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Tài liệu Báo cáo khoa học: Isoprenoid biosynthesis via the methylerythritol phosphate pathway Mechanistic investigations of the 1-deoxy-D-xylulose 5-phosphate reductoisomerase ppt

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Tiêu đề Isoprenoid Biosynthesis Via The Methylerythritol Phosphate Pathway Mechanistic Investigations Of The 1-Deoxy-D-Xylulose 5-Phosphate Reductoisomerase
Tác giả Jean-François Hoeffler, Denis Tritsch, Catherine Grosdemange-Billiard, Michel Rohmer
Trường học Universite Louis Pasteur
Chuyên ngành Biochemistry
Thể loại báo cáo khoa học
Năm xuất bản 2002
Thành phố Strasbourg
Định dạng
Số trang 12
Dung lượng 385,7 KB

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This transformation is a two-step process involving a rearrangement of DXP into the putative inter-mediate 2-C-methyl-D-erythrose 4-phosphate followed by a NADPH-dependent reduction of t

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Isoprenoid biosynthesis via the methylerythritol phosphate pathway

Jean-Franc¸ois Hoeffler, Denis Tritsch, Catherine Grosdemange-Billiard and Michel Rohmer

Universite´ Louis Pasteur/CNRS, Institut Le Bel, Strasbourg, France

The 1-deoxyxylulose 5-phosphate reductoisomerase (DXR,

EC 1.1.1.267)catalyzes the conversion of 1-deoxy-D-xylulose

5-phosphate (DXP)into 2-C-methyl-D-erythritol

4-phos-phate (MEP) This transformation is a two-step process

involving a rearrangement of DXP into the putative

inter-mediate 2-C-methyl-D-erythrose 4-phosphate followed by a

NADPH-dependent reduction of the latter aldehyde By

using [1-13C]DXP as a substrate, the rearrangement of DXP

into [5-13C]2-C-methyl-D-erythrose 4-phosphate was shown

to be NADPH dependent, although it does not involve

a reduction step The putative aldehyde intermediate,

obtained by chemical synthesis, was converted into MEP by

the DXR in the presence of NADPH and into DXP in the presence of NADP+, indicating the reversibility of the reaction catalyzed by the DXR This reversibility was con-firmed by the conversion of MEP into DXP in the presence

of NADP+ The equilibrium was, however, largely dis-placed in favour of the formation of MEP The reduction step required the presence of a divalent cation such as Mg2+

or Mn2+ Keywords: isoprenoid, 2-C-methyl-D-erythritol 4-phosphate, 1-deoxyxylulose 5-phosphate reductoisomerase,

2-C-methyl-D-erythrose4-phosphate

Many bacteria, the unicellular green algae and the

chlo-roplasts from phototrophic organisms synthesize their

isoprenoids via the mevalonate-independent

2-C-methyl-D-erythritol phosphate 5 (MEP)pathway (Fig 1)[1–3]

The initial step of this route is the formation of

1-deoxy-D-xylulose 5-phosphate 3 (DXP)by the condensation of

(hydroxyethyl)thiamine resulting from pyruvate 1

decarb-oxylation on glyceraldehyde 3-phosphate 2 catalyzed by

the thiamine diphosphate-dependent DXP synthase (DXS)

[4–6] The second enzyme of this biosynthetic pathway,

the DXP reductoisomerase (DXR), catalyzes the

trans-formation of DXP into MEP 5 in two steps DXR is a

class B dehydrogenase [7,8] The corresponding gene has

now been cloned from Escherichia coli [9], Zymomonas

mobilis [10], Mentha x piperita [11], Arabidopsis thaliana

[12], Synechocystis sp [7], Streptomyces coelicolor [13] and

Pseudomonas aeruginosa[14] In the postulated mechanism

of the reaction catalyzed by the DXR, DXP 3 is first

rearranged into 2-C-methyl-erythrose-4-phosphate 4 [15],

which is subsequently reduced by NADPH to yield MEP

5 The latter aldehyde intermediate 4 was, however, never

characterized, neither directly, nor indirectly It is appar-ently not released from the enzyme active site during the catalysis [16,17] Three reactions are successively per-formed on the MEP framework, yielding three additional intermediates of the MEP pathway: conversion of MEP 5 into 4-diphosphocytidyl-2-C-methyl-D-erythritol 6 [18,19], phosphorylation of the C-2 hydroxyl group of 6 yielding 7 [20,21] and conversion of 7 into 2-C-methyl-D-erythritol 2,4-cyclodiphosphate 8 [22,23] The two last steps of the pathway were identified by a combination of genetic and biochemical methods An E coli strain engineered for the utilization of exogenous mevalonate accumulated tritium-labelled 2-C-methyl-D-erythritol 2,4-cyclodiphosphate upon incubation of [1-3H]-2-C-methyl-D-erythritol and after disruption of the gcpE gene, suggesting that

2-C-methyl-D-erythritol 2,4-cyclodiphosphate 8 is the substrate of the GcpE protein [24] Incubation of [3-14

C]-2-C-methyl-D-erythritol 2,4-cyclodiphosphate 8 with a crude cell-free system from an E coli strain overexpressing gcpE resulted

in the formation of 4-hydroxy-3-methylbut-2-enyl diphos-phate 9 [25,26] Deletion of the lytB gene in a similarly engineered E coli strain, resulted in the accumulation of the same diol diphosphate 9 [27] In addition, feeding with uniformly labelled [U-13C5]-1-deoxy-D-xylulose E coli strains overexpressing the gene of the xylulose kinase (responsible for the phosphorylation of free 1-deoxy-D -xylulose)as well as of all genes of the enzymes down-stream of gcpE or lytB resulted in the accumulation of uniformly labelled 4-hydroxy-3-methylbut-2-enyl diphos-phate 9 or of isopentenyl diphosdiphos-phate (IPP) 10 and dimethylallyl diphosphate 11, respectively [28,29] The nature of the cofactors required for the conversion of 2-C-methyl-D-erythritol 2,4-cyclodiphosphate 8 into IPP 10 and dimethylallyl diphosphate 11 is still a matter of investigation (Fig 1)

This paper focuses on the two intriguing consecutive steps catalyzed by the DXR from E coli Recently,

Correspondence to M Rohmer, Universite´ Louis Pasteur/CNRS,

Institut Le Bel, 4 rue Blaise Pascal, 67070 Strasbourg Cedex, France.

Fax: +33 3 90241345, E-mail: mirohmer@chimie.u-strasbg.fr

Abbreviations: AHIR, acetohydroxy acid isomeroreductase;

H 2 -NADPH, dihydro-NADPH; DXP, 1-deoxy- D -xylulose

5-phosphate; DXR, 1-deoxy- D -xylulose 5-phosphate

reducto-isomerase; DXS, 1-deoxy- D -xylulose 5-phosphate synthase;

H-DXR, His-tagged DXR; IPP, isopentenyl diphosphate;

MEP, 2-C-methyl- D -erythritol 4-phosphate.

Enzymes: acetohydroxy acid isomeroreductase (EC 1.1.1.86),

1-deoxy- D -xylulose 5-phosphate reductoisomerase (EC 1.1.1.267),

1-deoxy- D -xylulose 5-phosphate synthase (EC 4.1.3.7),

NADP-dependent alcohol dehydrogenase (EC 1.1.1.2).

