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Báo cáo khoa học: Functional characterization of artemin, a ferritin homolog synthesized in Artemia embryos during encystment and diapause doc

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The encysted embryos cysts are exceptionally resistant to physiologic stress [4–6], undoubtedly due in part to the regulated synthesis of small heat shock proteins sHSPs [7,8].. Monomers

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synthesized in Artemia embryos during encystment and diapause

Tao Chen1,2,*, Tania S Villeneuve1,*, Katy A Garant1, Reinout Amons3 and Thomas H MacRae1

1 Department of Biology, Dalhousie University, Halifax, NS, Canada

2 The College of Animal Science and Technology, Hunan Agricultural University, Changsha, Hunan, China

3 Molecular Cell Biology, LUMC, Leiden University, the Netherlands

Embryos of the crustacean Artemia franciscana may

undergo oviparous development, which involves

cessa-tion of development as gastrulae, encystment, and

dia-pause, the last of these characterized by extremely low

metabolic activity [1–4] The encysted embryos (cysts)

are exceptionally resistant to physiologic stress [4–6],

undoubtedly due in part to the regulated synthesis of

small heat shock proteins (sHSPs) [7,8] As an

exam-ple, the Artemia sHSP p26, present in large amounts in

cysts, functions as a molecular chaperone in vitro

[9–11] In addition, p26 confers thermotolerance on transformed bacteria and transfected mammalian cells and inhibits apoptosis [7,9–12]

Another abundant protein found in Artemia cysts is artemin, which represents 10–15% of the postribosomal protein pool [13] Artemin was purified and sequenced

by Edman degradation, revealing similarity to ferritin but with high content of histidine and cysteine⁄ cystine [14,15] Monomers of artemin are 26 kDa in molecular mass and, like ferritin, they form rosette-like oligomers

Keywords

Artemia franciscana; artemin; diapause;

ferritin; molecular chaperone

Correspondence

T H MacRae, Department of Biology,

Dalhousie University, Halifax, NS, B3H 4J1,

Canada

Fax: +1 902 494 3736

Tel: +1 902 494 6525

E-mail: tmacrae@dal.ca

*These authors contributed equally to this

work

(Received 2 September 2006, revised 8

November 2006, accepted 19 December

2006)

doi:10.1111/j.1742-4658.2007.05659.x

Oviparously developing embryos of the crustacean Artemia franciscana encyst and enter diapause, exhibiting a level of stress tolerance seldom seen

in metazoans The extraordinary stress resistance of encysted Artemia embryos is thought to depend in part on the regulated synthesis of artemin,

a ferritin superfamily member The objective of this study was to better understand artemin function, and to this end the protein was synthesized

in Escherichia coli and purified to apparent homogeneity Purified artemin consisted of oligomers approximately 700 kDa in molecular mass that dis-sociated into monomers and a small number of dimers upon SDS⁄ PAGE Artemin inhibited heat-induced aggregation of citrate synthase in vitro, an activity characteristic of molecular chaperones and shown here to be shared

by apoferritin and ferritin This is the first report that apoferritin⁄ ferritin may protect cells from stress other than by iron sequestration Stably trans-fected mammalian cells synthesizing artemin were more resistant to heat and H2O2 than were cells transfected with vector only, actions also shared

by molecular chaperones such as the small heat shock proteins The data indicate that artemin is a structurally modified ferritin arising either from a common ancestor gene or by duplication of the ferritin gene Divergence, including acquisition of a C-terminal peptide extension and ferroxidase cen-ter modification, eliminated iron sequestration, but chaperone activity was retained Therefore, because artemin accumulates abundantly during devel-opment, it has the potential to protect embryos from stress during encyst-ment and diapause without adversely affecting iron metabolism

Abbreviations

sHSP, small heat shock protein.

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of approximately 600 kDa consisting of 24 subunits.

