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Tiêu đề Cloning and expression of sterol D14-reductase from bovine liver
Tác giả Rita Roberti, Anna Maria Bennati, Giovanni Galli, Donatella Caruso, Bruno Maras, Cristina Aisa, Tommaso Beccari, Maria Agnese Della Fazia, Giuseppe Servillo
Trường học University of Perugia
Chuyên ngành Biochemistry
Thể loại bachelor thesis
Năm xuất bản 2002
Thành phố Perugia
Định dạng
Số trang 8
Dung lượng 458,14 KB

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Amino- acid sequence analysis of a 38-kDa protein purified from bovine liver in our laboratory revealed > 90% similarity with a human sterol reductase, SR-1, encoded by the TM7SF2 gene,

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Cloning and expression of sterol A14-reductase from bovine liver

Rita Roberti', Anna Maria Bennati', Giovanni Galli?, Donatella Caruso2, Bruno MarasỶ, Cristina Aisa‘, Tommaso Beccari*, Maria Agnese Della Fazia* and Giuseppe Servillo*

' Department of Internal Medicine, University of Perugia, Italy; * Department of Pharmacological Sciences, University of Milan, Italy; *Department of Biochemical Sciences ‘A Rossi Fanelli’, Universita ‘La Sapienza Roma, Italy;

4 Department of Biochemical Sciences and Molecular Biotechnology, University of Perugia, Italy

Biosynthesis of cholesterol represents one of the funda-

mental cellular metabolic processes Sterol Al4-reductase

(A14-SR) is a microsomal enzyme involved in the con-

version of lanosterol to cholesterol in mammals Amino-

acid sequence analysis of a 38-kDa protein purified from

bovine liver in our laboratory revealed > 90% similarity

with a human sterol reductase, SR-1, encoded by the

TM7SF2 gene, and with the C-terminal domain of human

lamin B receptor A cDNA encoding the 38-kDa protein,

similar to human TM7SF2, was identified by analysis

of a bovine expressed sequence tag (EST) database

The cDNA was synthesized by RT-PCR, cloned, and

sequenced The cDNA encodes a 418 amino-acid poly-

peptide with nine predicted transmembrane domains The

deduced amino-acid sequence exhibits high similarity with

Al4-SR from yeasts, fungi, and plants (55-59%), sug- gesting that the bovine cDNA encodes Al4-SR Northern blot analysis of bovine tissues showed high expression of mRNA in liver and brain The polypeptide encoded by the cloned cDNA was expressed in COS-7 cells Immu- nofluorescence analysis of transfected cells revealed a distribution of the protein throughout the ER COS-7 cells expressing the protein exhibited Al4-SR activity about sevenfold higher than control cells These results demonstrate that the cloned bovine cDNA encodes A14-

SR and provide evidence that the human 7M7SF2 gene encodes Al4-SR

Keywords: sterol biosynthesis; sterol reductase; cloning; endoplasmic reticulum

Sterol Al4-reductase (Al4-SR), an essential enzyme for

sterol biosynthesis in eukaryotic cells, is an integral protein

of the ER that acts on A'“(>-ynsaturated sterols in different

organisms In mammalian cells the elimination of a

14a-methyl group from the C30 sterols, lanosterol and

24,25-dihydrolanosterol, during conversion to cholesterol

(C27A°) generates the intermediates 4,4-dimethyl-S-cho-

lesta-8,14,24-trien-3B-ol (C29A*!*™*) and 4,4-dimethyl-So-

cholesta-8,14-dien-3B-ol [1] that are transformed into

4,4-dimethyl-5o-cholesta-8,24-dien-3B-ol (C29A*?*) and

4,4-dimethyl-Sa-cholesta-8-en-3f-ol, respectively, by the

action of Al4-SR [2] The saturation of the Cl4=C15

Correspondence to R Roberti, Department of Internal Medicine,

Laboratory of Biochemistry, University of Perugia, Via del Giochetto,

06122 Perugia, Italy Fax: + 39 0755857428, Tel.: + 39 0755857426,

E-mail: roberti@unipg.it

Abbreviations: A14-SR, sterol Al4-reductase; SR-1, sterol reductase 1;

LBR, lamin B receptor; C29A81424 4,4-dimethyl-S5a-cholesta-8, 14,24-

trien-3B-ol; C29A**, 4,4-dimethyl-5e-cholesta-8,24-dien-3B-ol;

C27A° 4 5a-cholesta-8,14-dien-3B-ol; C27AŸ, 5œ-cholesta-8-en-3-ol;

