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Báo cáo khoa học: Discovery and characterization of a Coenzyme A disulfide reductase from Pyrococcus horikoshii Implications for the disulfide metabolism of anaerobic hyperthermophiles doc

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The enzyme does not show significant NADH peroxidase activity and is not active in the reduction of glutathi-one, cystine, or 3¢ dephospho-CoA disulfide unlike the staphylococcal enzyme, w

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reductase from Pyrococcus horikoshii

Implications for the disulfide metabolism of anaerobic

hyperthermophiles

Dennis R Harris*, Donald E Ward1, Jeremy M Feasel2, Kyle M Lancaster2, Ryan D Murphy2,

T Conn Mallet3and Edward J Crane III2

1 Genencor International, Palo Alto, CA, USA

2 Department of Chemistry, Pomona College, Claremont, CA, USA

3 Center for Structural Biology, Wake Forest University School of Medicine, Winston-Salem, NC, USA

While surveying the genomes of hyperthermophilic

and thermophilic Archaea for homologues of the

flavoprotein disulfide reductases, many homologues

with a high degree of identity to the branch of this

family represented by glutathione reductase were

found [1] Most of the homologues appear to belong

to the subfamily that depend on a redox-active single cysteine, analogous to the NADH oxidase and per-oxidase of Enterococcus and the coenzyme A disulfide reductase (CoADR; EC 1.8.1.14) of Staphylococcus

Correspondence

E J Crane III, Department of Chemistry,

Pomona College, 645 North College

Avenue, Claremont, CA 91711, USA

Fax: +1 909 607 7726

Tel: +1 909 607 9634

E-mail: ej.crane@pomona.edu

Website: http://www.userwebs.

pomona.edu/ejc14747/EJ_web.htm

*Present address

Department of Biochemistry, University of

Wisconsin-Madison, Madison, WI, USA

(Received 20 July 2004, revised 7 December

2004, accepted 4 January 2005)

doi:10.1111/j.1742-4658.2005.04555.x

We have cloned NADH oxidase homologues from Pyrococcus horikoshii and P furiosus, and purified the recombinant form of the P horikoshii enzyme to homogeneity from Escherichia coli Both enzymes (previously referred to as NOX2) have been shown to act as a coenzyme A disulfide reductases (CoADR: CoA-S-S-CoA + NAD(P)H + H+fi 2CoA-SH + NAD(P)+) The P horikoshii enzyme shows a kcat app of 7.2 s)1 with NADPH at 75C While the enzyme shows a preference for NADPH, it is able to use both NADPH and NADH efficiently, with both giving roughly equal kcats, while the Kmfor NADPH is roughly eightfold lower than that for NADH The enzyme is specific for the CoA disulfide, and does not show significant reductase activity with other disulfides, including dephos-pho-CoA Anaerobic reductive titration of the enzyme with NAD(P)H pro-ceeds in two stages, with an apparent initial reduction of a nonflavin redox center with the first reduction resulting in what appears to be an EH2form

of the enzyme Addition of a second of NADPH results in the formation

of an apparent FAD-NAD(P)H complex The behavior of this enzyme is quite different from the mesophilic staphylococcal version of the enzyme This is only the second enzyme with this activity discovered, and the first from a strict anaerobe, an Archaea, or hyperthermophilic source P furio-suscells were assayed for small molecular mass thiols and found to contain 0.64 lmol CoAÆg dry weight)1 (corresponding to 210 lm CoA in the cell) consistent with CoA acting as a pool of disulfide reducing equivalents

Abbreviations

CoADR, coenzyme A disulfide reductase (EC# 1.8.1.14); pfCoADR, P furiosus coenzyme A disulfide reductase; phCoADR, P horikoshii coenzyme A disulfide reductase; DTNB, 5,5¢ dithiobis(2-nitrobenzoic acid); EH 2 , two-electron reduced enzyme; EH 4 , four-electron reduced enzyme; HEPPS, N-(2-hydroxyethyl)piperazine-N¢-3-propanesulfonic acid; NOX, NADH oxidase; NPX, NADH peroxidase; TCA, trichloroacetic acid.