Artemin cDNA has been cloned and sequenced,

confirming that the protein is a ferritin homolog [16]

Artemin oligomers appear not to bind iron [15], a

finding corroborated by molecular modeling, which

indicates that the internal metal-binding cavity

charac-teristic of ferritin is filled by a C-terminal peptide

exten-sion of 35 amino acid residues [16,17] Only oviparously

developing Artemia embryos produce artemin [18], and

it is degraded in larvae along with artemin mRNA

[14,16,19,20] Artemin is extremely heat-stable and binds

RNA at high temperature in vitro, suggesting a role in

RNA protection [13], as was proposed for a 19S protein

shown to be artemin [19,20] However, in spite of these

results, artemin function during Artemia embryo

development remained uncertain

It is shown in this article that artemin prevents

heat-induced denaturation of citrate synthase in vitro, a

capability shared by apoferritin and ferritin, and

con-fers stress tolerance on transfected mammalian cells

Artemin and ferritin may have arisen from the same

ancestor gene or by duplication of the ferritin gene

Subsequent divergence yielded a protein that no longer

sequesters metal but retains activities characteristic of

molecular chaperones Thus, the results suggest that

artemin, which accumulates in large amounts, protects

oviparously developing Artemia embryos from stress

without affecting iron metabolism

Results

Artemin synthesis and purification

Coomassie Blue-stained gels of protein extracts from

Artemia cysts contained a major artemin polypeptide

that migrated at approximately 32 kDa, a molecular

mass greater than that observed in earlier work [13]

This protein reacted strongly with antibody to artemin

on western blots, as did a second, lighter-staining

band, of approximately twice the molecular mass

(Fig 1A,B, lane 1) Protein extracts from

anhydrotetra-cycline-induced Escherichia coli transformed with an

artemin cDNA-containing expression vector also

exhibited two antibody-reactive polypeptides of

equiv-alent relative sizes, both of which were missing from

bacteria transformed with vector lacking artemin

cDNA (Fig 1A,B, lanes 2 and 3) These polypeptides

were larger than artemin in cyst extracts, due to the

6xHN tag, and they migrated more slowly than

antici-pated on the basis of calculated molecular mass, as

observed for artemin from Artemia Purification on

TALON yielded a single polypeptide as indicated by

Coomassie Blue staining, although silver staining

detected three polypeptides, including a light band twice the mass of the major band, and a smaller poly-peptide (Fig 1A, lanes 4 and 5) All three polypoly-peptides detected by silver staining reacted with antibody to artemin (Fig 1B, lane 4), and the major band (single arrowhead) was identified as artemin by mass spectometry

Artemin oligomerization

As determined by sucrose density gradient centrifuga-tion and chromatography on Sepharose 6B, bacterially produced artemin consists of oligomers approximately

700 kDa in molecular mass (24 monomers) and a les-ser amount of smaller aggregates (Fig 2A,B) Purifica-tion had little effect on oligomer mass (Fig 2C), indicating that the protein retained its native confor-mation and was suitable for use in chaperone assays Electron microscopy of negatively stained samples revealed well-defined particles 14–16 nm in diameter,

A

B

Fig 1 Purification of artemin Protein samples were electrophore-sed in SDS polyacrylamide gels that were stained with Coomassie Blue (lanes 1–4) and silver (lane 5) (A), or blotted onto nitrocellulose and stained with antibody to artemin (B) Lane 1, protein extract from Artemia cysts; lane 2, protein extract from E coli transformed with vector containing artemin cDNA; lane 3, protein extract from

E coli transformed with vector only; lane 4, purified artemin; lane 5, purified artemin Lanes 1–3 received 5 lg of protein, and lanes 4 and 5 received approximately 1 lg of protein , artemin in cyst extract; *, artemin in E coli extract; single arrowhead, artemin monomer; double arrowhead, artemin doublet Molecular mass markers · 10)3are on the left.

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although particles as large as 18 nm were sometimes

observed, and confirmed the oligomeric status of

puri-fied artemin (Fig 2D) In contrast to apoferritin, and

more so for ferritin, which contains iron (Fig 2E,F),

the absence of electron-dense central regions within

negatively stained particles of artemin indicated the

lack of metal storage capacity

Artemin, apoferritin and ferritin inhibit citrate

synthase denaturation

Artemin, apoferritin and ferritin protected citrate

syn-thase against denaturation at 43C in a

concentration-dependent manner (Fig 3A–C) Maximal protection

was obtained at a chaperone⁄ substrate molar ratio of

2 : 1, and increasing this ratio to 4 : 1 had little effect

on activity (not shown) At a molar ratio of 0.5 : 1,

protection was marginal BSA and IgG at 600 nm

(molar ratio of 4 : 1) failed to prevent heat-induced

denaturation of citrate synthase, indicating the absence

of nonspecific protection (Fig 3D)