C27A°, cholesterol; E-64, N-[N-(L-3-trans-carboxyrane-2-carbonyl)-L-

leucyl]-agmantine; EST, expressed sequence tag; DMEM, Dulbecco’s

modified Eagle’s medium; PVDF, poly(vinyiledene difluoride);

FITC-conjugated, fluorescein isothiocyanate-conjugated; EPT,

ethanolaminephosphotransferase

Note: the nucleotide sequence reported in this paper has been

submitted to GenBank and is available under accession number

AY03968 1

(Received 2 August 2001, revised 26 October 2001, accepted 31

October 2001)

double bond may occur at different stages of the pathway leading from C30 to C27 sterols [3,4]

Biochemical characterization, solubilization, and purifi- cation of Al4-SR from rat liver have been reported [5,6] The liver enzyme is responsive to cholesterol lowering agents, as well as to changes in diet and circadian rhythm [6] Al4-SR has been cloned from yeast [7-9] and fungi [10] Gene cloning of Al4-SR from Arabidopsis thaliana and analysis of mutants has highlighted the role of the protein in cell growth and embryonic development of the plant [11,12]

Inherited human disorders caused by defects in choles- terol biosynthesis have been identified, suggesting a major role for cholesterol and/or intermediates of biosynthesis in embryogenesis and morphogenesis [13] Among these, the Greenberg skeletal dysplasia has been hypothesized to originate from Al4-SR deficiency [14] In addition, interest

in the C29A*!*** and C29A**" sterols has been consid- erably stimulated by the finding that they play a crucial role during meiosis in mammals [15] The C29A*!4™* sterol is a positive regulator of the nuclear receptor LXRa [16] These data indicate that Al4-SR is one of the regulatory enzymes in the complex pathway of cholesterol biosynthesis

Recently the human lamin B receptor (LBR), an integral protein of the inner nuclear membrane, has been shown to exhibit Al4-SR_ activity [17] Two protein paralogues of human LBR, sharing high similarity with plant and yeast sterol reductases, have been identified These proteins, sterol reductase 1 and 2 (SR-1 and SR-2), are encoded by TM7SF2 and DHCR7 genes, respectively [18-20] SR-2 is sterol A7-reductase, a Smith—Lemli—Opitz syndrome-related

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protein [19-22], whereas no functional characterization of

the TM7SF2 gene product has been reported It has been

hypothesized that human 7M7SF2 encodes A14-SR [13,23],

but upon expression in yeast, no sterol Al4-, A7-, or A24-

reductase activities were detected [13]

We isolated a 38-kDa protein from bovine liver ER witha

high degree of identity with both human SR-1 and human

LBR A cDNA encoding this protein was identified by

bovine expressed sequence tag (EST) analysis, cloned, and

expressed as a functional Al4-SR

MATERIALS AND METHODS

Chemicals

M-MLYV reverse transcriptase, lipofectamine reagent, Dul-

becco’s modified Eagle’s medium (DMEM), and foetal

bovine serum were purchased from Gibco-BRL (Milan,

Italy) TOPO-cloning kit was from Invitrogen (Leek, the

Netherlands) RNAse inhibitor was from Ambion (Austin,

TX, USA) The Expand Long Template PCR System,

Staphylococcus aureus V8 protease, N-[N-(L-3-trans-carb-

oxyrane-2-carbonyl)-L-leucyl]-agmantine (E-64), leupeptine,

phenylmethylsulfonyl fluoride (PMSF), and thesit were all

purchased from Roche Molecular Biochemicals (Milan,

Italy) Q-Sepharose fast flow, 5a-cholestane, glucose oxi-

dase, reduced glutathione, NADPH, commercial antibod-

ies, protein A-Sepharose CL 4B, SDS/PAGE reagents, and

enhanced chemiluminescence reagents were from Sigma

(Milan, Italy) Biogel HTP was from Bio-Rad (Milan,

Italy) Poly(vinylidene difluoride) (PVDF) membranes

(Immobilon PS) were purchased from Millipore (Bedford,

MA, USA) 5o-cholesta-8,14-dien-3B-ol (C27A*") was

synthesized according to Fieser & Ourisson [24] Diacyl-

glycerol was prepared from egg yolk as described previously

[25] Other reagents were from Gibco-BRL and Sigma

Isolation of sterol A14-reductase

Bovine A14-SR was co-purified from liver ER together with

the previously reported ethanolaminephosphotransferase

(EPT) [25] Briefly, microsomes (3 mg proteinmL™') were

solubilized with 1.5% thesit in the presence of | mm NaCl

and diacylglycerol (0.3 mgmL7') The purification proce-

dure included chromatography on Biogel HTP and two

chromatographic steps on Q-Sepharose, performed at

pH 7.0 and pH 8.5, as described previously [25] The

protein preparation was concentrated and freed of lipids

as follows The sample was dialysed extensively against

distilled water and freeze-dried The residue was suspended

in a 10-mL mixture of chloroform/methanol (1 : 9, v/v) for

10 min at 37 °C The insoluble protein pellet was recovered

by centrifugation and the extraction was repeated twice The

protein pellet was vacuum dried, resuspended in 5% SDS

and adjusted to 100 mm Tris/HCl (pH 6.8), 1% SDS (w/v),

10% glycerol (v/v), and 100 mm dithiothreitol (SDS/PAGE

sample buffer)

