ライフサイエンスコーパス: tRNA(Leu)

1 euRS, are required for editing of mischarged tRNALeu.

2 e folding of an Escherichia coli cytoplasmic tRNALeu.

3 nd interacts with the corner of the L-shaped tRNALeu.

4 that DeltaAla(P) would be condensed with Leu-tRNA(Leu).

5 to significantly hydrolyze misaminoacylated tRNA(Leu).

6 es a TTA codon predicted to be recognized by tRNA(leu).

7 tation that hydrolyzes correctly charged Leu-tRNA(Leu).

8 e yielded a mutant LeuRS that hydrolyzes Leu-tRNA(Leu).

9 ions, including introns and the anticodon of tRNA(Leu).

10 show a decrease in the cellular abundance of tRNA(Leu).

11 T mutation in the leucine transfer RNA gene (tRNAleu)].

12 Mutations in the anticodon and extra arm of tRNALeu-1 do not measurably effect its ability to serve

13 wild type Leu-tRNALeu-4 (UAA) or mutant Leu-tRNALeu-4 (CUA) are each 0.4 +/- 0.2 microM.

14 een L/F-transferase and either wild type Leu-tRNALeu-4 (UAA) or mutant Leu-tRNALeu-4 (CUA) are each 0

15 to characterize the determinants of the Leu-tRNALeu-4 acceptor stem recognized by the L/F-transferas

16 itioning of G18 and G19 that is found in all tRNA(Leu); a base was inserted at position 47n between t

17 aled differences in the contributions of the tRNA(Leu) acceptor stem base-pairs to tRNA(Leu) function

18 ficity was contingent on the presence of the tRNA(Leu) acceptor stem sequence.

19 cyl-tRNA synthetase by formation of a stable tRNA(Leu)-AN2690 adduct in the editing site of the enzym

20 Herein, we describe the smallest tRNA(leu) analog that has been aminoacylated to a signif

21 A series of tRNA(leu) analogs with various domains and combinations

22 8ph by mutant H3S28A repressed Brf1, TBP and tRNA(Leu) and 5S rRNA expression and decreased occupancy

23 cer cells (MCF-7) decreases the induction of tRNA(Leu) and 5S rRNA genes by alcohol, whereas reductio

24 Reduction of Brf1 significantly decreased tRNA(Leu) and 5S rRNA transcription and repressed EGF-in

25 induce H3S28ph, which, in turn, upregulates tRNA(Leu) and 5S rRNA transcription through Brf1 and TBP

26 EGFR, but not PI3K, reduced both H3S28ph and tRNA(Leu) and 5S rRNA transcription.

27 ced occupancy of H3S28ph in the promoters of tRNA(Leu) and 5S rRNA.

28 urnover, thus inhibiting synthesis of leucyl-tRNA(Leu) and consequentially blocking protein synthesis

29 Experiments monitoring deacylation of Ile-tRNA(Leu) and misactivated adenylate turnover revealed t

30 ichia coli LeuRS abolished aminoacylation of tRNALeu and also amino acid editing of mischarged tRNA m

31 equence alters mitochondrial localization of tRNA(Leu), and in vivo studies also show a decrease in t

32 d containing three tRNA genes, tRNA(1)(Ser), tRNA(Leu), and tRNA(2)(Ser).

33 quence changes, as significant levels of Ile-tRNA(Leu) are formed in the presence of high concentrati

34 When the 3' end of tRNA(Leu) binds to the editing active site, the boron cr

35 Thus, these LeuRS mutants charge tRNA(Leu) but fail to translocate these products to the

36 uggested that other tRNAs can substitute for tRNA(Leu) but that interactions in addition to pairing o

37 ing function to correct misaminoacylation of tRNA(Leu) by isoleucine and methionine.

38 The rate of misaminoacylation of tRNA(Leu) by isoleucine and valine increases with the in

39 rase-dependent increase in the proportion of tRNA(Leu(CAA)) containing m(5)C at the wobble position,

40 constant of 22 nM for one of its substrates, tRNA(Leu)(CAG).

41 the substrate for the condensation with Leu-tRNA(Leu) catalyzed by the C-terminal domain of DhpH.

42 tRNA(Leu) charging decreased, but only small increases i

43 d an archaeal leucyl-tRNA synthetase (LeuRS):tRNA(Leu) complex.

44 The gene arrangement and lack of a tRNA(Leu(CUN)) gene in P. opilio is most parsimoniously

45 which probably destroyed the function of the tRNA(Leu(CUN)) gene.

46 cantly decreased use of codons recognized by tRNA(Leu(CUN)), likely due to selection to utilize the m

47 ochondrial tRNA genes and lacks the gene for tRNA(Leu(CUN)).

48 niversally conserved aspartic acid abolished tRNA(Leu) deacylation.

49 tide linker and allows interactions with the tRNA(Leu) elbow.