Artemin confers stress resistance on stably

transfected mammalian cells

Artemin promoted survival of stably transfected

mam-malian cells upon exposure to thermal and oxidative

stress (Fig 4A,B) For example, approximately 90% of

artemin-containing cells endured a 30 min heat shock,

as opposed to only 17% of those lacking the protein

(Fig 4A) In comparison, 55% of cells containing

arte-min survived incubation in 0.50 mm H2O2 for 45 min,

whereas only 15% without artemin were viable

(Fig 4B) The presence of artemin in transfected but

not nontransfected cells was verified by probing of western blots (Fig 4C,D) Occasionally, an antibody-reactive polypeptide comigrated with artemin on western blots containing cell-free extract from non-transfected cells, but when present, it stained very lightly and was considered to result from nonspecific antibody cross-reactivity The production of

aB-crys-A

B

C

Fig 2 Oligomer formation by artemin (A) Artemin-containing

bac-terial extracts were centrifuged on sucrose gradients, and samples

obtained after fractionation were electrophoresed in SDS

polyacryl-amide gels, blotted onto nitrocellulose, stained with antibody to

artemin (inset), and scanned The pixel density in arbitrary units of

each protein band was plotted against fraction number The bottom

of the gradient is on the left, and fractions are numbered All lanes,

with the exception of lanes 5 and 6, which received 0.5 lL, were

loaded with 6 lL of sample (B) Artemin-containing bacterial

extracts were fractionated in Sepharose CL-6B, and samples were

probed with antibody to artemin, as described for sucrose gradients

(inset) (C) Purified artemin was centrifuged in sucrose gradients,

and the A280of each fraction was plotted against fraction number.

Molecular mass markers carbonic anhydrase (29 kDa) BSA

(66 kDa), alcohol dehydrogenase (150 kDa), b-amylase (200 kDa),

apoferritin (443 kDa) and thyroglobulin (669 kDa) are indicated by

numbered open circles Purified artemin (D), apoferritin (E) and

ferri-tin (F) were negatively stained with uranyl acetate, and examined

by electron microscopy The bar represents 100 nm.

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tallin, HSP27, HSP60, HSP70 and HSP90 was not

enhanced in transfected cells, indicating that protection

against stress was not due to induction of these

molecular chaperones by artemin (Fig 5)

Discussion

Encysted Artemia embryos exhibit a level of stress

tolerance almost unknown among other metazoans,

and unusual characteristics such as the capacity to

sur-vive extended anoxia [4–6] and repeated

dehydra-tion⁄ rehydration [21] require exceptional biochemical

adaptation Resistance to stress is provided by the cyst

wall, which is impervious to most substances and

offers structural support [22,23] Another protective

mechanism entails drastic reduction of metabolic

activ-ity, thus limiting resource utilization and

macromolec-ular degradation to a rate sustainable for years [3,4]

Trehalose and molecular chaperones, including the

sHSPs, are produced in excess and are thought to

shield encysted Artemia embryos [2,3,7,8] At least

three sHSPs occur in oviparous Artemia embryos

(unpublished data), of which p26 has been described

[2,9,11,12] Another plentiful cyst protein is artemin,

an oligomeric, heat-stable ferritin homolog that binds

mRNA at high temperature in vitro, but that has an uncertain role in vivo [13,15,16]

A 6xHN-tagged derivative of artemin was synthes-ized in E coli and purified by affinity chromatography,

a relatively mild procedure Purified artemin occurred mainly as large oligomers similar to those in protein extracts from transformed bacteria and Artemia cysts [15], indicating minimal disruption of structure during chromatography Artemin dimers were observed upon electrophoresis, perhaps reflecting the presence of sta-ble disulfide bonds formed during oligomerization by the many cysteines that characterize the protein [16] Artemin effectively prevented heat-induced denatura-tion of citrate synthase at artemin⁄ substrate molar

A

B

D C

Fig 4 Artemin confers stress tolerance upon mammalian cells (A) Mammalian cells transfected with the artemin cDNA-containing expression vector (nonshaded bars) or with vector only (shaded bars) were heated at 46 C for the indicated times, and viability was determined by crystal violet staining The data represent the mean ± standard error of three independent experiments Inset, stained flasks of cells transfected with vectors containing (left) and lacking (right) artemin cDNA that were heated for 30 min (B) Mam-malian cells transfected with the artemin cDNA-containing expres-sion vector (nonshaded bars) or with vector only (shaded bars) were exposed to either 0.25 m M (1, 2) or 0.50 m M (3, 4) H 2 O 2

(exposures follow the same order at each time), and then proc-essed as described Inset, crystal violet-stained flasks of cells trans-fected with vectors containing (left) and lacking (right) artemin cDNA that were exposed to 0.50 m M H 2 O 2 for 30 min Protein samples obtained from transfected cells prior to stressing were electrophoresed in SDS polyacrylamide gels and either stained with Coomassie Blue (C) or blotted onto nitrocellulose and probed with antibody to artemin (D) 1, cells transfected with empty vector; 2, cells transfected with the artemin cDNA-containing vector.