Sequence analysis of sterol A14-reductase

A 20-ug aliquot of lipid-free protein was subjected to SDS/

PAGE, electroblotted on a PVDF membrane, and stained

with Coomassie blue The N-terminal amino-acid sequence

was determined by automated Edman degradation using a PerkinElmer model AB 476A sequencer For internal sequence determination the protein (30 1g) was subjected

to SDS/PAGE After staining the gel with Coomassie blue, the 38-kDa band was cut and equilibrated for 10 min with

100 mm Tris/HCl (pH 6.8) containing 12% (v/v) glycerol,

50 mm 2-mercaptoethanol, and 2% (w/v) SDS (buffer A) The slice was then inserted into a gel well and covered with buffer A containing 20% glycerol (v/v) Staphylococcus aureus V8 protease solution (2 ug in 10 uL of buffer A) was layered onto the top [26] The separating gel contained 15% (w/v) polyacrylamide (acrylamide/bisacrylamide

30 : 0.8, w/w) After the sample had been stacked with a 4-mA constant current, the power was turned off for 2 h

at room temperature to achieve proteolysis Fragments were separated by applying a 30-mA constant current and electroblotted on PVDF membrane Bands were excised and amino-acid sequence analysis was performed as described above

The amino-acid sequences were analysed using the BLAST search program (National Center for Biotechnology Infor- mation; http://www.ncbi.nlm.nhi.gov) [27]

Antibody production Polyclonal antibodies against Al4-SR were raised in rabbits

by multiple subcutaneous injections of a solution containing

~50 ug of lipid-free protein preparation in 0.9% NaCl mixed with an equal volume of Freund’s complete adjuvant Boost injections of 50-ug protein were performed 21 and

42 days after the initial administration The IgG fraction was purified on a protein A-Sepharose CL 4B column equilibrated with 0.1 m Tris/HCl (pH 8.0) and eluted with 0.1 m glycine buffer (pH 3.0) [28]

RT-PCR cloning of the bovine cDNA encoding sterol A14-reductase

BLASTN search of the bovine EST database was performed

to identify bovine cDNA clones homologous to human SR-1 cDNA [27] The putative bovine cDNA was used to design PCR primers for amplification of the ORF Total RNA (5 ug), purified from liver as described below, was used to synthesize first-strand cDNA using a reaction mixture containing 50 mm Tris/HCl (pH 8.3), 40 mm KCl, 6mm MgCl, | mm dithiothreitol, 40 UmL™! of RNase inhibitor, 2.5 mm dNTP, 0.2 mm oligo-dT 15—18mer, and

200 U of M-MLYV reverse transcriptase First-strand syn- thesis was performed at 42 °C for 45 min and then the enzyme was inactivated at 90 °C for 5 min Following first- strand synthesis, PCR of 4/4-SR cDNA was carried out using appropriate primers and the Expand Long Template PCR System The two primers used were the sense primer (ŠS-ATTCTAGAAGCGGAGACCATGGCCCCTCCTC AG-3’) and the antisense primer (5-ATTCTAGATAG GGTACAGGCCCTTGTGTCCCG-3’), both bearing the Xbal restriction site (underlined) PCR conditions were as follows: 4 min at 94 °C (1 cycle); 1 min at 94 °C, 1 min at

65 °C, 1 min at 68 °C (30 cycles); 5 min at 68 °C (1 cycle) The RT-PCR product was cloned into the pCR2.1 vector

by TOPO-cloning kit and bidirectionally sequenced at MWG Biotech (Mtinchen, Germany) The PCR product (1370 bp) was used as a probe for Northern blot analysis

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RNA isolation and Northern blot analysis

Total RNA was isolated from different bovine tissues (liver,

brain, lung, skeletal muscle, heart, adrenal, and testis) by

homogenizing the samples in guanidium isothiocyanate

solution (100 mg tissuemL™') followed by CsCl step

gradient centrifugation [29] RNA was denatured in

formamide, separated in denaturing agarose gel (1%

agarose/2.2 m formaldehyde), and blotted onto a nitrocel-

lulose filter The RNAs (20 pg) extracted from different

tissues were hybridized with random priming P cDNA

specific for bovine 4/4-SR [30]