50 limiting C-terminal domain accessibility to tRNA(Leu) facilitates its role in protein synthesis and

51 e is imported rapidly, while the mature-size tRNA(Leu) fails to be imported in this system.

52 TM84 requires tRNA(Leu) for tight binding to the LeuRS synthetic activ

53 ermine the nucleotides that are required for tRNA(Leu) function.

54 of the tRNA(Leu) acceptor stem base-pairs to tRNA(Leu) function: in the type I, but not the type II f

55 thogenicity island (Pai) that is linked to a tRNA(Leu) gene found also in Pseudomonas aeruginosa but

56 e complete initiator tRNA(Met) gene, metY; a tRNA(Leu) gene; the tpiA gene product; and the MrsA prot

57 hat the association of BRF1 and pol III with tRNA(Leu) genes in cells decreases when ERK is inactivat

58 n in the occupancy of all TFIIIB subunits on tRNA(Leu) genes, whereas prolonged PTEN expression resul

59 es of tRNASer genes, 7 from five families of tRNALeu genes, and 3 from three families of tRNAAla gene

60 The trapping of enzyme-bound tRNA(Leu) in the editing site prevents catalytic turnove

61 The substrate, composed of tRNA(Ser) and tRNA(Leu), is transcribed in tandem with a 59-nucleotide

62 so dispensable for hydrolysis of the charged tRNA(leu) mimics.

63 fer editing activity that efficiently clears tRNA(Leu) mischarged with isoleucine.

64 's post-transfer hydrolytic activity against tRNA(Leu) mischarged with methionine is weak.

65 ino acid residue in the presence of a mutant tRNA(Leu) molecule containing the extra nucleotide, U, a

66 ) aminoacylates up to six different class II tRNA(leu) molecules.

67 e II counterparts.A minimum of six conserved tRNA(Leu) nucleotides were required to change the amino

68 Binding of gold-labeled tRNA(Leu) places leucyl-tRNA synthetase and the bifuncti

69 sidue group I intron of the Anabaena PCC7120 tRNAleu precursor.

70 Using tRNA(Leu) purified from a DUS 2 knockout strain of yeast

71 .5-7.3 kb of dissimilar intervening DNA with tRNA(Leu)-queA-tgt sequences that are also found in Pseu

72 st enough to completely block mischarging of tRNA(Leu), resulting in codon ambiguity and statistical

73 leucine occurs through misaminoacylation of tRNALeu, similar to the misincorporation of norleucine f

74 RNA promoters, including that for the major tRNALeu species in Escherichia coli, tRNA1Leu.

75 a activity, but increased the k(cat) for Leu-tRNA(Leu) synthesis approximately 8-fold.

76 es a single nucleotide in the anticodon of a tRNA(Leu) that changes its normal 5'CAG3' leucine antico

77 by proline and that sncB69 encodes a mutant tRNA(Leu) that corrects the mutation.

78 c tRNA loci (e.g., the nuclear tRNA(Gly) and tRNA(Leu), the mitochondrial tRNA(Val) and tRNA(Pro)) we

79 bstrate with a uridine at position 38 (human tRNA(Leu)), there was very slight formation of pseudouri

80 c precursors containing the tRNA(1)(Ser) and tRNA(Leu) transcripts with a 59-nucleotide intergenic se

81 RNA Pol III-dependent genes (Pol III genes), tRNA(Leu), tRNA(Tyr), 5S rRNA and 7SL RNA.

82 found to interrupt the anticodon loop of the tRNA(Leu)(UAA) gene in a bacterium belonging to the gamm

83 -proteobacteria, and the first instance of a tRNA(Leu)(UAA) group I intron to be found in a group of

84 and processing of the genes tRNA(Thr)(UGU), tRNA(Leu)(UAA), and tRNA(Phe) (GAA) therefore attributes

85 Many tRNA(Leu)UAA genes from plastids contain a group I intro

86 The phylogenetic distribution of the tRNA(Leu)UAA intron follows the clustering of rRNA seque

87 Our data support the notion that the tRNA(Leu)UAA intron was inherited by cyanobacteria and p

88 nd secondary structural similarities between tRNA(Leu)UAA introns found in strains of the cyanobacter

89 either does with other known cyanobacterial tRNA(Leu)UAA introns.

90 Extra copies of the tRNA(Leu)(UAG) gene rescued the cold sensitivity and in

91 ue, the levels of three point mutations, the tRNA(Leu(UUA)) 3243 mutation causing mitochondrial encep

92 In particular, the tRNA(Leu(UUR)) A3243G mutation causes mitochondrial ence

93 pathogenetic mechanism of the mitochondrial tRNA(Leu(UUR)) A3243G transition associated with the mit

94 ribosomes, possibly as a consequence of the tRNA(Leu(UUR)) aminoacylation defect.

95 75%) reduction in the level of aminoacylated tRNA(Leu(UUR)) and a decrease in mitochondrial protein s

96 high affinity wild-type and mutant human mt-tRNA(Leu(UUR)) and mt-tRNA(Lys), and stabilize mutant mt

97 ue to selection to utilize the more specific tRNA(Leu(UUR)) anticodon.