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aureus [2,3] These enzymes are proposed to be

involved in the robust oxygen-defense systems of

aerobic and facultatively anaerobic organisms [4,5]

and would not be expected to be present in the

mostly strictly anaerobic hyperthermophiles Evidence

is mounting, however, for the presence of a vigorous

oxidative stress response in Pyrococcus, including the

discovery of both a novel peroxide-producing

super-oxide reductase [6] and an NADH oxidase [1]

Addi-tionally, an oxidative stress response has been

characterized in the strictly anaerobic bacterium

Clos-tridium perfringens [7]

Microorganisms in the genus Pyrococcus are strictly

anaerobic hyperthermophiles (Topt¼ 100 C) isolated

from marine hydrothermal vents [8–10] The genomes

of P horikoshii, P furiosus and P abyssii each contain

at least two NADH oxidase homologues

Characteriza-tion of one of these homologues (NOX1) from

P furiosus has been described previously [1] NOX1

shows a novel H2O and H2O2producing NADH

oxid-ase activity in both the absence and presence of

exo-genous FAD The second NOX homologue examined

(from P horikoshii, previously referred to as NOX2)

showed a slow NAD(P)H oxidase activity in the

pres-ence of high concentrations of substrate-level FAD,

i.e., in addition to the enzyme bound FAD The results

described here demonstrate that this enzyme is not

likely to act as an NADH oxidase in vivo, instead

act-ing as a CoADR This is only the second

demonstra-ted CoA reductase activity, and the first appearance of

this activity in both the Archaea and in a strict

anaer-obe While the best known small molecular mass thiol

is probably glutathione, a number of novel thiols such

as mycothiol, c-glutamyl cysteine, and trypanithione

have been found in microorganisms [11] The function

of these thiols appears to be the maintenance of a

reducing intracellular environment Due to the

pres-ence of a CoADR homologue in all three pyrococcal

genomes, P furiosus cells were assayed for the

pres-ence of small molecular mass thiols in order to better

understand the role of this enzyme and thiol⁄ disulfide systems in pyrococcal metabolism The results presen-ted below provide an insight into the use of a small molecular mass thiol system for the maintenance of the internal redox environment in an anaerobic hyper-thermophile

Results

Characterization of the recombinant CoADR The recombinant CoADR from P horikoshii (phCo-ADR) was purified 15-fold with a yield of 58% and

a specific activity of 3.26 UÆmg)1 (oxidase activity) (Table 1) and 8.3 UÆmg)1 (CoADR activity) The phCoADR had a subunit m¼ 50 k as determined by SDS⁄ PAGE, and was shown by both HPLC and con-ventional size-exclusion chromatography to be a tetra-meric enzyme of m ¼ 198 k The enzyme obtained from the overexpression host is approximately 20% holoenzyme After reconstitution with FAD the enzyme contains 0.92 flavin per subunit based on the ratio of protein concentration to flavin concentration (as determined at 460 nm) blast and tfasta analysis

of the phCoADR revealed a significant level of identity

to putative NADH oxidases from hyperthermophiles and bacterial NADH oxidases from mesophilic sources (Fig 1) Of particular interest was the identity to the well characterized NOXs from mesophilic organisms, with the highest levels of identity found with the NADH oxidases from E faecalis (28%), Streptococcus mutans (26%), and Brachyspira (Serpulina) hyodysente-riae(24%) The CoADR from S aureus is 26% identi-cal to the P horikoshii CoADR As shown in Fig 1, the P furiosus NOX1 and the pf and ph CoADRs con-tain a cysteine which corresponds to the single redox active cysteine of the E faecalis NOX and NPX, as well as considerable identity in areas that have been shown to be important for NADH and FAD binding

in these enzymes

Table 1 Purification of the recombinant coenzyme A disulfide reductase from P horikoshii For the purposes of this table, purification was monitored by the FAD-dependent NADH oxidase activity of the enzyme, with a unit equal to the amount of enzyme required to oxidize

1 lmol NADH in 1 min in the presence of 100 lm NADH, 100 lm FAD, in 50 mm potassium phosphate, pH 7.50 at 75 C The specific activity of the purified enzyme in terms of coenzyme A disulfide reductase activity is 8.3 UÆmg)1.

Fraction Total units Total protein (mg)

Specific activity (unitsÆmg)1) Purification (fold) Yield (%)

Heat-treated extract 134 77.2 1.73 7.83 68.0

Size-exclusion 114 35.0 3.26 14.8 57.8

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In order to determine the extinction coefficient of

the enzyme-bound FAD, the FAD was released from

the holoenzyme by trichloroacetic acid (TCA)

precipi-tation of the protein The e460 of the enzyme-bound

FAD was determined to be 10 200 m)1Æcm)1 It is

interesting to note that attempts to remove the FAD

from the enzyme by treatment in 6.0 m guanidine⁄ HCl

were unsuccessful, even with overnight incubation at

90C This result is consistent with the extreme stabil-ity of this enzyme, and consistent with the observation that thermostable proteins, including the NOX1 from

P furiosus, are frequently stable in organic solvents and in the presence of denaturants [1] The visible spectrum of the enzyme as purified (Fig 2) has the same distinct shoulder in the area of 470 nm as the mesophilic staphylcoccal enzyme [12]

Fig 1 Multiple sequence alignment of

P horikoshii and P furiosus CoADRs to

known NADH oxidases ⁄ NADH peroxidase ⁄

CoADR The alignment was performed with

CLUSTAL W The GenBank accession numbers

for the other enzymes are as follows:

Staphylococcus aureus CoADR (AF041467),

E faecalis NOX (P37061), E faecalis NPX

(P37062), P furiosus NOX (PF_1430634).