Fig 3 Artemin, apoferritin and ferritin prevent heat-induced

dena-turation of citrate synthase (A) Purified artemin was incubated at

43 C with 150 n M citrate synthase, and solution turbidity was

measured at 360 nm Artemin concentrations were: 1, 0.0 n M ;

2, 75 n M ; 3, 150 n M ; 4, 225 n M ; 5, 300 n M Experiments were done

in duplicate, and the standard error ranged from 0 to 0.005 The

assays were repeated in duplicate for apoferritin (B) and ferritin (C)

at the concentrations used for artemin, with standard error ranging,

respectively, from 0 to 0.004 and from 0 to 0.003 (D) Citrate

syn-thase at 150 n M was incubated at 43 C in the absence of other

proteins (1) and in the presence of either BSA (2) or IgG (3) at

600 n M

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ratios of 2 : 1, and similar results were obtained for

apoferritin and ferritin Moreover, like the Artemia

sHSP p26 [9,11], artemin functions in the absence of

ATP, presumably a benefit during diapause, when

metabolism is reduced Transfected mammalian cells

synthesizing artemin were substantially more tolerant

of heat and oxidative stress than cells transfected with

vector only However, artemin accumulation was

relat-ively low as judged by staining intensity on western

blots and in comparison to the protein in cyst extracts,

suggesting that it protected transfected cells in a way

other than by indiscriminate binding to denaturing

proteins In this vein, Artemia p26 inhibits apoptosis in

transfected mammalian cells [12] On the basis of these

observations, artemin has the potential to protect

Artemia embryos during physiologic insult, either by

influencing discrete cellular processes, as a molecular

chaperone with a broad substrate range, or by a

com-bination of these capabilities Moreover, the results

expand the potential protective role of apoferritin⁄

ferritin in stressed cells, which was previously restricted

to defense against oxidative damage through

modula-tion of iron availability [24–28], although there was a

previous report that ferritin mRNA translation is

enhanced by heat shock [29]

Artemia organisms contain H-ferritin, of which

arte-min is a homolog (Fig 6A,B) The Artemia genes for

artemin and ferritin may have originated from a

com-mon ancestor, or one gene may have arisen by

duplica-tion of the other Of these opduplica-tions, the ubiquitous

phylogenetic distribution of ferritin, in contrast to the apparent restricted dispersal of artemin, implies that a ferritin gene duplicate diverged to yield artemin Sub-sequent mutation of the ferritin gene duplicate elimin-ated the ability of its product to oxidize and sequester iron, but chaperone activity was maintained, ultimately generating artemin, a novel developmentally regulated protein with a potentially important role in Artemia embryogenesis, stress tolerance and diapause

In the proposed evolutionary scheme, artemin and ferritin retained significant sequence identity and

sim-Fig 6 Sequence comparison of artemin and ferritin (A) CLUSTALW

was used to compare ferritin sequences ON, Oncometopia nigri-cans, accession number AAU95196; HC, Homalodisca coagulata, AAT01076; AF, Artemia franciscana, AAL55398; ON2, Oncorhyn-chus nerka, AAK08117; SS, Salmo salar, AAB34575; TN, Tetraodon nigroviridis, CAF92096; RC, Rana catesbeiana, AAA49525; XL, Xen-opus laevis, AAB20316; AJ, ApostichXen-opus japonicus, AAY89589 (B) CLUSTALW was used to compare Artemia ferritin and artemin Boxed residues, ferritin di-iron ferroxidase center; boxed and sha-ded residues, pore gate paired residues; shasha-ded cysteines may function in oligomer formation and protein stabilization; the artemin C-terminal extension is shaded *, identical residues; :, conserved substitution; , semiconserved substitution; –, no residue.