(Received 12 June 2002, accepted 24 July 2002)

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experiments performed using different combinations of

substrate, inhibitor and NADPH have been reported [17]

They suggested that NADPH binds before the normal

substrate DXP 3 or an inhibitor such as fosmidomycin

and were consistent with an ordered mechanism DXR,

like all enzymes of the MEP pathway, is a potential target

for inhibitors acting as antibacterial or antiparasitic drugs

or as herbicides Fosmidomycin, an inhibitor of the latter

enzyme [30], has been shown to be active against the

parasite responsible for malaria [31] Knowledge of the

intimate mechanism of the reaction catalyzed by DXR is

required for the design of such inhibitors The following

questions were thus addressed: (1)What is the role of

methylerythrose phosphate in the conversion of DXP into

MEP? (2)Is the cofactor NADPH required for the sole

isomerization of DXP into methylerythrose phosphate? (3)

Is the reaction catalyzed by DXR reversible? (4)What

kind of mechanism is involved in the rearrangement

leading to the branched MEP carbon skeleton? An a-ketol

rearrangement or a retroaldolization/aldolization would

both afford the same reaction product

M A T E R I A L S A N D M E T H O D S

General methods

Unlabelled DXP was prepared either enzymatically [32],

or chemically (Hoeffler et al., unpublished results) [1-13C]

DXP and [2-13C]DXP were prepared enzymatically from

glyceraldehyde phosphate and from [3-13C]pyruvate

(Isotec, Miamisburg, OH, USA)or from [2-13C]pyruvate (Isotec, Saclay, France), respectively MEP was obtained either by chemical synthesis [33], or by enzymatic synthesis [9] [5-13C]MEP or [2-13C]MEP were prepared enzymati-cally from [1-13C]DXP or [2-13C]DXP, respectively [2-13C] Glycerol was purchased from Euriso-top (Saclay, France) Unless otherwise indicated, substrates, coen-zymes and encoen-zymes were from Sigma Dihydro-NADPH (H2-NADPH)was synthesized from NADPH by catalytic hydrogenation as previously described [34] The concentra-tion of H2-NADPH was determined from the absorbance at

263 nm (e¼ 18 500M )1Æcm)1) All enzymatic DXR assays were recorded on an Uvikon 933 spectrophotometer (Kontron Instruments)by following the variation of the NADPH concentration Glycoaldehyde 2-phosphate 12 was synthesized from glycerol 3-phosphate by treatment with sodium metaperiodate and purified by anion exchange chromatography.D-Erythrose 4-phosphate was purchased from Fluka

All nonaqueous reactions were run in dry solvents under

an argon atmosphere Dried and concentrated refers to the removal of residual amounts of water with anhydrous

Na2SO4followed by evaporation of the solvent on a rotary evaporator Flash chromatography [35] (Merck silica gel, 40–63 lm)and TLC (Merck 1.05553)were performed using the same solvent system TLC plates were developed by heating up to 100C after spraying with an ethanol solution

of p-anisaldehyde (2.5%), sulfuric acid (3.5%) and acetic acid (1.6%)or with an ethanol solution of phosphomolybdic acid reagent (10% w/v) NMR spectra were recorded on a

Fig 1 2-C-Methyl- D -erythritol 4-phosphate pathway for isoprenoid biosynthesis.

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Bruker AC200 spectrometer at 200 MHz for1H-NMR and

50 MHz for13C-NMR, on a Bruker AC300 at 300 MHz for

1H-NMR, at 75 MHz for13C-NMR and at 121.5 MHz for

31P-NMR and also on Bruker ARX 500 at 500 MHz

for1H-NMR, 125 MHz for13C-NMR and 202 MHz for

31P-NMR 31P NMR spectra were calibrated against an

external H3PO4standard (d¼ 0.00 p.p.m.) NMR

experi-ments were carried out in CDCl3or D2O using as internal

standard CHCl3(d¼ 7.26 p.p.m.), DHO (d ¼ 4.56 p.p.m.)

for 1H-NMR and 13CDCl3 (d¼ 77.03 p.p.m.)for

13C-NMR Negative mode electrospray mass spectrometry

was performed on a Hewlett Packard 1100MS spectrometer

using acetonitrile/water (1 : 1)as solvent GC-MS by

chemical ionization was performed on a Finnigan-MAT

TSQ 700 spectrometer with a 70 eV ionization energy using

i-butane as gas

Synthesis of 2-C-methyl-D-erythrose 4-phosphate 4

2-O-Benzyl-2-C-methyl-D-erythrose 4-dibenzylphosphate 13

[33] was hydrogenated (200 mg, 0.41 mmol)over 10%

Pd/C (20 mg)in methanol (10 mL)for 30 min at room

temperature and atmospheric pressure (Fig 2) The mixture

was filtered, and the filtrate diluted in water (15 mL),

concentrated in order to remove the methanol and treated

with a 1MNaOH solution to reach pH 7.5, yielding a

mixture of 2-C-methyl-D-erythrose 4-phosphate 4 and its

dimethylacetal This mixture was treated with an ion

exchange resin (Dowex 50 W-X4, H+ form)in water

(10 mL)at 37C for 2 h [36] After filtration, the pH of the

filtrate was adjusted to 7.5 with a 1MNaOH solution For

NMR and mass spectra analyses, an aliquot of the solution

was lyophilized to dryness to afford the sodium salt of

2-C-methyl-D-erythrose 4-phosphate 4 This aldehyde

can-not be stored pure or in concentrated solution and was

accordingly kept in water solution The aldehyde

concen-tration was determined using the DXR assay 1H-NMR

(500 MHz, D2O, 1 : 2 mixture of the aldehyde and of the

hydrate): d¼ 0.93 (2H, s, CH3, hydrate) ; 1.10 (1H, s, CH3,

aldehyde) ; 3.62 (2H, m, 2· 4-H) ; 3.76 (1H, m, 3-H) ; 4.74

(0.7H, s, 1-H, hydrate); 9.41 (0.3H, s, 1-H, aldehyde).13

C-NMR (125 MHz, D2O): d¼ 16.34 (CH3) ; 18.25 (CH3);

63.65 (d, J¼ 4.8 Hz, C-4); 65.12 (d, J ¼ 4.8 Hz, C-4);

73.78 (d, J¼ 7.2 Hz, C-3); 74.11 (d, J ¼ 7.2 Hz, C-3);

75.27 (C-2); 79.83 (C-2); 91.78 (C-1, hydrate); 205.72 (C-1,

aldehyde) 31P-NMR (202 MHz, D2O): d¼ 5.2 and 5.0

Electrospray MS: m/z¼ 213 (M-H, molecular ion of the

2-C-methyl-D-erythrose 4-phosphate mono-anion)

Synthesis of (3S )-3-hydroxypentan-2-one

5-phosphate 14

(S)-2-Hydroxy-c-butyrolactone

tert-butyldimethylsilyl-ether 16 To a solution of (S)-2-hydroxy-c-butyrolactone

15 (1.1 g, 10.3 mmol, 1 equivalent)and 2,6-lutidine

(3.0 mL, 25.8 mmol, 2.5 equivalents)in dichloromethane

(20 mL)at)5 C, was added tert-butyldimethylsilyl triflate (3.6 mL, 15.5 mmol, 1.5 equivalents) After 1 h at)5 C, the reaction was quenched with water (15 mL), diluted with diethyl ether (45 mL), washed with 1MHCl (15 mL), 5% aqueous NaHCO3(15 mL)and brine (15 mL) The organic layer was dried and concentrated The residue was purified

by flash chromatography to afford 16 as colourless oil (2.2 g, 97%, Rf¼ 0.48, hexane/ethyl acetate, 80 : 20).1 H-NMR (300 MHz, CDCl3): d¼ 0.14 (3H, s); 0.16 (3H, s); 0.90 (9H, s); 2.21 (1H, dddd, J¼ 12.6 Hz, J ¼ 9.1 Hz,

J¼ 9.1 Hz, J¼ 8.6 Hz, 3-Ha); 2.46 (1H, dddd,

J¼ 12.6 Hz, J ¼ 9.1 Hz, J ¼ 6.4 Hz, J ¼ 3.4 Hz, 3-Hb); 4.18 (1H, ddd, J¼ 9.1 Hz, J ¼ 9.1 Hz, J ¼ 6.4 Hz; 4-Ha); 4.38 (2H, m, 4-Hband 2-H).13C-NMR (75 MHz, CDCl3):

d¼)4.90 (CH3); 17.86 (quaternary C); 25.57 (CH3); 38.12 (C-3); 68.08 (C-2); 76.08 (C-4); 175.63 (C-1)

(3S)-3-(tert-Butyldimethylsiloxy)pentan-2-one 5-dibenzyl-phosphate 17 Methyl lithium (1.6M solution in diethyl ether, 5.9 mL, 9.5 mmol, 1.1 equivalents)was added dropwise to a stirred solution cooled to )78 C of silyl ether 16 (1.9 g, 8.5 mmol, 1 equivalent)in tetrahydofuran (40 mL) After stirring at)78 C for 3 h, the reaction was quenched by addition of water (20 mL)and diluted with diethyl ether (40 mL) The organic layer was separated, and the aqueous layer was extracted with diethyl ether (3· 40 mL) The combined organic extracts were dried and concentrated in vacuo to give crude (3S)-3-(tert-butyldi-methylsiloxy)-2-methyltetrahydrofuran-2-ol (1.8 g, 90%) as

a colourless oil corresponding to the mixture of diastereo-mers at C-2, which was used for the next step without further purification