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CoADR activity of the recombinant P furiosus

CoADR homologue

The CoADR from P horikoshii has a homolouge in

P furiosus that is 92% identical (Fig 1), indicating

that this gene product was also likely to be a CoADR

The recombinant P furiosus CoADR (pfCoADR) was

expressed in E coli Heat-treated FAD-reconstituted

extracts of the putative pfCoADR showed a strong

CoADR activity corresponding to a specific activity of

11 UÆmg)1 of heat-treated extract This result

com-pares favorably with the specific activity obtained

dur-ing the production of the recombinant CoADR from

P horikoshii Like the phCoADR, the pfCoADR is

active with both NADH and NADPH CoADR

activ-ity was also detected in crude extracts of P furiosus,

however, the level of activity was low and difficult to

distinguish from background reactions

Steady-state kinetics of the CoADR and oxidase

reactions

The kinetic constants for the CoADR and oxidase

activities of phCoADR are listed in Table 2 The

enzyme does not show significant NADH peroxidase

activity and is not active in the reduction of

glutathi-one, cystine, or 3¢ dephospho-CoA disulfide (unlike the

staphylococcal enzyme, which has a 40 lm Kmfor the

dephospho substrate) The enzyme also does not show

significant 5,5¢ dithiobis(2-nitrobenzoic acid) (DTNB)

reductase in a standard aerobic steady-state kinetic

assay; however, in the anaerobic assays of free thiols

discussed below the enzyme does show DTNB turn-over with NADPH at a very high concentration of enzyme (30–60 lm) While NADPH is the preferred substrate for the CoADR activity based on Km, the two nucleotide substrates have almost identical kcats This result is quite distinct from the substrate specifi-city observed with the staphylococcal enzyme, which shows a marked preference for NADPH [12]

While phCoADR shows a low level of NAD(P)H oxidase activity (in the absence of CoA disulfide) in the absence of substrate level FAD (i.e., FAD added

in addition to that present in the enzyme-bound form),

a significant amount of oxidase activity can be observed in the presence of additional substrate-level FAD (Table 2) The kcat app obtained in the presence

of 100 lm NADH and FAD and 115 lm O2 is 8.2 s)1, which correlates well with the catalytic constant observed for the CoADR reaction

Thermostability and thermoactivity of the CoADR phCoADR is stable for months at both )80 C and )20 C, and has half-lives of > 100 and 39 h at 85 and 95C, respectively Figure 3 shows the dependence

of the oxidase and phCoADR activities on tempera-ture While both activities show the preference for high temperature expected of an enzyme from a hyper-thermophile, at temperatures above 75C both activit-ies appear to plateau slightly, rather than increasing all the way to the optimal growth temperature for Pyro-coccus

Anaerobic reduction with NAD(P)H and redox state of the proposed cysteine nonflavin redox center

As shown in Fig 2, when phCoADR is titrated anaero-bically at 60C with NADPH the titration shows two main phases, each corresponding to the addition of

300

0.6

0.4

0.2

0

Wavelength, nm

0

NADPH, eq

A600.7200.040 0.080

Fig 2 Anaerobic reductive titration with NADPH at 60 C 56 l M

phCoADR in 50 m M potassium phosphate at pH 7.50 was titrated

with NADPH Spectra are shown at 0 (—), 1.1 (- - -) and 2.0 (ÆÆÆÆ)

NADPH Inset, Change in absorbance at 600 (s) and 720 (d) nm

during titration.

Table 2 Michaelis constants for the P horikoshii CoADR, deter-mined at 75 C in 50 m M potassium phosphate, pH 7.50.

Activity-substrate Km app(l M ) kcat app(s)1) CoADR-NADHa 73 8.1 CoADR-NADPH a < 9.0 7.2 CoADR-CoANaCl ⁄ CitoA b 30 7.1 Oxidase-NADHc 73 8.2 Oxidase-NADPH c 13 2.0 Oxidase-FAD d 22 5.9

a Determined at 200 lm CoA-S-S-CoA, b determined at 100 lm NADPH, cdetermined at 100 lm FAD, ddetermined at 100 l M

NADH.