98 ate levels and the aminoacylated fraction of tRNA(Leu(UUR)) are likely to contribute to the decreases

99 by reduced the aminoacylated efficiencies of tRNA(Leu(UUR)) as well as tRNA(Ala) and tRNA(Met).

100 showed that the alteration of aminoacylation tRNA(Leu(UUR)) caused by the A3243G mutation led to mito

101 The T3271C mutation in tRNA(Leu(UUR)) did not affect the efficiency of aminoacy

102 ions of the mutation at position 3243 in the tRNA(Leu(UUR)) gene associated with the MELAS encephalom

103 zes a mtDNA segment within the mitochondrial tRNA(Leu(UUR)) gene immediately adjacent to and downstre

104 3G and T3271C mutations in the mitochondrial tRNA(Leu(UUR)) gene on the aminoacylation of tRNA(Leu(UU

105 ing analysis of the mtDNA segment within the tRNA(Leu(UUR)) gene that binds the transcription termina

106 ription termination region (TERM) within the tRNA(Leu(UUR)) gene was consistently and strongly protec

107 ated mutations are known to affect the hs mt tRNA(Leu(UUR)) gene, and the molecular-level properties

108 e if the decreased fraction of aminoacylated tRNA(Leu(UUR)) in A3243G mutant cells was due to a defec

109 in the amount of ND1 mRNA and co-transcribed tRNA(Leu(UUR)) in mutant cells.

110 f the D, TPsiC, and anticodon loops of hs mt tRNA(Leu(UUR)) in the structure and function of this mol

111 uences, indicating that this region of hs mt tRNA(Leu(UUR)) is not involved in recognition by LeuRS.

112 ted either with the m.3243A>G mutation in mt-tRNA(Leu(UUR)) or with mutations in the mt-tRNA(Ile), bo

113 tion efficiencies among wild-type and mutant tRNA(Leu(UUR)) transcripts.

114 Native A3243G mutant tRNA(Leu(UUR)) was 25-fold less efficiently aminoacylate

115 zed nucleotides in the loop regions of hs mt tRNA(Leu(UUR)), and tRNA variants that were aminoacylate

116 rs more structured than wild-type (WT) hs mt tRNA(Leu(UUR)), indicating that the entirely AU stem of

117 noacylation kinetics of wild-type and mutant tRNA(Leu(UUR)), using both native and in vitro transcrib

118 The results indicate that hs mt tRNA(Leu(UUR)), which is known to have structurally weak

119 ion was an inefficient aminoacylation of the tRNA(Leu(UUR)).

120 )) and mt-tRNA(Lys), and stabilize mutant mt-tRNA(Leu(UUR)).

121 lated in vitro, compared to native wild-type tRNA(Leu(UUR)).

122 , using both native and in vitro transcribed tRNA(Leu(UUR)).

123 creased steady-state levels of mitochondrial tRNA(Leu(UUR)).

124 tRNA(Leu(UUR)) gene on the aminoacylation of tRNA(Leu(UUR)).

125 a decrease in the fraction of aminoacylated tRNA(Leu(UUR)).

126 ially denatured for the wild type (WT) hs mt tRNALeu(UUR) and were significantly stabilized by mutati

127 as further elucidated with a mutant of hs mt tRNALeu(UUR) containing a stabilized D stem and a pathog

128 structure of the human mitochondrial (hs mt) tRNALeu(UUR) features several domains that are predicted

129 n at position 3256, within the mitochondrial tRNALeu(UUR) gene in a patient with a multisystem disord

130 process of charged and uncharged tRNALys and tRNALeu(UUR) has revealed that the separation of the two

131 tRNALeu(UUR), an etiologic hot spot for such diseases, h

132 ease in steady-state levels of mitochondrial tRNALeu(UUR), and a partial impairment of mitochondrial

133 n pattern was observed between the wild-type tRNALeu(UUR)and its counterpart carrying the A3243G muta

134 Complementary sequencing of tRNALeu(UUR)has allowed the localization of this modific

135 The expected tRNALeu-UUR gene was not revealed between COI and COII.

136 vivo and in vitro characteristics of type I tRNA(Leu) variants with their type II counterparts.A min

137 In this way, a group I intron located in tRNA(Leu), which has been used extensively for phylogene

138 anscript of the A14G pathogenic mutant of mt-tRNA(Leu), which is known to dimerize, and find that the

139 of tandem UAGA quadruplets by an engineered tRNA(Leu) with an eight-base anticodon loop, has been in

140 lation is facilitated by the misacylation of tRNA(Leu) with methionine by the methionyl-tRNA syntheta

141 allowing the enzyme to conditionally charge tRNA(Leu) with methionine.

142 The decoding properties of tRNA(Leu) with U at position 33.5 of its eight-membered