Dibenzylphosphorochloridate [37] (1.6 g, 5.4 mmol, 1.5 equivalents)was added under stirring to a solution of (3S)-3-(tert-butyldimethylsiloxy)-2-methyltetrahydrofu-ran-2-ol (1.0 g, 4.3 mmol, 1 equivalent)in pyridine (20 mL)

at 0C The reaction was stirred at room temperature for

2 h After quenching by addition of water (2 mL), the solvents were removed under vacuum by azeotropic distil-lation with toluene Flash chromatography gave 17 as colourless oil (340 mg, 16%, Rf¼ 0.35, hexane/ethyl acet-ate, 60 : 40).1H-NMR (300 MHz, CDCl3): d¼ 0.03 (3H, s) ; 0.05 (3H, s) ; 0.90 (9H, s) ; 1.91 (1H, m, 4-Ha) ; 1.92 (1H, m, 4-Hb) ; 2.13 (3H, s, 1-H) ; 4.12 (3H, m, 3-H, 5-H) ; 5.02 (4H,

m, CH2Ph); 7.28–7.35 (10H, m) 13C-NMR (75 MHz, CDCl3): d¼)5.18 (CH3);)4.99 (CH3); 18.03 (quaternary C); 25.30 (C-1); 25.66 (3· CH3) ; 35.04 (d, J¼ 6.6 Hz, C-4); 63.41 (d, J¼ 4.9 Hz, C-5); 69.28 (d, J ¼ 4.9 Hz,

2· CH2); 75.06 (C-3); 127.94, 128.53, 135.74 and 135.90 (aromatic C); 210.97 (C-2).31P-NMR (121.5 MHz, CDCl3):

d¼)3.46

(3S)-3-Hydroxypentan-2-one 5-dibenzylphosphate 18 To

a stirred solution of the silyl ether 17 (200 mg, 0.41 mmol, 1 equivalent)in tetrahydofuran (5 mL)was added tetrabutyl-ammonium fluoride (160 mg, 0.49 mmol, 1.2 equivalents)

Fig 2 Synthesis of 2-C-methyl- D -erythrose 4-phosphate 4 (i)H 2 , Pd/C in methanol; (ii)DOWEX 50 W-X4, H + , in water at

40 C.

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The mixture was stirred at room temperature for 30 min

and evaporated to dryness, and the residue was purified by

flash chromatography to afford 18 as a colourless oil

(135 mg, 88%, Rf¼ 0.41, ethyl acetate/hexane, 90 : 10)

1H-NMR (300 MHz, CDCl3): d¼ 1.77 (1H, m, 4-Ha) ; 2.14

(1H, m, 4-Hb) ; 2.15 (3H, s, 1-H) ; 3.74 (1H, s, OH) ; 4.17 (3H,

m, 3-H, 5-H); 4.97 (1H, d, J¼ 11.8 Hz, CH2Ph), 5.01 (1H,

d, J¼ 11.6 Hz, CH2Ph) , 5.04 (1H, d, J¼ 11.8 Hz,

CH2Ph), 5.08 (1H, d, J¼ 11.6 Hz, CH2Ph); 7.34 (10H,

m).13C-NMR (75 MHz, CDCl3): d¼ 25.11 (C-1); 33.79 (d,

J¼ 6.6 Hz, C-4); 63.56 (d, J ¼ 6.6 Hz, C-5); 69.38 (d,

J¼ 4.9 Hz, 2 · CH2); 73.20 (C-3); 127.97, 128.56, 135.64

and 135.77 (aromatic C); 209.40 (C-2) 31P-NMR

(121.5 MHz, CDCl3): d¼)3.35

(3S)-3-Hydroxypentan-2-one 5-phosphate 14

(3S)-3-Hydroxypentan-2-one 5-dibenzylphosphate 18 (35 mg,

0.01 mmol)was hydrogenated over 10% Pd/C (4 mg)in

ethanol (2 mL)for 2 h at room temperature and

atmo-spheric pressure The mixture was filtered, and the filtrate

concentrated The residue was dissolved in water (1 mL),

and the pH adjusted to 7.5 with a 1MNaOH solution The

mixture was lyophilized to give the sodium salt of 18

(20 mg, 98%) 1H-NMR (200 MHz, D2O): d¼ 1.60

(1H, m, 4-Ha) ; 1.93 (1H, m, 4-Hb) ; 2.01 (3H, s, 1-H) ; 3.69

(2H, ddd, J4a,5¼ J4b,5¼ J5,P¼ 6.2 Hz, 5-H); 4.23 (1H,

dd, J¼ 8.9 Hz, J ¼ 3.7 Hz, 3-H) 13C-NMR (75 MHz,

D2O): d¼ 25.30 (C-1); 33.45 (C-4); 60.53 (C-5); 73.95 (C-3);

215.15 (C-2).31P-NMR (121.5 MHz, D2O): d¼ 4.25

Synthesis of (4S)-4-hydroxypentan-2-one 5-phosphate 19

(R)-(tert-Butyldiphenylsiloxymethyl)oxirane 21 To a

stirred solution of (R)-glycidol 20 (2.7 g, 36.0 mmol, 1

equivalent)and imidazole (3.0 g, 44 mmol, 1.2 equivalents)

in dry dichloromethane (30 mL)was added at 0C

tert-butylchlorodiphenylsilane (10.5 mL, 40 mmol, 1.1

equiva-lents) After 1 h at room temperature, the reaction mixture

was poured into water (30 mL), and the organic layer was

separated The aqueous layer was extracted three times with

dichloromethane (250 mL) The combined extracts were

dried, filtered, concentrated and purified by flash

chroma-tography to give 21 as a colourless oil (10.4 g, 92%,

Rf¼ 0.21, hexane/ethyl acetate, 95 : 5) 1H-NMR

(200 MHz, CDCl3): d¼ 1.09 (9H, s); 2.63 (1H, dd,

J¼ 5.2 Hz, J ¼ 2.5 Hz, 3-Ha) ; 2.76 (1H, dd, J¼ 5.2 Hz,

J¼ 4.2 Hz, 3-Hb) ; 3.15 (1H, m, 2-H) ; 3.73 (1H, dd,

J¼ 11.8 Hz, J¼ 4.7 Hz, 1-Ha) ; 3.88 (1H, dd,

J¼ 11.8 Hz, J ¼ 3.2 Hz, 1-Hb); 7.36–7.49 (6H, m); 7.69–

7.75 (4H, m) 13C-NMR (50 MHz, CDCl3): d¼ 19.27

(quaternary C); 26.78 (3· CH3); 44.45 (C-3); 52.25 (C-2);

64.34 (C-1); 127.74, 129.77, 133.31 and 135.64 (aromatic C)

(2S)-4-Methylpent-4-ene-1,2-diol 22 Into a flask

equip-ped with a mechanical stirrer, an addition funnel and

containing anhydrous copper iodide (110 mg, 0.58 mmol,

0.1 equivalents)was added tetrahydofuran (20 mL) After

cooling at)30 C, isoproprenylmagnesium bromide (0.5M

in tetrahydofuran, 58 mL, 28.8 mmol, 5 equivalents)was

drop wise added The temperature never exceeded)30 C

After stirring for 30 min at)30 C

(R)-(tert-butyldiphenyl-siloxymethyl)oxirane 21 (1.8 g, 5.8 mmol, 1 equivalent)in

tetrahydofuran (10 mL)was slowly added, maintaining the

temperature at)30 C After stirring for 1 h at )30 C, the reaction was quenched by addition of a saturated NH4Cl solution and warmed up to room temperature The reaction was filtered through a sintered glass funnel containing celite and the tetrahydofuran was removed under reduce pressure The filtrate was diluted with diethyl ether (50 mL)and the organic layer was washed with water (20 mL)and brine (20 mL), dried and concentrated in vacuo Purification by flash chromatography afforded (2S)-1-tert-butyldiphenyl-siloxy-2-hydroxypent-4-ene as a colourless oil (1.9 g, 98%,