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roughly one equivalent of NAD(P)H At 720 nm the

majority of the change occurs during the addition of

the first equivalent of the reducing agent as seen in

Fig 2 (inset) Little change is observed at 361 nm

dur-ing addition of the first equivalent of NADPH, while

an increase is observed during the addition of the

sec-ond and subsequent equivalents of NADPH With the

exception of the expected increase at 340 nm from the

addition of free NADPH, little additional change is

seen in the spectra when NADPH is added to a total of

six equivalents No reduction of the FAD is observed

during addition of excess NAD(P)H Anaerobic

titra-tion of phCoADR with NADH shows very similar

spectral results to those obtained with NADPH (results

not shown) During anaerobic reduction with dithionite

(data not shown) the FAD becomes reduced upon the

addition of a second equivalent of dithionite, consistent

with initial reduction of a nonflavin redox center,

fol-lowed by reduction of the FAD by the strongly

redu-cing dithionite

While the spectral changes upon addition of

NADPH appear to correlate well with enzyme states

corresponding to the addition of roughly 1 and 2

equivalents of NADPH, it is difficult to determine

directly from the spectrum the fate of the reduced

pyr-idine nucleotide During the addition of the first

equiv-alent of NADPH, there is a blue shift in the 380 nm

peak and subsequent small increase in absorbance at

340 nm, although the increase is much less than that

expected for the amount of NADPH added (the

increase corresponds to the addition of 15 lm

NADPH, when 50 lm NADPH had been added)

When the titration is performed at room temperature,

no additional absorbance is observed at 340 nm during the addition of the first equivalent of NADPH con-firming that the pyridine nucleotide is consumed during the addition of the first equivalent (data not shown)

Determination of free thiol content

In order to characterize the redox state of the pro-posed active site cysteine on the enzyme as purified and after addition of 0.8 equivalent of NADPH, as well as any small molecular mass thiols released by the enzyme, we used the thiol specific reagent DTNB Because the enzyme contains only one cysteine residue, there is only one possible reactive thiol on the enzyme,

in addition to any small molecular mass thiol trapped

in the form of a mixed-disulfide with the cysteine (Cys-S-S-R) The results of these experiments are shown in Table 3 The enzyme as purified contains 0.00 equiva-lents of DTNB reactive thiol Following anaerobic reduction with NADPH, less than 0.01 equivalent of small molecular mass thiol was detected, indicating that little if any of the enzyme is purified in the mixed disulfide form If the NADPH reduced enzyme is kept anaerobic and assayed for thiol content, 0.85 equival-ent of thiol is detected, indicating that reduction by NADPH produces a reactive thiol If the enzyme is exposed to air following reduction, this thiol becomes unreactive, suggesting that it is rapidly oxidized to the sulfenic acid

Determination of CoA levels and relative stability

in P furiosus

To determine whether CoA might play a role as a pool

of reducing equivalents in Pyrococcus, as suggested by the presence of a CoADR homologue in all three pyrococcal genomes, cells of P furiosus were assayed for small molecular thiols CoA was present at a con-centration of 0.64 lmol CoAÆg dry weight)1, which corresponds roughly to 210 lm CoA in the cell (assu-ming a wet⁄ dry weight ratio of 3 : 1 [13]) Glutathione was not detected CoA was present almost entirely

100

75

50

25

0

Temperature

Fig 3 NADH oxidase (d) and CoA disulfide reductase (j) activity

of phCoADR at varying temperatures Activities at 81.3 (oxidase)

and 85.0 C (disulfide reductase) were set at 100%.

Table 3 Equivalents of free thiol, as detected by DTNB.

Equivalents

of free thiol phCoADR, as purified 0.00 NADPH reduced phCoADR, anaerobic 0.85 Small molecular mass thiol

released upon NADPH reduction

0.01 NADPH reduced, exposed to air 0.00

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in the thiol form, as there was < 5% detected in the

disulfide form, as determined by the concentration of

(thiol + disulfide)–(thiol)

CoA has previously been shown to be four times

more stable than glutathione and 180 times more

sta-ble than cysteine to the Cu2+-catalyzed oxidation to

the disulfide form in the presence of oxygen [14]

Because CoA is significantly more complex than either

cysteine or glutathione, we were interested in

determin-ing whether the increased stability to overoxidation

extends to higher temperatures For this reason, the

oxidation of thiols at a high temperature was assayed

It was found that CoA oxidizes approximately 4.4

times slower than glutathione at 88C in 50 mm

imi-dazole buffer, 1.0 lm Cu2+ pH 7.50, as shown in

Fig 4 (under these conditions cysteine oxidizes too

quickly to be measured using conventional techniques)