Fig 5 Artemin does not induce synthesis of stress proteins in

transfected cells Protein samples from 293H cells prior to

stress-ing were electrophoresed in SDS polyacrylamide gels, blotted onto

nitrocellulose, and stained with antibody to aB-crystallin (aB-cry),

HSP27, HSP60, HSP70 and HSP90 1, 20 lg of nontransfected

293H cell lysate; 2, 20 lg of lysate from 293H cells transfected

with empty vector; 3, 20 lg of lysate from 293H cells transfected

with vector containing artemin cDNA; 4, 0.1 lg of purified

a-crystal-lin (top panel) and 20 lg of lysate from heat-shocked HeLa cells

(lower four panels).

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ilar oligomer size, but differences accrued A major

change was the acquisition by artemin of a C-terminal

extension thought to fold inward and fill the cavity

enclosed by the oligomer shell The equivalent space in

ferritin sequesters iron [17,30–33], and each H-ferritin

subunit possesses a dinuclear ferroxidase center

com-posed of six conserved residues arranged as catalytic

sites A and B, which, by using Fe2+ and oxygen as

substrates, produce a hydrous ferric oxide mineral

within the protein cavity Artemin lacks all but one of

the residues constituting the di-iron ferroxidase center,

although these residues are conserved in Artemia

ferr-itin (Fig 6A,B), and as a consequence artemin does

not catalyze iron mineralization Because metal

bind-ing is prevented, artemin is unlikely to disrupt iron

homeostasis during embryo encystment and early

dia-pause, when cysts are metabolically active [34], and the

concentration of the protein is high Embryos would

also be compromised if intracellular iron were

unavail-able when diapause was broken, because inorganic

constituents of metabolic pathways would not be able

to traverse the cyst shell Despite the modifications to

the ferroxidase center residues, artemin retains three of

four pore gate paired residues, with the fourth residue

being a conserved substitution (Fig 6A,B)

The chaperone activity of artemin relative to

apo-ferritin⁄ ferritin is essentially unaffected by the

struc-tural differences between the proteins, but artemin is

available in large quantities during development The

advantage to oviparously developing embryos of

arte-min accumulation is that chaperoning capacity is

greatly increased, thus improving stress endurance

Accumulation may occur because the artemin gene is

under control of a regulatory element that promotes

transcription during oviparous development Other

possibilities include enhanced mRNA stability and⁄ or

high translation rate, low susceptibility to proteolytic

degradation as a result of disulfide bridges arising from

increased cysteine content, or a combination of these

factors It is of interest, in the context of artemin

sta-bility, that disulfide bond formation in Hsp16.3, an

sHSP from Mycobacterium tuberculosis, disrupts

chap-erone activity, and this was offered as an explanation

for the low number of cysteines in molecular

chaper-ones [35] This idea does not hold for artemin, and

may reflect mechanistic differences between artemin

and the sHSPs

To summarize, apoferritin and ferritin possess the

ability to inhibit heat-induced protein denaturation, an

activity characteristic of molecular chaperones and that

suggests for the first time that their ability to protect

cells subject to stress extends beyond iron

sequestra-tion and prevensequestra-tion of oxidative damage Moreover,

the data support the proposal that artemin arose from ferritin by gene duplication; subsequent divergence eliminated a role in iron homeostasis, but left the chaperone activity intrinsic to apoferritin⁄ ferritin unchanged Accumulation of artemin in large amounts

by one or more undetermined mechanisms, but per-haps dependent on the stabilization of artemin by disulfide bonds, has the potential to increase stress resistance in oviparously developing Artemia embryos Thus, artemin has the characteristics of a novel molecular chaperone, and it will be interesting to determine how it functions in vivo, because it may have both RNA and protein substrates

Experimental procedures

Construction of expression plasmids

Artemin cDNA (accession number AY062896) was ampli-fied by PCR, employing primers 5¢-GTGGTCGACATGGC AACAGAAGGTGCAAG-3¢ and 5¢-GGGATCCAACTTG GACGGGCAACTC-3¢, respectively, containing Sal1 and BamH1 restriction sites, inserted into the TA cloning vector pCR2.1 (Invitrogen, San Diego, CA, USA), and used to transform E coli DH5a The artemin cDNA insert was excised from the TA vector with SalI and BamHI, and fol-lowing electrophoresis in agarose, was recovered with the GFX PCR and Gel band purification kit (Amersham Bio-sciences, Piscataway, NJ, USA) Artemin cDNA was then cloned into the 6xHN-tagged prokaryotic expression vector pPROTet.E133 (BD Biosciences Clontech, Mississauga,