Rf¼ 0.28, ethyl acetate/hexane, 10 : 90)

To a stirred solution of the former silyl ether (1.9 g, 5.7 mmol, 1 equivalent)in tetrahydofuran (50 mL)was added tetrabutylammonium fluoride (2.0 g, 6.2 mmol, 1.1 equivalents) The mixture was stirred at room temperature for 3 h and evaporated to dryness The residue was purified

by flash chromatography to afford 22 as colourless oil (610 mg, 91%, Rf¼ 0.33, ethyl acetate) 1H-NMR (200 MHz, CDCl3): d¼ 1.74 (3H, s, 4-CH3) ; 2.14 (2H, m,

2· 3-H); 3.17 (2H, -OH); 3.42 (1H, dd, J ¼ 11.3 Hz,

J¼ 7.1 Hz, 1-Ha) ; 3.63 (1H, dd, J¼ 11.3 Hz, J ¼ 3.0 Hz, 1-Hb) ; 3.84 (1H, m) ; 4.77 (1H, m, 2-H) ; 4.83 (1H, m, 4-H)

13C NMR (50 MHz, CDCl3): d¼ 22.42 (4-CH3) ; 41.69 (C-3); 66.44 (C-1); 69.69 (C-2); 113.35 (C-3); 141.93 (quaternary C-4)

(2S)-2-Hydroxypent-4-en-1-ol dibenzylphosphate 23 Dibenzylphosphorochloridate [36] (1.6 g, 5.4 mmol, 1.2 equivalents)was added under stirring to a solution of (2S)-4-methylpent-4-ene-1,2-diol 22 (520 mg, 4.5 mmol, 1 equi-valent)in pyridine (10 mL)at)40 C during a period of

20 min The reaction was stirred at)40 C for 2 h, quenched

by addition of water (2 mL), and the solvents were removed under vacuum by azeotropic distillation with toluene Flash chromatography gave 23 as a colourless oil (920 mg, 54%) (Rf¼ 0.24, ethyl acetate/hexane, 65 : 35) 1H-NMR (200 MHz, CDCl3): d¼ 1.72 (3H, s, 4-CH3) ; 2.13 (2H, m, 3-H) ; 2.69 (1H, -OH) ; 3.93 (3H, m, 1-H, 2-H) ; 4.75 (1H, m, 5-Ha) ; 4.83 (1H, m, 5-Hb) ; 5.07 (4H, m, 2· -CH2Ph); 7.35 (10H, m) 13C-NMR (50 MHz, CDCl3): d¼ 22.39 (4-CH3); 41.19 (C-3); 68.09 (d, J¼ 6.1 Hz, C-2); 69.50 (d,

J¼ 5.1 Hz, 2 · CH2); 71.49 (d, J¼ 5.8 Hz, C-1); 113.64 (C-5); 127.97, 128.58, 135.60 and 135.74 (aromatic C); 141.33 (C-4).31P-NMR (121.5 MHz, CDCl3): d¼)2.55

(4S)-4-Hydroxypentan-2-one 5-dibenzylphosphate 24 To

a biphasic solution of (2S)-2-hydroxypent-4-en-1-ol diben-zylphosphate 23 (110 mg, 0.29 mmol, 1 equivalent)and NaIO4(263 mg, 1.2 mmol, 4.2 equivalents)in a mixture of acetonitrile/carbon tertrachloride/H2O (2 : 2 : 3, 7 mL) was added ruthenium trichloride (7 mg, 0.03 mmol, 0.1 equivalents)[38] After vigorous stirring for 15 min at room temperature, water (10 mL)and dichloromethane (10 mL) were added, and the two phases were separated The upper aqueous phase was extracted four times with dichlorome-thane (4· 25 mL) The combined organic extracts were dried and concentrated The residue was purified by flash chromatography to afford 24 as a colourless oil (88 mg, 80%, Rf¼ 0.41, ethyl acetate/hexane, 80 : 20).1H-NMR (200 MHz, CDCl3): d¼ 2.13 (3H, s, 1-H); 2.55 (2H, m, 3-H) ; 3.40 (1H, broad s, -OH) ; 3.94 (2H, m, 5-H) ; 4.18 (1H,

m, 4-H); 4.99 (1H, d, J¼ 11.6 Hz, CH2Ph) , 5.03 (1H, d,

J¼ 11.8 Hz, CHPh) , 5.05 (1H, d, J¼ 11.6 Hz, CHPh),

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5.09 (1H, d, J¼ 11.8 Hz, CH2Ph) ; 7.34 (10H, m) ; 13

C-NMR (50 MHz, CDCl3): d¼ 30.70 (C-1); 45.73 (C-3);

66.45 (d, J¼ 6.5 Hz, C-4); 69.55 (d, J ¼ 5.0 Hz, 2 · CH2);

70.41 (d, J¼ 6.2 Hz, C-5); 127.84, 128.01, 128.61, 135.57

and 135.68 (aromatic C); 207.82 (C-2) 31P-NMR

(121.5 MHz, CDCl3): d¼)2.73

(4S)-4-Hydroxypentan-2-one 5-phosphate 19

(4S)-4-Hydroxypentan-2-one 5-dibenzylphosphate 24 (55 mg,

0.15 mmol)was hydrogenated over 10% Pd/C (6 mg)in

ethanol (2 mL)for 2 h at room temperature and

atmo-spheric pressure The mixture was filtered, and the filtrate

and evaporated to dryness The residue was dissolved in

water (1 mL), and the pH adjusted to 7.5 with a 1MNaOH

solution The mixture was lyophilized to give the sodium

salt of 19 (35 mg, 99%) 1H-NMR (500 MHz, D2O):

d¼ 2.06 (3H, s); 2.55 (1H, dd, J ¼ 16.8 Hz, J ¼ 8.9 Hz,

3-Ha); 2.61 (1H, dd, J¼ 16.8 Hz, J ¼ 4.1 Hz, 3-Hb) ; 3.51

(1H, m, 5-Ha) ; 3.57 (1H, m, 5-Hb) ; 4.07 (1H, m, 4-H)

13C-NMR (75 MHz, D2O): d¼ 29.66 (CH3); 45.64 (CH2);

46.02 (d, J¼ 19.4 Hz, CH2); 66.95 (d, J¼ 12.1 Hz, CH);

213.59 (CO).31P-NMR (121.5 MHz, D2O): d¼ 4.10

Purification of His-tagged deoxyxylulose 5-phosphate

reductoisomerase

The coding region for the dxr gene from E coli was cloned

into the pRSET vector (Invitrogen)between the BglII and

HindIII restriction sites This vector contains a DNA

sequence encoding for six histidine residues Plasmid

pRSET-DXR was introduced into E coli strain

BL21(DE3)pLysE After induction of enzyme expression

by addition of IPTG (0.4 mM)at mid-log phase (OD600,

0.7)at 37C, the culture was incubated for additional 3 h

at the same temperature Cells (from 3· 500 mL cultures)

were harvested by centrifugation and washed with water

They were resuspended in a 50 mM Tris/HCl, 250 mM

NaCl, 5 mM2-mercaptoethanol pH 8 buffer (10 mL)and

disrupted by sonication (8· 30 s pulses at 40-W output,

duty cycle 50%)with cooling in an ice bath The cell-free

system was centrifuged at 18 000 g for 30 min at 4C in a

Sigma 3K30 centrifuge The crude cell extract was applied

on a column of Ni-nitrilotriacetic acid agarose (Qiagen,

0.8· 2 cm)equilibrated with the same buffer The column

was first washed with the same buffer, and then with the

buffer containing imidazole (5 mM) The enzyme was eluted

by applying a linear gradient of imidazole (5–120 mM)in the

same buffer (2· 30 mL) Fractions containing His-tagged

DXR (H-DXR)were pooled and concentrated by

ultrafil-tration on a Centricon 30 unit (Millipore) The enzymatic

solution was dialysed against 50 mM Tris/HCl, 100 mM

NaCl, dithiothreitol (2 mM), pH 8 buffer by several

concentration/dilution steps using Centricon 30 units The

concentration of protein was determined using the method

of Bradford [39]