Under conditions in which the copper and any trace

contaminating metals were chelated with EDTA and

phosphate (50 mm potassium phosphate, 0.50 mm

EDTA, pH 7.50), no significant oxidation of CoA was

observed over 100 min at 88C

Discussion

The phCoADR is only the second CoADR

character-ized to date, and is the first from a hyperthermophile

and Archaeon Moreover, the enzyme displays distinct

differences from the S aureus CoADR The enzyme is

quite distinct from the staphylococcal enzyme in its

ability to use both NADPH and NADH as substrates

With the S aureus enzyme, substitution of NADH as

the reducing nucleotide gives approximately 17% of the rate observed with NADPH [12], while the pyro-coccal enzyme gives almost identical kcat values with either reduced nucleotide substrate The Kmappof < 9 and 73 lm for NADPH and NADH, respectively, do differ significantly, with NADPH appearing to be the more efficient substrate

The reduced nucleotide concentrations have been determined for P furiosus [15], and while the total concentration of NAD(P)(H) was found to be about half the value seen in the mesophilic Salmonella typhimurium, the pyrococcal NADP(H)⁄ NAD(H) ratio was found to be more than twice that found in

S typhimurium This result is not surprising, given the presence of several unique NADP+-dependent cata-bolic enzymes present in Pyrococcus [15] The kcat of 7.2 s)1determined for the phCoADR with NADPH as the reducing substrate is similar to the kcat of 27 s)1 observed for the staphylococcal enzyme, although it is lower [12]

Stabilization of enzyme intermediates Different enzymes within the disulfide reductase family stabilize different intermediates upon anaerobic reduc-tion with their nucleotide substrates The H2 O-produ-cing NADH oxidases are reduced by their nucleotide substrates by four electrons to an EH4 or EH4ÆNAD+ form, as shown in Scheme 1 [16,17] In this case the first reducing equivalent reduces the active site cysteine residue, which serves as a nonflavin redox center, from the oxidized sulfenic acid to a reduced thiol species This 2e– reduced form of the enzyme is referred to as the EH2 species [17] Addition of a second equivalent

of reduced nucleotide substrate results in reduction

of the enzyme-bound FAD, forming the EH4 or

EH4ÆNAD(P)+species In the case of a true oxidase, it makes sense for the enzyme to stabilize the EH4 form, since the reduced flavin is reactive with O2

Other enzymes in the family, such as the NADH peroxidase or glutathione reductase, tend to stabilize the enzyme-reduced nucleotide complex referred to

as EH2ÆNAD(P)H (Scheme 1) [18,19] On the EH2Æ NADH complex of the NADH peroxidase from

E faecalis[20] (Npx: NADH + H++ H2O2fi NAD+ + 2H2O), the reducing equivalents of NADH are held

in the nicotinamide ring on the re-side of the flavin isoalloxazine ring with the C4 position of the nicotina-mide ring located 3.49 A˚ from N5 of the isoalloxazine ring The active site cysteine thiolate is 3.48 A˚ from N5 on the si-side of the flavin, which allows for oxida-tion of this residue by peroxide, followed by reducoxida-tion

by NADH via the flavin This configuration ensures

0

0.4

0.6

0.8

1

Time (min)

Fig 4 Autoxidation of glutathione (d) and CoA (s) at high

tem-perature (88 C) in the presence of Cu 2+ The observed rates of

oxi-dation correspond to pseudo first order rate constants of 5.7 · 10)3

and 1.3 · 10)3min)1for glutathione and CoA, respectively.

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that NADH is available to be used ‘on demand’ when

a substrate appears while at the same time avoiding

the stabilization of a reduced flavin intermediate that

could react undesirably with O2

In Fig 2, the redox state of the enzyme-bound FAD

is indicated by the peaks at 380 and 460 nm, with

for-mal reduction and⁄ or charge transfer to the

isoalloxa-zine ring resulting in a loss of absorbance at these

wavelengths During the addition of the first equivalent

of NADPH there is a decrease in absorbance at

460 nm with a concomitant increase in long

wave-length (> 510 nm) absorbance The observed spectral

changes are consistent with the reduction of a

nonfla-vin redox center and the formation of an EH2 species,

with charge transfer possibly developing between the

FAD and the conserved active site cysteine thiol or

thiolate

During the anaerobic reduction of the S aureus

enzyme there is loss of roughly 50% of the absorbance

at 452 nm In that case, the loss of absorbance is

attributed to an asymmetric reduction of the dimeric

enzyme, with the net result of reduction by the first

equivalent being an oxidized flavin⁄ oxidized cys

resi-due in the form of a mixed disulfide on one subunit

and a reduced flavin⁄ reduced cys in the form of a thiol

on the other subunit [12] The decrease of 460 nm

absorbance during titration of the phCoADR

corres-ponds to at most a 24% loss, which is inconsistent

with the scheme proposed for the S aureus CoADR

It is interesting to note, however, that the overall

shape of the titration curve at 452 nm for the

sta-phylococcal enzyme and 460 nm for the phCoADR is

nearly identical, with most of the decrease in

absorb-ance occurring during addition of the first reducing

equivalent

Addition of a second equivalent of NADPH to the

EH2 form of phCoADR results in an increase in

absorbance in the regions between 507 and 700 nm

and 400 and 500 nm There is also an increase and

blue shift in the peak which corresponds to the 380 and 360 nm peaks of the E and EH2 forms, respect-ively This result is inconsistent with reduction of the FAD and consistent with the formation of an EH2Æ NADPH complex, although further characterization is currently underway to determine definitively the nature

of this enzyme species It is apparent, however, that lit-tle if any of the enzyme is stabilized in the FADH2 form It was this finding that led us to originally con-clude that this enzyme was not likely to act as an NAD(P)H oxidase in vivo