ON, Canada) and transformed into E coli strain BL21PRO (BD Biosciences Clontech) For expression in mammalian cells, artemin cDNA was amplified by PCR with primers 5¢-GATCCTCGAGTTAACTATAGAAGACACGGG-3¢

inserted into pCR2.1, and used to transform E coli DH5a The insert was recovered from pCR2.1 with BamHI and XbaI, and cloned into the eukaryotic expression vector pcDNA3.1(+) (Invitrogen) cDNA was sequenced at the DNA Sequencing Facility, Centre for Applied Genomics, Hospital for Sick Children, Toronto, ON, Canada

Artemin purification

Transformed E coli cells were grown at 37C with shaking

in Difco Luria Broth Base, Miller (LB) (Becton, Dickinson and Co., Sparks, MD, USA) containing spectinomycin

(Sig-ma, Oakville, ON, Canada) at 50 lgÆmL)1 and chloram-phenicol (Sigma) at 34 lgÆmL)1 Anhydrotetracycline (BD Biosciences Clontech) was added to 400 ngÆmL)1when cul-ture A600 reached approximately 0.5, and incubation was continued for 8 h at 37C, after which protein extracts were prepared [10] Induction of bacteria under reduced

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aeration improved artemin yield over that obtained in

well-aerated flasks Artemin was purified on BD TALON

Metal Affinity Resin (BD Biosciences Clontech), following

the manufacturer’s instructions and using an equilibration⁄

washing buffer of 50 mm Na2HPO4, 500 mm NaCl, and

10 mm imidazole (pH 7.5) Artemin purification was

evalu-ated by electrophoresis in SDS polyacrylamide gels

fol-lowed by either Coomassie Blue or silver staining [36]

Artemin purification was also monitored by blotting

pro-teins resolved in SDS polyacrylamide gels onto

nitrocellu-lose membranes and probing with antibody to artemin

followed by horseradish peroxidase-conjugated goat

anti-rabbit IgG (Jackson ImmunoResearch, Mississauga, ON,

Canada) [12] The primary antibody to purified bacterially

produced artemin was prepared in rabbit using TitreMax

Gold Adjuvant (Sigma) Rabbits were obtained from

Charles River Canada (St Constant, Quebec, Canada) and

cared for in accordance with guidelines in ‘Guide to the

Care and Use of Experimental Animals’ available from the

Canadian Council on Animal Care The identity of

anti-body-reactive purified proteins as artemin was confirmed by

mass spectometry [36]

Artemin oligomerization

Bacterial extracts containing artemin were applied to

con-tinuous 10 mL, 10–40% sucrose gradients in 0.1 m

Tris⁄ glycine buffer (pH 7.4), and centrifuged at 200 000 g

for 15 h at 4C in a Beckman SW41 Ti rotor Fractions

of 0.74 mL were collected, and samples were

electrophore-sed in 12.5% SDS polyacrylamide gels, blotted onto

nitro-cellulose membranes, and probed with antibody to

artemin Bacterial extracts containing artemin were also

chromatographed at 10 mLÆh)1 in Sepharose CL-6B (Sigma)

columns (1.0 cm diameter· 50 cm length) equilibrated

with 0.1 m Tris⁄ glycine (pH 7.4) One-milliliter fractions

were collected and probed with antibody to artemin after

SDS⁄ PAGE and blotting onto nitrocellulose membranes

Artemin band densities on blots were measured at

400 dots per inch with an UMAX Astra 1200S scanner

(Dallas, TX, USA) and plotted against fraction numbers

[12] Purified artemin was centrifuged on sucrose gradients

as described above, with the protein being detected by

reading the A280 of fractions The monomer molecular

mass of bacterially produced artemin, including the 6xHN

tag, was determined by generunner (version 3.05)

(Hast-ings Software Inc., Hast(Hast-ings on Hudson, NY, USA) to be

28.8 kDa, and this value was used to calculate oligomer

subunit number Molecular mass markers (Sigma) of

14.2 kDa (a-lactalbumin), 29 kDa (carbonic anhydrase),

66 kDa (BSA), 150 kDa (alcohol dehydrogenase), 200 kDa

(b-amylase), 443 kDa (apoferritin) and 669 kDa

(thyro-globulin) were centrifuged separately in gradients or

chro-matographed in Sepharose CL-6B columns, and the A280

values of fractions were determined

Artemin purified on TALON Metal Affinity Resin, horse spleen apoferritin (Sigma) and horse spleen ferritin (Sigma) was applied to formvar-coated copper grids, and samples were stained with 1% uranyl acetate in H2O The grids were examined with a Philips Tecnai transmission electron microscope, and images were captured using analysis, version 2.1 (Soft Imaging System Corp., Lakewood, CO, USA)