H-DXR enzymatic activity

The enzymatic activity was determined routinely at 37C in

a 50 mM Tris/HCl, 1 mM MnCl2, 2 mM dithiothreitol

pH 7.5 buffer containing 0.15 mM NADPH and 0.5 mM

DXP H-DXR was added to have an absorbance decrease

of about 0.1 min)1 The rate was measured by following the

decrease of the absorbance at 340 nm due to the formation

of NADP+from NADPH

To compare the kinetic parameters (Kmand V)of DXP 3 and 2-C-methyl-D-erythrose 4-phosphate 4, assays were carried out in a 50 mMtriethanolamine/HCl, 1 mMMnCl2 (or 3 mMMgCl2) , 2 mMdithiothreitol, pH 7.7, at a fixed concentration of NADPH (0.15 mM) The concentration of DXP varied from 31 to 310 lM, while the concentration of 2-C-methyl-D-erythrose 4-phosphate 4 varied from 93 to

620 lM The concentrations of the stock solutions of substrate were determined enzymatically using the H-DXR The enzyme (4.3 lg) was added lastly in order

to initiate the reaction

D-Erythrose 4-phosphate was tested as the substrate of H-DXR at concentrations up to 1 mMand H-DXR con-centrations up to 13 lgÆmL)1 The influence ofD-erythrose 4-phosphate (1 mM)on the activity of H-DXR was checked with DXP (96 lM)as the substrate The kinetic parameters (Kmand V)in the reverse reaction were determined at a fixed concentration of NADP+(0.15 mM) The assays were performed at 37C in a 50 mM Tris/HCl, 1 mM MnCl2,

2 mM dithiothreitol pH 7.5 buffer The concentration of MEP 5 varied from 75 to 375 lM The concentration of the stock solution of MEP 5 was determined by titration of the phosphate according to the method of Leloir & Cardini [40] The enzyme (4 lg)was added lastly in order to initiate the reaction

Reduction of 2-C-methyl-D-erythrose 4-phosphate 4 to 2-C-methyl-D-erythritol 4-phosphate 5 by H-DXR

To show that the reduction of 2-C-methyl-D-erythrose 4-phosphate 4 really gives 2-C-methyl-D-erythritol 4-phos-phate 5, the aldehyde 4 (10 mg)was treated overnight with DXR (1.2 mg)in the presence of NADPH (0.5 mM)in a triethanolamine/HCl, 1 mM MnCl2, 2 mM dithiothreitol

pH 7.7 buffer at 37C (4 mL final volume) NADPH was regenerated using the isopropanol/alcohol dehydrogenase system from Thermoanaerobium brockii [41] After hydro-lysis of the phosphate esters with alkaline phosphatase (bovine intestinal mucosa, Sigma, 0.5 mg)for 4 h at 37C, the medium was lyophilized, and the residue was acetylated overnight with a mixture of acetic anhydride and pyridine (0.2 mL, 1 : 1 v/v) After evaporation of the reagents, the residue was analysed by TLC Methylerythritol triacetate was isolated and identified by1H-NMR (Rf¼ 0.41, ethyl acetate/hexane, 50 : 50) 1H NMR (200 MHz, CDCl3):

d¼ 1.24 (3H, s, CH3) ; 2.04 (3H, s, CH3COO); 2.09 (3H, s, CH3COO) ; 2.11 (3H, s, CH3COO) ; 2.49 (1H, s, OH); 3.89 (1H, d, J1a,1b¼ 11.6 Hz, 1 Ha) ; 4.15 (1H, d,

J1a,1b¼ 11.6 Hz, 1-Hb); 4.16 (1H, dd, J4a,4b¼ 12.1 Hz,

J3,4a¼ 8.1 Hz, 4-Ha) ; 4.56 (1H, dd, J4a,4b¼ 12.1 Hz,

J3,4b¼ 2.7 Hz, 4-Hb) ; 5.18 (1H, dd, J3,4a¼ 8.1 Hz,

J3,4b¼ 2.7 Hz, 3-H); 13C-NMR (50 MHz, CDCl3):

d¼ 19.80 (CH3); 20.62 (CH3); 20.71 (CH3); 62.67 (CH2); 68.02 (CH2); 71.95 (quaternary C, C-2); 72.54 (CH, C-3); 169.99 (CO); 170.85 (2· CO)

Isomerization of 2-C-methyl-D-erythrose 4-phosphate 4 into DXP 3 by H-DXR

2-C-Methyl-D-erythrose 4-phosphate 4 (10 mg)was treated overnight with H-DXR (1.2 mg)in the presence of NADP+

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(0.5 mM)in a 5 mM triethanolamine/HCl, 1 mM MnCl2,

2 mM dithiothreitol pH 7.7 buffer at 37C (4 mL, final

volume) The carbohydrate phosphates were identified after

dephosphorylation and acetylation by the usual method

The acetylated crude residue was analysed by GCMS, and

the analytical data compared with those of a synthetic

reference of deoxyxylulose triacetate

Reversibility of the formation of DXP 3 from MEP 5

by H-DXR

MEP 5 (10 mg)was treated overnight with H-DXR

(1.2 mg)in the presence of NADP+(0.5 mM)in a 5 mM

triethanolamine/HCl, 3 mM MgCl2, 2 mM dithiothreitol

pH 7.7 buffer at 37C (4 mL final volume) NADP+was

regenerated using the acetone/alcohol dehydrogenase from

Thermoanaerobium brockii [40] After dephosphorylation

using an alkaline phosphatase, the mixture was lyophilized

and acetylated Deoxyxylulose triacetate was isolated by

TLC and identified by1H-NMR [6]

In other experiments, [5-13C]MEP or [2-13C]MEP (8 mM)

was treated overnight with H-DXR (1.1 mg)in the presence

of NADP+(3 mM)in a 50 mMNH4HCO3, 3 mMMgCl2

and 2 mM dithiothreitol buffer at 37C (0.5 mL, final

volume) NADP+ was regenerated using the acetone/

alcohol dehydrogenase from Thermoanaerobium brockii

The reaction was directly performed in a NMR tube and

monitored by13C-NMR (50 MHz)using [2-13C]glycerol as

internal reference (d¼ 71.3 p.p.m.)

Determination of the apparent equilibrium constant

of the DXR reaction

The assays were performed in a 50 mM Tris/HCl pH 7.5

buffer containing 1 mMMnCl2and 2 mMdithiothreitol at

37C H-DXR (12 lg)was incubated in the presence of

0.116 mM MEP and NADP+at different concentrations

(0.088–0.352 mM)or at fixed concentration of NADP+

(0.176 mM)with MEP at different concentrations (0.058–

1.16 mM) The reactions were followed at 340 nm until the

absorbance reached a plateau The concentration of

produced NADPH was determined from the absorbance

(e¼ 6220M )1cm)1, kmax¼ 340 nm) The influence of

DXP 3 (0.51–0.153 mM final concentration)or NADPH

(6.9–20.4 lMfinal concentration)on the concentration of

NADPH formed during the incubation of the enzyme with

NADP+ (0.176 mM)and MEP 5 (0.116 mM)was

deter-mined by the same UV absorption method

13

C-NMR study of the rearrangement reaction of H-DXR

The reactions were directly performed in NMR tubes

(5 mm diameter)in a 50 mMNH4HCO3buffer containing

3 mM MgCl2 and 2 mM dithiothreitol at 37C The

[1-13C]DXP concentration was 12.5 mM H-DXR (100 lg)

was added to initiate the enzymatic reaction The influence

of 0.5 mM NADP+, 0.5 mMATP-ribose and 0.5 mMH2

-NADPH was tested The activity of the enzyme was

demonstrated by adding NADPH (0.3 mM)and its

regen-erating system, isopropanol/alcohol dehydrogenase from

Thermoanaerobium brockii.The reaction medium (620 lL

final volume)contained D2O (100 lL)and [2-13C]glycerol

(1 mg)as an internal reference (d¼ 71.3 p.p.m.) 13

C-NMR spectra were recorded after 4 h incubation The13C chemical shifts of the possible metabolites resulting from the retro-aldol cleavage of DXP are hydroxyacetone 25 and glycoaldehyde phosphate 12 The 13C shifts of hydroxy-acetone 25 (0.7M)and glycoaldehyde phosphate 12 (0.3M) were determined in the same medium Hydroxyacetone 25:

13C-NMR (50 MHz, 50 mM NH4HCO3): d¼ 24.0 (C-3,

CH3), 66.7 (C-1, CH2OH), 211.0 (C-2, CO) Glycoaldehyde 2-phosphate 12:13C-NMR (50 MHz, 50 mMNH4HCO3):

d¼ 66.0 (d, C-2, J ¼ 3.3 Hz, CH2OP) , 88.4 [d, C-1,

J¼ 6.6 Hz, CH(OH)2]

Kinetic studies of (3S )-3-hydroxypentan-2-one 5-phosphate 14 and (4S )-4-hydroxypentan-2-one 5-phosphate 19 with H-DXR

H-DXR was incubated with (3R)-3-hydroxypentan-2-one 5-phosphate 14 (0.5 mM)or (4S)-4-hydroxypentan-2-one 5-phosphate 19 (0.5 mM)and NADPH (0.15 mM)in a

50 mMTris/HCl, 1 mMMnCl2, 2 mMdithiothreitol pH 7.5 buffer The reaction was followed at 340 nm to observe the formation of NADP+ The inhibition of the enzymatic activity of DXR by (3S)-3-hydroxypentan-2-one 5-phos-phate 14 and (4S)-4-hydroxypentan-2-one 5-phos5-phos-phate 19 was studied by determining the influence of the two compounds [0.8–2.4 mM for (3S)-3-hydroxypentan-2-one 5-phosphate 14, 0.022–0.110 mM for (4S)-4-hydroxypen-tan-2-one 5-phosphate 19] on the enzymatic rate The concentration of DXP 3 varied between 75 and 510 lM DXR (4 lg)was added last to initiate the reaction

R E S U L T S A N D D I S C U S S I O N 2-C-Methyl-D-erythrose 4-phosphate 4 as intermediate

in the DXR-catalyzed reaction 2-C-Methyl-D-erythrose 4-phosphate 4 was postulated as an intermediate in the first step of the reaction catalyzed by DXR It results from an a-ketol rearrangement of DXP and, after reduction, yields MEP 5 From the analogy of the latter reaction sequence with that involved in the formation

of the carbon skeleton of amino acids with a branched side-chains, aldehyde 4 was expected to be only a transient intermediate not released from the enzyme active site, much like 3-hydroxy-3-methyl-2-oxobutyrate resulting from rear-rangement of 2-acetolactate by acetohydroxy acid isomero-reductase (AHIR; EC 1.1.1.86)in the biosynthesis of branched-chain amino acids [42]

For testing its possible role, unlabelled

2-C-methyl-D-erythrose 4-phosphate 4 was synthesized by an adaptation

of our former synthesis of MEP 5 (Fig 2)[33] 2-O-Benzyl-2-C-methyl-D-erythrose 4-dibenzylphosphate 13 was obtained as previously described in six steps from commer-cially available 1,2-O-isopropylidene-a-D-xylofuranose 26 Hydrogenolysis of the benzyl groups in methanol yielded the 2-C-methyl-D-erythrose 4-phosphate dimethylacetal, which upon hydrolysis with an acidic Dowex resin afforded 2-C-methyl-D-erythrose 4-phosphate 4 The puta-tive intermediate was tested as substrate of H-DXR assays and was utilized as reference material for the detection of this aldehyde in the DXR enzyme tests

Preliminary kinetic studies were performed in order to determine the optimal conditions for the DXR-catalyzed

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enzymatic reaction Assays were performed in a

triethanol-amine/HCl buffer instead of the usual Tris/HCl buffer [9]

because Tris is known to react with aldehydes [43] DXR

requires divalent cations such as Mn2+, Co2+or Mg2+for

its catalytic activity [9,16] For our enzyme system,

maxi-mal rates were found for 1 mM Mn2+and 3 mM Mg2+

concentrations, indicating that the enzyme has more affinity

for Mn2+cations than for Mg2+cations The usual

concen-tration of NADPH is 0.3 mM [9] However, a 0.15 mM

concentration was chosen for NADPH because higher

concentrations resulted in lower rates When

2-C-methyl-D-erythrose 4-phosphate 4 was incubated with H-DXR in the

presence of NADPH, consumption of the cofactor was

shown by the decrease in the absorption at 340 nm,

suggesting that the enzyme reduced the aldehyde 4 For the

identification of MEP, the expected reaction product, the

reaction mixture obtained after the reduction of

2-C-methyl-D-erythrose 4-phosphate 4 with NADPH was

dephosphory-lated using an alkaline phosphatase and freeze-dried The

crude residue was acetylated, and TLC allowed the isolation

of methylerythritol triacetate, which was identified by NMR

by comparison with a synthetic reference sample [44] This

confirmed that 2-C-methyl-D-erythrose 4-phosphate 4 was

effectively reduced to MEP 5 by H-DXR in the presence of

NADPH Under these reaction conditions, deoxyxylulose

triacetate could not be isolated after TLC The reverse

reaction, isomerization of 2-C-methyl-D-erythrose

4-phos-phate 4 into DXP 3 did not take place significantly in the

presence of NADPH The formation of DXP 3 from

methylerythrose 4 by H-DXR was, however, observed by

incubating the aldehyde in the presence of NADP+ As

methylerythrose and DX, as well as the diacetate of

methylerythrose and the triacetate of DX, have the same

Rf, the presence of DX triacetate was checked by GC and

GCMS The retention times of the detected products were

compared with those of synthetic 1-deoxy-D-xylulose

triace-tate In contrast with the almost quantitative formation of

MEP 5 from aldehyde 4, the formation of DXP 3 was very

low ( 7% yield as shown by GC detection of DX

triacetate) Furthermore, GC-MS (chemical ionization with

i-butane)of the acetylated crude reaction mixture showed a

peak with the retention time of deoxyxylulose triacetate and

characterized by a pseudo molecular ion at (M + H)+

(m/z¼ 261)and by an ion corresponding to the loss of acetic

acid from the deoxyxylulose triacetate (m/z¼ 201) This

confirmed the presence of small amounts of

1-deoxy-D-xylulose triacetate

The Kmvalues measured for methylerythrose phosphate

(294 lMin the presence of 1 mMMnCl2and 158 lMin the

presence of 3 mM MgCl2)for the E coli H-DXR were significantly higher than those found for DXP (73 lMfor

1 mMMnCl2and 97 lMfor MgCl2) and also depended on the nature of the divalent cation Despite several reprodu-cible measurements, for unknown reasons the Kmvalues we determined for DXP 3 in the presence of MnCl2(1 mM) differed significantly from those found in the literature for the same enzyme from E coli (Km¼ 250 lM)[45] or from

Z mobilis(Km¼ 300 lM)[10] However, the Kmvalues for DXP (Km¼ 97 lM)when MgCl2was used were similar to those published for the purified E coli enzyme wild-type (Km¼ 99 lM)[45] and for S coelicolor DXP reductoiso-merase (Km¼ 60 lM)[13] The results obtained with an enzyme bearing a His-tag, like most those of the literature concerning His-tagged proteins, may not be directly exten-ded to the native enzyme As the amino-terminal part of DXR is involved in the binding of the cofactor [46], the His-tag, which is localized at the N-terminal end, may influence the enzymatic activity of H-DXR

As for AHIR [42], the reduction step required the presence of a divalent metal cation, which may be involved

in the binding of the aldehyde and/or the cofactor to the enzyme Whether such a metal cation is also required for the isomerization remains to be shown With DXP 3 as a substrate, no significant difference of the kinetic constants was observed at optimal concentrations of Mn2+(1 mM) and Mg2+(3 mM)(Table 1) The influence of the nature of the divalent cation was, however, more pronounced for methylerythrose phosphate 4 In the presence of Mn2+, the binding of the aldehyde 4 was less efficient than in the presence of Mg2+ Indeed, although the chemical and biochemical behaviour of Mn2+resembles that of Mg2+,

Mn2+(0.75 A˚)is somewhat larger than Mg2+(0.65 A˚) In addition, Mn2+ binds more readily to a site containing nitrogen in addition to oxygen than Mg2+, which prefers oxygen only [47] These peculiar properties of the two metal cations may influence the binding of methylerythrose phosphate 4 to the active site, and thus explain the different

Kmvalues for the aldehyde 4 The higher rate of reduction observed with Mn2+ could be due to a faster release of MEP, the reaction product

Interestingly, the methyl group of methylerythrose phos-phate 4 is essential for the binding to the enzyme In our reaction conditions,D-erythrose 4-phosphate was neither a substrate, nor an inhibitor of the H-DXR (data not shown)

It was recently reported thatD-erythrose 4-phosphate is a poor substrate of DXR [17] According to our results, methylerythrose phosphate apparently has a good affinity with the enzyme, at least as compared with that of DXP 3

Table 1 Determination of the kinetic parameters (K m and V) of DXP 3 and 2-C-methyl- D -erythrose 4-phosphate 4 Assays were carried out in a

50 m M triethanolamine/HCl, 1 m M MnCl 2 (or 3 m M MgCl 2 ) , 2 m M dithiothreitol pH 7.7 buffer at a fixed concentration of NADPH (0.15 m M ) The concentration of DXP varied from 31 to 310 l M while the concentration of 2-C-methyl- D -erythrose 4-phosphate 4 varied from 93 to 620 l M The concentrations of the stock solutions of substrate were determined enzymatically using the H-DXR The enzyme (4.3 lg)was added last in order to initiate the reaction.