The difference in the reductive half reaction, inclu-ding the apparent lack of subunit asymmetry, and the difference in quaternary structure (the S aureus enzyme is a dimer) suggest that the mesophilic and thermophilic enzymes, which operate at very different temperatures, may use different mechanisms These differences are currently being investigated

Redox state of the single cysteine Based on homology to the single cysteine members of the disulfide reductase family, it seems likely that the CoADR uses its single cysteine to catalyze its redox chemistry As purified, the CoADR cysteine is not reactive with DTNB The observation that the cysteine becomes reactive following reduction with NADPH, along with the absence of small molecular mass thiols released upon reduction, leads to the conclusion that the enzyme is likely to be purified in the sulfenic acid form (Scheme 1) This result is not surprising, given that most of the enzyme is obtained in the apo form from the overexpression host It is also not particularly surprising that this enzyme, whose physiological func-tion appears to be to serve as a CoADR, is easily oxidized to the sulfenic acid form, when the anaerobic nature of Pyrococcus is taken into account While Pyrococcus may encounter some oxidative stress, it seems unlikely that it would be regularly subjected to

Scheme 1 Possible redox states for

single-cysteine containing disulfide reductases.

During reduction from ‘E’ to ‘EH2’ the

hydride passes from the NAD(P)H through

the FAD to the nonflavin redox center An

additional possible species, EH2-NAD(P) + , is

not shown.

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the levels of O2present in ambient air Even if it were,

however, this apparent sulfenic acid state is freely

reducible, so that its production would not seem to

put the enzyme at a disadvantage

Physiological role of CoADR and NAD(P)H

in Pyrococcus

The maintenance of low intracellular levels of cysteine

in organisms has been attributed to the avoidance of

the hydrogen peroxide produced during the rapid O2

-dependent oxidation to cystine, necessitating the use of

other small molecular mass thiols such as glutathione

for the maintenance of internal redox levels The

results presented above are consistent with a role for

CoA in maintaining a reducing environment or serving

as a pool of reducing equivalents at the very high

tem-peratures and high concentrations of metals found in

the natural environment of Pyrococcus The observed

CoA concentration of 0.64 lmol CoAÆg dry weight)1

compares favorably with the result of 1.1 lmolÆg)1dry

weight obtained for S aureus [14], and the

correspond-ing intracellular concentration of 210 lm CoA is well

above the Km app of 30 lm for the CoA disulfide The

pfCoADR (nox A-2 in the annotation of the P

furio-sus genome) was found to be upregulated more than

fivefold by growth on elemental sulfur (S0) [21], a

result which suggests a role for this enzyme in the

eventual transfer of electrons to S0 Because CoA

lev-els were determined in cells which were grown in the

absence of S0, future studies will determine whether

CoA levels increase during growth in the presence of

S0 It is also worth noting that the low CoADR

activ-ity noted in crude extracts of P furiosus was obtained

from cells grown in the absence of elemental sulfur, so

it seems likely that greatly increased activity will be

seen in extracts of cells grown in the presence of S0

The NAD(P)H dependence of enzymes in the

disul-fide reductase family can be divided into two classes:

(a) enzymes whose function appears to be the

main-tenance of a high R-SH⁄ R-S-S-R ratio, such as

glutathione reductase, trypanathione reductase and

thi-oredoxin reductase, which tend to be NADPH

depend-ent; and (b) enzymes that appear to be involved more

directly in the reduction of oxidizing compounds and

in the regeneration of oxidized nucleotides for

glycoly-sis, which show a distinct preference for NADH, such

as the NADH oxidase, NADH peroxidase, the NOX1

of P furiosus, alkyl hydroperoxide reductase, and

lipo-amide dehydrogenase

The pyrococcal CoADR described in this work is

able to efficiently utilize both NADPH and NADH, a

result which is consistent with the unusual utilization

of reduced nucleotide coenzymes by Pyrococcus The central metabolism of this organism uses an unusual NADPH-dependent sulfide dehydrogenase which is capable of both the NADPH-dependent reduction of elemental sulfur and the NADP+-dependent oxida-tion of ferredoxin [22] A unique NADPH-dependent alcohol dehydrogenase with wide substrate specificity and a strong preference for the reduction of alde-hydes to alcohols is also found in this organism [23] This unusual mix of NADH and NADPH dependent reactions in catabolic processes may account for the finding that the pyrococcal CoADR, which would be expected to show a strong preference for NADPH, is able to efficiently utilize either reduced nucleotide substrate