Inhibition of citrate synthase denaturation by artemin, apoferritin and ferritin

Citrate synthase (Sigma) at 150 nm in 40 mm Hepes⁄ KOH buffer (pH 7.5) was heated at 43C as done previously to determine sHSP chaperone activity [9–11], although in this case the assay was performed in the absence and presence

of artemin, apoferritin and ferritin Molarity was based on monomer molecular mass for all proteins The purified arte-min was centrifuged (1500 g at room temperature for 2 min, using Spectrofuge 16M centrifuged with an 18 place rotor) through Pierce Protein Desalting Spin columns equil-ibrated with 40 mm Hepes⁄ KOH buffer (pH 7.5) to remove imidazole Solution turbidity was monitored at 360 nm with

a Perkin Elmer (Montreal, QB, Canada) Lambda 3B

UV⁄ VIS spectrophotometer

Stress resistance of mammalian cells containing artemin

Mammalian 293H kidney cells were transfected in the pres-ence of Lipofectamine 2000 (Invitrogen) [12] with the expression vector pcDNA3.1(+) (Invitrogen) either con-taining or lacking artemin cDNA, and stable transfectants were selected in Geneticin (Invitrogen) Artemin synthesis was detected by probing western blots containing protein extracts of transfected cell lines resolved in SDS polyacryla-mide gels To prepare protein extracts, cells grown to con-fluence in 100 mm tissue culture dishes were rinsed with NaCl⁄ Pi (140 mm NaCl, 2.7 mm KCl, 8.0 mm Na2HPO4, 1.5 mm KH2PO4, pH 7.4), recovered by scraping in 100 lL

of whole cell extraction buffer (25 mm Na2HPO4, 400 mm NaCl, 0.5% SDS, 0.04 mgÆmL)1 each of soybean trypsin inhibitor, leupeptin and pepstatin A, 0.08 mgÆmL)1 phenyl-methylsulfonyl fluoride, pH 7.2), transferred to an Eppen-dorf tube, and placed in a boiling H2O bath for 10 min The homogenate was cooled, and centrifuged for 10 min in

a microcentrifuge; the supernatant was either used immedi-ately or frozen at ) 20 C Protein concentrations were determined with the Bio-Rad (Mississauga, ON, Canada) protein assay

To test stress resistance, transfected 293H cells were seeded at 5· 105cellsÆmL)1in 30 mm dishes and incubated

at 37C for 24 h under 5% CO2 in DMEM (Invitrogen) containing 10% fetal bovine serum (Invitrogen) and 1%

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antibiotic–antimycotic (Invitrogen) The dishes were sealed

with Parafilm, heated at 46C for up to 1 h, and then

incubated at 37C for 24 h, with cell viability being

deter-mined by use of crystal violet (Sigma), except that cells

were incubated for 1 week before staining [12] The results

were plotted as the average, with standard error, of three

experiments Stably transfected cells prepared as described

above were also exposed to either 0.25 or 0.50 mm H2O2

(Sigma) for up to 1 h, and then incubated at 37C for 24 h

before determination of viability Artemin production was

confirmed by electrophoresis of transfected cell protein

extract in SDS polyacrylamide gels, blotting onto

nitrocel-lulose, and reacting with antibody

Protein extracts from transfected mammalian cells were

probed with antibodies to aB-crystallin, HSP27, HSP60,

HSP70 and HSP90 (Stressgen, Victoria, BC, Canada) to

deter-mine whether artemin induced their synthesis aB-crystallin

(Stressgen) and HeLa cell lysates (Stressgen) were used to

confirm antibody activity

Acknowledgements

This work was supported by the Heart and Stroke

Foundation of Nova Scotia, the Natural Sciences and

Engineering Research Council of Canada, the Nova

Scotia Health Research Foundation, and the Canadian

Institutes of Health Research The authors thank Paul

O’Connell, Devanand Pinto and Alan Doucette for

assistance with mass spectometry

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