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(Table 1) As erythrose 4-phosphate has a very weak affinity

with the DXR, it appears that the methyl group at C-2 must

play a crucial role for the binding of the substrate to the

enzyme active site

DXR and AHIR, an enzyme involved in the

biosynthe-sis of branched-chain amino acids [42], catalyze similar

reactions The latter converts 2-acetolactate or

2-aceto-2-hydroxybutyrate into dihydroxy-3-isovalerate or

2,3-dihydroxy-3-methylvalerate This reaction proceeds in two

steps: an isomerization, consisting of an alkyl migration, is

followed by an NADPH-dependent reduction of the oxo

group to give the final product In the reactions catalyzed by

the two enzymes, the ketol-acid and the DXP

isomero-reductase, the formation of the expected intermediates,

3-hydroxy-3-methyl-2-oxo-butyrate or methylerythrose

phosphate, respectively, has never been shown For AHIR,

it was suggested that the intermediate may be tightly bound

to the enzyme or that the reduction takes place during the

alkyl transfer so that the intermediate is never really formed

[42] In none of our assays could the formation of

methylerythrose phosphate 4 be detected Assays designed

to dissociate the transposition step from the reduction when

using DXP 3 as substrate were performed for a tentative

direct identification of methylerythrose phosphate In the

absence of cofactor, no isomerization was observed

Accord-ingly, the simultaneous presence of the divalent cation and

of the cofactor might be required for the subsequent fixation

of DXP 3 or methylerythrose phosphate 4 [17]

Dihydro-NADPH, an NADPH analogue [34] which is not a reducing

cofactor, was expected to bind to the enzyme much like the

natural coenzyme [17] Inhibition of the reaction by

dihydro-NADPH would suggest that this analogue was

bound to the active site of the enzyme It was, however,

impossible to induce the isomerization of DXP 3 into

methyl erythrose phosphate 4

The reduction step seems to represent the driving force to

perform the rearrangement The fact that the postulated

oxo intermediate in both isomeroreductase-catalyzed

reac-tions are substrates for the reduction step with higher Km

than those of the normal substrates suggests that the first

proposition, their tight binding to the enzyme, is rather

improbable The reduction step might be necessary in order

that the isomerization takes place

Reversibility of the DXR-catalyzed reaction: formation

of DXP 3 from MEP 5

In order to verify that the H-DXR is capable of catalyzing

the reverse reaction, the enzyme was incubated with MEP 5

and NADP+ A first series of experiments was performed

with13C-labelled MEP When H-DXR was incubated in the

presence of [5-13C]MEP or [2-13C]MEP and NADP+, a

decrease of the C-5 (d¼ 17.7 p.p.m.)or of the C-2

(d¼ 73.2 p.p.m.)signals from MEP was observed,

accom-panied by a concomitant appearance and following increase

of new signals corresponding to C-1 (d¼ 25.5 p.p.m.)and

C-2 (d¼ 212.4 p.p.m.)from [1-13C]DXP or [2-13C]DXP,

respectively A second experiment was performed with

unlabelled MEP The increase of the absorbance at 340 nm,

due to the formation of NADPH, suggested that MEP 5

was at least oxidized to 2-C-methyl-D-erythrose 4-phosphate

4, the supposed intermediate of the reaction To show that

the enzyme is capable of performing the two steps of the

reverse process, converting MEP 5 into DXP 3, i.e oxidation of MEP into 4 and rearrangement of 4 into DXP 3, MEP 5 was treated with H-DXR in the presence

of NADP+and a regeneration system of the coenzyme to favour the reaction in the direction of the formation of DXP

3 After dephosphorylation and acetylation of the reaction mixture, 1-deoxy-D-xylulose triacetate and

2-C-methyl-D-erythritol triacetate were isolated by TLC and identified

by1H-NMR, proving that H-DXR catalyzed the reverse transformation of MEP 5 into DXP 3, including not only the oxidation of MEP 5 to 2-C-methyl-D-erythrose 4-phosphate

4, but also the rearrangement of the latter aldehyde into DXP 3 Methylerythrose diacetate, which coelutes with DX triacetate, was not observed

When the reverse reaction with MEP 5 (115 lM)and NADP+ (175 lM)was followed during several minutes the absorbance increase stopped completely when about 13–14% of the MEP 5 was transformed, corresponding to the production of some NADPH (15.6 lM) The addition of more H-DXR to the reaction medium did not induce any additional absorbance increase Ceasing NADPH forma-tion was not due to the inactivaforma-tion of the enzyme, but rather to the fact that the equilibrium had been reached This low production of NADPH suggests that the reaction equilibrium is largely in favour of the production of MEP 5 from DXP 3 In order to confirm this hypothesis, the influence of the concentrations of NADP+and MEP 5, the substrates of the reverse reaction, and of NADPH and DXP

3, the products of the reaction, on the total amount of NADPH produced were analysed

The apparent equilibrium constant

K¼½DXPeq ½NADPHeq ½H

þ

½MEPeq ½NADPþeq where [DXP], [MEP], [NADPH] and [NADP+] represent the concentrations of the different compounds at the equilibrium, was calculated in each case and found to be approximately the same (average value 4.6 ± 0.5· 10)10M

at 37C) Attempts to determine the Km of MEP 5 showed that the Kms of MEP 5 (116 lM)and DXP 3 (76 lM)had similar values The V of the reverse reaction (3.5 mMÆmin)1Æmg protein)1)was about 60% of that of the formation of MEP 5 from DXP 3 (5.6 mMÆmin)1Æmg protein)1)

Even the very transitory existence of methylerythrose phosphate 4 is no longer an assumption, as this aldehyde 4

is the substrate of the DXP reductoisomerase with a good affinity It is converted into MEP 5, as well as into DXP 3 Furthermore, our NMR data afforded direct evidence for the reversibility of the reaction catalyzed by the DXR by the conversion of MEP 5 into DXP 3

Rearrangement of DXP 3 to 2-C-methyl-D -erythrose-4-phosphate 4: the role of NADPH

The conversion of DXP 3 into MEP 5 by the DXR requires the presence of NADPH as cofactor The first step of this conversion, i.e the rearrangement of DXP 3 into methyl-erythrose phosphate 4, is, however, formally fully inde-pendent of this cofactor, as this rearrangement only corresponds to an isomerization In order to try to shed light on the possible role of methylerythrose phosphate 4,

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the DXR-catalyzed reaction was followed by 13C-NMR

using a13C-labelled substrate (99% isotope abundance)in

order to improve the sensitivity of the detection method

[1-13C]DXP was incubated in the presence of NADPH and

of a NADPH regenerating system The enzyme preparation

was active The decrease of the intensity of the C-1 signal of

[1-13C]DXP (d¼ 25.5 p.p.m.)was accompanied by the

concomitant increase of the C-5 signal of [5-13C]MEP

(d¼ 17.7 p.p.m.) In a second experiment, NADPH was

omitted in order to check whether the presence of the

reducing cofactor is essential in the transposition step When

[1-13C]DXP was incubated alone in the absence of

NADPH, no additional 13C signal was observed, and

especially no signal corresponding to the C-5 methyl group

of methylerythrose phosphate 4 (d¼ 16.34 p.p.m.,

alde-hyde form; d¼ 18.25 p.p.m hydrate form), indicating that

no reaction had occurred, at least within the limits of the

13C-NMR detection The presence of the native coenzyme

seems essential for the rearrangement, although it is not

formally required In the presence of NADPH analogues,

such as NADP+, dihydro-NADPH or ATP-ribose, DXP

remained intact and no conversion into methylerythrose

phosphate was observed

In conclusion, direct evidence for the formation of

2-C-methyl-D-erythrose 4-phosphate 4 was not obtained in this

enzymatic reaction, and no isomerization took place in the

absence of NADPH These results were consistent with

those of previous observations reported in the literature: the

binding of NADPH first only allowed the binding of the

DXP 3 [17]

Formation of 2-C-methyl-D-erythrose 4-phosphate

4 from DXP: an a-ketol rearrangement or a retro-aldolization reaction?

