarged (with Ser or Gly) tRNA(Ala).

10 These also recognize mischarged tRNA(Ala).

11 eptor stem and/or the TPsiC loop stem of the tRNA(Ala).

12 the major determinant for identity of Dm mt tRNA(Ala).

13 acylation of the most deleterious mutants of tRNA(Ala).

14 tochondrial enzyme cannot charge cytoplasmic tRNA(Ala).

15 (37) to m(1)I(37) modification in eukaryotic tRNA(Ala).

16 inates adenosine 37 to inosine in eukaryotic tRNA(Ala).

17 In the case of tRNAAla a single acceptor stem G.U base pair at position

18 typically recognizes the G3:U70 base pair of tRNA(Ala); a G3A change in Ashbya tRNA(Ala)UAG abolishes

19 n structure of a microhelix derived from the tRNAAla acceptor end has been determined at high precisi

20 The tRNAAla acceptor end is overall similar to A-form RNA, b

21 The anticodon stem-loop of tRNA(Ala) alone is not a functional substrate for hADAT1

22 ->A in the mt-tRNA(Ala)) destabilizes the mt-tRNA(Ala) aminoacyl stem, we designed a compensatory m.5

23 could restore the secondary structure of the tRNA(Ala) aminoacyl stem.

24 solely responsible for the change in cognate tRNA(Ala) aminoacylation observed under oxidative stress

25 The reduced mt-tRNA(Ala) amounts in these cells were increased after ed

26 Total mt-tRNA(Ala) amounts were restored in heart and muscle by t

27 gans mitochondrial C-Ala robustly bound both tRNA(Ala) and DNA and maintained targeting specificity f

28 ion into Escherichia coli EF-Tu, whereas Ala-tRNA(Ala) and Gly-tRNA(Gly) were unaffected.

29 aRS) were investigated in vivo for wild-type tRNA(Ala) and mutant tRNAs with G.U substitutions.

30 C.A, or G.A gave similar amounts of charged tRNA(Ala) and supported viability of E. coli lacking chr

31 Thus, cdc64-1 might affect charging of tRNA(Ala) and thereby initiation of cell division.

32 bicans have thus been identified: tRNA(Asp), tRNA(Ala) and tRNA(Ile).

33 Mutation of tRNA(Ala) and tRNA(Lys) had little effect on either MprF

34 ed efficiencies of tRNA(Leu(UUR)) as well as tRNA(Ala) and tRNA(Met).

35 yl-tRNA synthetase efficiently aminoacylates tRNAAla and an RNA minihelix that comprises just one dom

36 ri and Sulfolobus solfataricus hydrolyze Ser-tRNAAla and Gly-tRNAAla substrates.

37 erent amino acids; MprF1 is specific for Ala-tRNA(Ala), and MprF2 utilizes Lys-tRNA(Lys).

38 AlaRS mischarged serine and glycine to tRNA(Ala), as observed in other bacteria, and also trans

39 yl-tRNA synthetase (AlaRS) and can form BMAA-tRNA(Ala) by escaping from the intrinsic AlaRS proofread

40 ruption of translation, consumption of seryl-tRNA(Ala) by MurM may represent a first line of defense.

41 ecognition of mitochondrial from cytoplasmic tRNA(Ala) by translocation of G:U.

42 and in vitro deamination of adenosine 37 of tRNAala by ADAT1.

43 on aminoacylation of alanine-specific tRNA (tRNA(Ala)) by alanyl-tRNA synthetase (AlaRS) gave rise t

44 rosophila melanogaster mitochondrial (Dm mt) tRNA(Ala) contains a G:U base pair that has been translo

45 d phosphatidylglycerol (PG) catalyzed by Ala-tRNA(Ala)-dependent alanyl-phosphatidylglycerol synthase

46 original m.5024C->T mutation (G->A in the mt-tRNA(Ala)) destabilizes the mt-tRNA(Ala) aminoacyl stem,

47 umed that the specificity for recognition of tRNA(Ala) for editing was provided by the same structura

48 ch the G3.U70 pair marks the acceptor end of tRNAAla for aminoacylation with alanine has not been cla

49 6-fold decrease in efficiency of cognate Ala-tRNA(Ala) formation.

50 ly deaminates A(37) in the anticodon loop of tRNA(Ala) from higher eukaryotes and with lower efficien

51 s assay of the expression and utilization of tRNA(ala)(GAC) also can be used to study a variety of tR

52 ssense suppression is blocked by mutation of tRNA(ala)(GAC) at a site that prevents aminoacylation by

53 Bombardment of a highly expressed dicot tRNA(ala)(GAC) gene into Zea mays bz-E2 or bz-E5 coleopt

54 c for the mouse m.5024C>T mutation in the mt-tRNA(Ala) gene and its delivery to mice intravenously us

55 an AUX/IAA gene, but rather a mutation in a tRNA(ala) gene in which the anticodon was found changed

56 model of mtDNA disease (m.5024C>T in the mt-tRNA(Ala) gene).

57 ISR1 contained a tRNA(Ala) gene, while ISR2 contained a tRNA(Ile) gene.

58 c pathogenic mtDNA mutation (m.C5024T of the tRNAAla gene) into Slirp knockout mice causes an additiv

59 itochondrial transfer RNA (tRNA) alanine (mt-tRNA(Ala)) gene.