Comparison of the phCoADR to the pyrococcal NADH oxidase

There are now two members of the disulfide reductase family that have been characterized from Pyrococcus, the NADH oxidase and the CoADR These two enzymes display unique biochemical and enzymatic properties that are not present in their mesophilic counterparts The P horikoshii CoADR and the

P furiosus NADH oxidase (NOX1) are 37% identical Each appears to play distinct roles in the fermentative metabolism of Pyrococcus and each is regulated differ-ently [1,21] The difference in their reactivity is reflec-ted in the behavior of these two enzymes in reductive anaerobic titrations As shown in Fig 2 and discussed above, upon addition of excess NAD(P)H the phCo-ADR forms what appears to be an EH2ÆNAD(P)H complex with little or no FADH2 character (Scheme 1) This can be contrasted to the behavior of the P furiosus NOX, which forms what appears to be

an EH4ÆNAD+ complex with a fully reduced FAD (Scheme 1) upon addition of two equivalents of NADH (data not shown) In-depth studies comparing the mechanisms of these two pyrococcal enzymes to each other and to their mesophilic counterparts will be presented in a future communication

Experimental procedures

Growth of microorganisms

as previously described [24] Cellobiose (30 mm), maltose

inclu-ded as primary carbon source E coli JM109(kDE3) and

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K2HPO4 (2.5 gÆL)1)] When required, the following

Cloning and expression of the gene encoding

the P horikoshii and P furiosus CoADRs

The structural gene encoding the CoADR [previously

referred to as NOX2 (PH0572)] was amplified from P

oligonucleo-tides TG100 (5¢-GGCCTCATGAAGAAAAAGGTCGTCA

TAATT-3¢), and TG101 (5¢-GGCCAAGCTTCTAGAAC

TTGAGAACCCTAGC-3¢) (for the P horikoshii CoADR),

and TG104 (5¢-CGCGCCATGGAAAAGAAAAAGGTA

GTCATAA-3¢) and TG105 (5¢-CGCGGTCGACCTAGAA

CTTCAAAACCCTGGC-3¢) for the P furiosus CoADR

The N terminus of the CoADRs were based on the

pres-ence and proper spacing of the ribosome binding site,

agreement with the NOX homologues from mesophilic

sources that had been characterized in detail PCR

amplifi-cation was carried out using Pfu polymerase (Stratagene,

La Jolla, CA), and the resulting 1.3 kb PCR product was

cloned in the NcoI and HindIII sites of pET-24d The

resulting plasmids, pSMC002 (P horikoshii) and pSMC004

(P furiosus) were transformed into E coli BL21(kDE3)

For production of the recombinant enzymes the strain

JM109 (kDE3) was used

Production and purification of recombinant

phCoADR

The phCoADR was overexpressed in E coli JM109(kDE3)

( 4.0 h) isopropyl thio-b-d-galactoside was added to a

final concentration of 1.0 mm to induce enzyme production

The culture was incubated for an additional 4.0 h and the

15 min The cells were washed with 50 mm Tris buffer

until purification

The thawed cells were resuspended in 50 mm Tris buffer

pH 7.5 (70 mL total volume) Eight-milliliter aliquots of

treat-ments Cell debris was removed by centrifugation at

and sonication treatments were repeated (20 mL total

vol-ume) and cell debris was removed by centrifugation

protein was removed by centrifugation at 15 000 g and

Chromatography was performed using an AKTA low-pressure chromatography system (FPLC) from Pharmacia Biotech (Piscataway, NJ) The supernatant was applied to a

25 mL Q-Sepharose Hi-Load column (Pharmacia Biotech) equilibrated with 50 mm Tris buffer pH 7.5 at 3.0 mLÆ

50 mm Tris pH 7.5 to remove excess protein phCoADR was eluted by a 120-mL linear gradient from 0.10 to 0.45 m KCl, with phCoADR eluting between 0.27 and 0.32 m KCl Fractions containing phCoADR were pooled and reconsti-tuted with a final concentration of 1 mm FAD by

concentrated and rinsed with 50 mm Tris buffer pH 7.50 by ultrafiltration with 30 k molecular mass limit filtration