Incubation of [4,5-13C2]glucose into triterpenoids of the hopane series from Methylobacterium fujisawaense demon-strated for the first time the presence of a rearrangement in the MEP pathway [48] By analogy with the biosynthesis of the amino acids with branched side-chains, the conversion

of DXP 3 into MEP 5 was considered as an a-ketol rearrangement (Fig 3) This mechanism involves the deprotonation of the hydroxyl group at C-3 of DXP 3, followed by the migration of the phosphate-bearing C2

subunit to afford methylerythrose phosphate 4 Examples

of reactions utilizing a retroaldolization/aldolization type mechanism in the place of an a-ketol rearrangement are also found in the literature, e.g the reaction catalyzed by the ribulose 5-phosphate 4-epimerase [49,50] In addition, such aldolization reactions often require the presence of a divalent cation [50], much like the reaction catalyzed by DXR For the formation of MEP 5 from DXP 3, such an alternative mechanism would involve the deprotonation of the C-4 hydroxyl group of DXP 3, followed by the cleavage

of the carbon–carbon bond between the carbon atoms C-3 and C-4 to give the enolate of hydroxyacetone 25 and glycoaldehyde phosphate 12 (Fig 3) Recombination of the two resulting moieties, rearranged via an aldolization by formation of a novel carbon–carbon bond between the carbon atoms derived from C-2 and C-4 of DXP 3, would give 2-C-methyl-D-erythrose 4-phosphate 4 In order to try

Fig 3 Conversion of DXP into MEP by the DXR: a-ketol rearrangement vs retro-aldolization/aldolization.

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to get more insight into the mechanism of the

DXR-catalyzed reaction, the DXP analogue 14 was synthesized

and analysed for its behaviour towards the DXR On

the one hand, if DXP analogue 14 is transformed to the

(2R)-2-hydroxy-2-methylbutanol 4-phosphate 27, the

reac-tion is most probably an a-ketol rearrangement On the

other hand, the retro-aldolization would imply the

interme-diary formation of glycoaldehyde phosphate 12 and of the

enol of hydroxyacetone 25 (Fig 3)

Formation of 2-C-methyl-D-erythrose 4-phosphate 4 from

DXP: an a-ketol rearrangement? The possibility that

DXR catalyzes the formation of 2-C-methyl-D-erythrose

4-phosphate 4 from DXP 3 via an a-ketol rearrangement

(Fig 3)was checked by testing (3S)-3-hydroxypentan-2-one

5-phosphate 14 as potential substrate of H-DXR This

compound was synthesized from the commercially available

(S)-2-hydroxy-c-butyrolactone 15, which has the required

configuration for the C-2 asymmetric carbon of 14 (Fig 4)

Protection of the secondary alcohol of 15 afforded the silyl

ether 16 in 97% yield Addition of methyl lithium gave a

lactol, which opened under standard phosphorylation

condition to the enantiomerically pure ketone 17, but with

low yield [37] Deprotection of the silyl ether 17 with fluoride

salts (TBAF), followed by hydrogenolysis of the benzyl

groups, afforded (3R)-3-hydroxypentan-2-one 5-phosphate

14 Incubation of the DXP analogue 14 with H-DXR in the

presence of NADPH did not induce any decrease of the

absorbance at 340 nm The DXP analogue 14 was not a

substrate of DXR It was, however, recognized by DXR

and reversibly inhibited the enzyme as a mixed-type

inhibitor (Ki¼ 120 lM) In conclusion, no information

was obtained on the reaction mechanism of the

DXR-catalyzed reaction, but the crucial role of the C-4 hydroxy

group of DXP 3 was pointed out in the isomerization steps

Furthermore, as the DXP analogue 14 inhibited the

DXR, its isomer, (4S)-4-hydroxypentan-2-one 5-phosphate

19, was also synthesized and tested on H-DXR The

synthesis started with the preparation of the silyl ether 21

from commercially available (R)-glycidol 20 (Fig 4)

Epox-ide opening of 21 with isoproprenylmagnesium bromEpox-ide in

the presence of CuI, followed by the deprotection of the silyl

ether, gave diol 22 in excellent yield Selective

phosphory-lation of the primary alcohol of 22 with dibenzylphosphate

chloride [37] at low temperature followed by oxidative

cleavage [38] of the double bond yielded the protected

ketone 23 in 39% yield over two steps Finally the benzyl

groups were quantitatively removed by hydrogenolysis in

the presence of a catalytic amount of palladium on activated

carbon to yield (4S)-4-hydroxypentan-2-one 5-phosphate 19

(Fig 4) Analogue 19 also inhibited the DXR as a mixed

type inhibitor (Ki¼ 800 lM)

Formation of 2-C-methyl-D-erythrose 4-phosphate 4 from

DXP: a retro-aldolization mechanism? In the case of an

alternative retro-aldolization mechanism, hydroxyacetone

25 and glycoaldehyde phosphate 12 are the two

intermedi-ates leading to the formation of methylerythrose phosphate

4 (Fig 3) Detection of hydroxyacetone 25 was attempted

by incubation of [1-13C]DXP and following the reaction by

13C-NMR spectroscopy No signal corresponding to the

C-3 of hydroxyacetone 25 (d¼ 24.0 p.p.m.), which was

expected to be labelled in the case of hydroxyacetone

formation, was observed next to those of C-1 of DXP (d¼ 25.5 p.p.m.)and C-5 of MEP (d ¼ 17.7 p.p.m.) In addition, the influence of hydroxyacetone 25 and glyco-aldehyde phosphate 12, the two intermediates in a retro-aldolization/aldolization mechanism (Fig 3), on the activity

of DXR was checked When the enzyme was incubated in the presence of the two compounds at concentrations up to

1 mM, and NADPH, no decrease of the absorbance at

340 nm was observed, indicating that no MEP 5 was produced In addition, the two compounds, either alone or together at concentrations of up to 1 mM, did not inhibit the production of MEP 5 from DXP 3 They do not seem to be recognized by DXR

These negative results did not enable us to retain or exclude either one or the other mechanism The absence of NADPH consumption during the incubation of the enzyme

Fig 4 Synthesis of (3S)-3-hydroxypentan-2-one 5-phosphate 14 and (4S)-4-hydroxypentan-2-one 5-phosphate 19 (A)Synthesis of (3R)-3-hydroxypentan-2-one 5-phosphate 14 (i)TBDMSOTf, 2,6-lutidine, dichloromethane, 97%; (ii)CH 3 Li, tetrahydofuran, )78 C, 67%; (iii)(BnO) 2 POCl, pyridine, 16%; (iv)Bu 4 NF, tetrahydofuran, 88%; (v)H 2 , Pd/C, EtOH, 100% (B)Synthesis of (4S)-4-hydroxypentan-2-one 5-phosphate 19 (i)TBDPSCl, imidazole, dichloromethane, 92%; (ii)CH 2 ¼ CHMgBr, CuI, tetrahydofuran; (iii)Bu 4 NF, tetrahydofu-ran, 89% from two steps; (iv)(BnO) 2 POCl, pyridine, )40 C, 54%; (v)RuCl 3 , NaIO 4 , CH 3 CN, CCl 4 , H 2 O, 72%; (vi)H 2 , Pd/C, EtOH, 100%.

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