60 ted viability of E. coli lacking chromosomal tRNA(Ala) genes.

61 wild-type and mutant versions of the Bombyx tRNAAla genes into Drosophila Schneider-2 cells and foun

62 tRNALeu genes, and 3 from three families of tRNAAla genes.

63 sophila melanogaster (Dm) mitochondrial (mt) tRNA(Ala) has a G2:U71 but not a G3:U70 pair.

64 s that mimic the amino acid acceptor stem of tRNA(Ala) has been shown, by analysis of variant minihel

65 The effect of tRNA(Ala) identity mutations on both aminoacylation effi

66 ncy between in vivo and in vitro analysis of tRNA(Ala) identity.

67 emonstrated that AlaXp deacylated mischarged tRNA(Ala) in vitro, the significance of this activity in

68 ifically and with a high efficiency on human tRNA(Ala) in vitro.

69 triking hinge-like movements in RqcH leading tRNA(Ala) into a hybrid A/P-state associated with peptid

70 Moreover, DTD's activity on non-cognate Gly-tRNA(Ala) is conserved across all bacteria and eukaryote

71 The structures explain how tRNA(Ala) is selected via anticodon reading during recru

72 nd can support growth of an Escherichia coli tRNAAla knockout strain, leading to the hypothesis that

73 produces approximately 50% reduction in the tRNA(Ala) level in mutant cells.

74 ant mtDNA with concomitant restoration of mt-tRNA(Ala) levels.

75 In contrast to full-length tRNAAla, minihelixAla was robustly mischarged and could

76 ges harbouring a heteroplasmic mitochondrial tRNA(Ala) mutation (m.5019A>G) to address this question.

77 Docking of tRNA(Ala) on AlaRS shows critical contacts with the thre

78 e independently can provide determinants for tRNA(Ala) recognition.

79 MurNAc pentapeptide and Escherichia coli Ala-tRNAAla, respectively, and exhibited a kcat value of 660

80 iation of the key G:U base pair seen in some tRNA(Ala)s.

81 Throughout evolution, tRNA(Ala) selection by alanyl-tRNA synthetase (AlaRS) ha

82 d these differences between minihelixAla and tRNAAla, several chimeric full tRNAs were constructed.

83 itecture can efficiently edit mischarged Gly-tRNA(Ala) species four orders of magnitude more efficien

84 positively selects the universally invariant tRNA(Ala)-specific G3*U70.

85 s solfataricus hydrolyze Ser-tRNAAla and Gly-tRNAAla substrates.

86 compromise the efficiency with which alanyl-tRNA(Ala) synthetase can avoid noncognate mischarging of

87 erexpression of the editing domain of alanyl-tRNA(Ala) synthetase that enables detoxification of tRNA

88 conjunction with homoplasmic ND1 T3308C and tRNA(Ala) T5655C mutations using cybrids constructed by

89 ir in Escherichia coli alanine transfer RNA (tRNA(Ala)) that are associated with aminoacylation by al

90 compensatory m.5081G->A edit (C->T in the mt-tRNA(Ala)) that could restore the secondary structure of

91 served invariant base G(18) in the D-loop of tRNA(Ala) through a highly conserved lysine residue, K93

92 hat catalyzes the transfer of l-Ala from Ala-tRNAAla to the epsilon-amino group of l-lysine of UDP-Mu

93 ular conditions, yeast tRNA(Phe) and E. coli tRNA(Ala) transcripts fold in a single, cooperative tran

94 the particular tRNA precursor substrate for tRNA(Ala), tRNA(Val), and tRNA(His).

95 a lesser extent, differences in the in vivo tRNA(Ala):tRNA(Ser) ratio in 159 and Pn16.

96 se pair of tRNA(Ala); a G3A change in Ashbya tRNA(Ala)UAG abolishes its recognition by AgAlaRS.

97 Enzymatic studies reveal that tRNA(Ala)UAG is efficiently recognized by A. gossypii mi

98 We further demonstrate that a predicted tRNA(Ala)UAG is transcribed and accurately processed in

99 corporate seryl groups from mischarged Seryl-tRNA(Ala)(UGC) into cell wall precursors with exquisite

100 factor, senses the obstruction and recruits tRNA(Ala(UGC)) to modify nascent-chain C termini with a

101 ial recombinant fragment, targets mischarged tRNA(Ala) using a structural motif unrelated to that for

102 It also clears mischarged tRNAAla using a specialized domain in its C-terminal hal

103 Tric1/2 binds tRNA(ala)via conserved residues in the C-terminal Steril

104 efect in this model, namely low levels of mt-tRNA(Ala), were markedly improved in treated muscles.

105 significance of this unique modification in tRNA(Ala), which is conserved from yeast to man.

106 tRNA(Ala) with G.C was inactive.

107 tRNA(Ala) with G.U, C.A, or G.A gave similar amounts of

108 uctures of an archaeal AlaRS in complex with tRNA(Ala) with G3*U70 and its A3*U70 variant.

109 Thus, the 3'-CCA region of tRNA(Ala) with G3*U70 is oriented to the reactive route

110 nthetase can avoid noncognate mischarging of tRNA(Ala) with serine, which is toxic to cells.