The concentrate (total volume 1.7 mL) was applied to a 120-mL Sephacryl S-200 HR (Pharmacia Biotech) size-exclusion column equilibrated with 50 mm Tris buffer

were pooled (total volume 20 mL) The procedure yields

35 mg of enzyme with little loss between the steps following heat treatment ( 30% of activity is lost during the heat treatment, which is assumed to be due to association of the enzyme with the large pellet of heat denatured protein obtained at this stage) The enzyme shows a single band

Fig 5 Coomassie blue stained SDS ⁄ PAGE analysis of the purifica-tion of the recombinant P furiosus CoADR Lane 1, crude extract (15 lg); lane 2, heat-treated extract (5 lg); lane 3, pooled fractions from the Q-sepharose column (5 lg); lanes 4 and 5, pooled frac-tions from the size-exclusion column (1 and 2 lg, respectively) The left lane contains marker proteins with the indicated subunit molecular mass (top to bottom): myosin, 195 k; b-galactosidase,

112 k; BSA, 59 k; carbonic anhydrase, 30 k.

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gives a single peak by both conventional and HPLC

size-exclusion chromatography A summary of the purification

spec-trum of phCoADR, which is typical of a flavoprotein, with

Production and assay of the recombinant

pfCoADR

pfCoADR was overexpressed in E coli JM109(kDE3) A

2.8-L Fernbach flask with 325 mL TYP media and

inoculation of overnight culture Cells were grown, protein

production was induced, and cells were harvested as

des-cribed above Cells were disrupted by sonicating for

precipi-tated during the heat treatment were removed by

centrifu-ging in a microcentrifuge for 15 min at 14 000 g

Standard assays

tempera-ture) in 1.5-mL cuvettes All substrates, including oxidized

CoA and dephosphoCoA, were from Sigma (St Louis,

MO) Enzyme and substrate(s) were added to preheated

buffer for a total reaction volume of 840–950 lL Oxidation

of NAD(P)H was monitored at 340 nm The standard

oxid-ase assay used to monitor the purification of phCoADR

was conducted with 100 lm NADH and FAD as above A

unit of CoADR activity is defined as the amount of enzyme

potassium phosphate pH 7.5, 230 lm CoA disulfide and

Protein and enzyme-bound FAD extinction

coefficient determinations

Protein concentrations were determined using a modified

Bradford assay (Bio-Rad Protein Assay, Hercules, CA)

The extinction coefficient of the enzyme-bound FAD in

50 mm Tris pH 7.50 was determined using the following

Quaternary structure determination

The 120-mL Sephacryl S-200 HR (Pharmacia Biotech)

size-exclusion column was used to determine the quaternary

molecular mass of phCoADR The column was eluted with

molecular mass of phCoADR was determined by

(gamma globulin), 44 k (ovalbumin), and 17 k (myoglobin) This result was confirmed by size exclusion HPLC

column

Determination of enzyme free and released thiols

DTNB was used to detect both protein and small molecular mass thiols All determinations used a final concentration

of DTNB of 200 lm Small molecular mass thiols that might be in the form of mixed disulfide on the enzyme (Cys-S-S-R) were determined by reducing the enzyme (56 lm) in an anaerobic titration with NADPH, followed

by cooling the cuvette on ice, opening the cuvette to air, and immediately centrifuging the enzyme on a 30 k mole-cular mass cut-off filter to separate the enzyme from small molecular mass thiols The flow-through from the filtration experiment was assayed for thiol content (providing a measure of small molecular mass thiols), while the retentate was rinsed three times with 50 mm potassium phosphate, 0.5 mm EDTA pH 7.5 and also assayed for thiol content (providing a measure of air-stable, accessible protein thiols)

In order to detect protein thiols that were not stable in air (such as those that may be converted to sulfenic acids), the enzyme was reduced by 0.8 equivalents of NADPH in an anaerobic titration at room temperature (because of a slow turnover of the enzyme with DTNB, more than one equiv-alent of NADPH would result in a DTNB reductase activ-ity), followed by a tip to DTNB The enzyme as purified was assayed for reactive thiols simply by adding DTNB, as above

Thiol stability assays

Thiol assays were performed using DTNB as a thiol detec-tion reagent in a modificadetec-tion of a previously published pro-cedure [25] An aliquot of the thiol to be assayed (generally

100 lL) was removed and added to 900 lL of assay buffer containing (final concentrations) 5 mm DTNB, 0.25 m potassium phosphate, 0.5 mm EDTA pH 7.2 After a 5-min incubation the absorbance was read at 412 nm Thiol con-tent was determined by comparison to a standard curve determined under the same conditions with an extinction

Thermostability and thermoactivity assays

of enzyme was placed in a 2.0-mL microcentrifuge tube and sealed with Parafilm For lower temperatures, the tube was placed in the respective freezer and standard activity assays were performed after 1 month At higher temperatures, a

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