Expression of sterol A14-reductase in COS-7 cells

Bovine 4/4-SR cDNA was subcloned in the Xbal site of the

eukaryotic expression vectors pCS2-myc-tag, containing the

CMV promoter [31], and modified pMT2, containing the

SV40 promoter [32], kindly provided by N S Foulkes

(IGBMC of Strasbourg, France) and F Grignani (Univer-

sity of Perugia, Italy), respectively The cDNA was subcl-

oned in pCS2-myc-tag 3’ to a sequence encoding six copies

of a 13-residue c-myc epitope COS-7 cells were grown in a

5% CO, incubator at 37 °C in DMEM supplemented with

10% foetal bovine serum and 2 mm glutamine Cells were

cultured in 10-cm Petri dishes until 50-80% confluence and

transfected for 5 h with the two plasmids (4 tug) separately,

using lipofectamine in serum-free DMEM Control cells

were transfected with empty pMT2 or pCS2-myc-tag

vectors After transfection, the medium was replaced with

complete DMEM and cells were incubated for 35 h at

37 °C Transfected cells were recovered with 0.9% NaCl

containing 1 mm EDTA, | um leupeptine, 0.1 mm PMSF,

0.3 um E-64 and then sonicated three times for 10 s The

microsomal fraction was prepared by centrifugation of the

500 g supernatant at 100 000 g for 1 h at 4 °C The pellet

was resuspended in 10 mm K-phosphate/0.05 mm EDTA

(pH 7.4) Protein concentration was determined by the

method of Bradford [33], using BSA as a standard

Microsomal proteins separated by SDS/PAGE were

blotted on PVDF membranes and incubated with poly-

clonal rabbit anti-(Al4-SR) Ig or monoclonal mouse anti-

(c-myc-tag) Ig, as indicated Peroxidase-conjugated goat

anti-(rabbit IgG) Ig or anti-(mouse IgG) Ig were used as

secondary antibodies The protein was detected by the

enhanced chemiluminescence assay

Indirect immunofluorescence

Transfected COS-7 cells, grown on coverslips, were washed

with NaCl/P; and fixed in ice-cold methanol for 10 min at

—20 °C Cells were subsequently permeabilized by treatment

with 0.1% Triton X-100 in NaCl/P; for 5 min at room

temperature, washed with NaCl/P;, blocked with 3% BSA

in NaCl/P;, and incubated for 60 min at room temperature

with rabbit anti-(Al4-SR) IgG After washing with NaCl/P;

containing 0.1% Tween-20, cells were incubated for 60 min

at room temperature with Cy3-conjugated sheep anti-

(rabbit IgG) Ig Cells transfected with the pCS2-myc-tag

vector were subsequently treated with monoclonal mouse

anti-(c-myc-tag) Ig and fluorescein isothiocyanate-conjugat-

ed (FITC-conjugated) goat anti-(mouse IgG) Ig The cells

were examined by fluorescence microscopy and the images

were acquired by using a Spot-2 cooled camera (Diagnostic Instruments)

Sterol A14-reductase assay A14-SR activity was assayed in microsomes prepared from Al4-SR cDNA-transfected COS-7 cells and from bovine liver, using 5a-cholesta-8,14-dien-3B-ol (C27A*"*) as a substrate [5] The sterol was added as a 0.3-mmM suspension

in 0.8% Tween-80, at 60 uM final concentration (13.5 Lug) to 0.5 mL of a mixture containing 0.1 mM K-phosphate buffer (pH 7.4), 0.5 mm EDTA, | mM reduced glutathione, 2 mm NADPH, 0.14 ™ glucose, and 10 U of glucose oxidase, that had been preincubated for 4 min at 37°C under N> atmosphere Incubation was carried out under N> for

30 min at 37 °C with 0.24 mg of microsomal proteins and terminated by the addition of 1 mL of 20% KOH in 50% methanol, followed by additional 30 min incubation at

37 °C After the addition of 5a-cholestane (5 wg) as an internal standard, sterols were extracted three times with

3 mL of petroleum ether and the organic phases were evaporated to dryness under nitrogen stream

The sterol extracts were acetylated with acetic anhydride- pyridine, 2 : 1 (v/v) for 1 hat 60 °C The samples were taken

to dryness and the residues were dissolved in ethyl acetate Aliquots of the samples were analysed by GC-MS in multiple ion detection mode using a Varian Saturn 2100T apparatus with a Varian CP-Sil8 CB low bleed/MS column Temperature was programmed from 150 to 300°C at

12 °C-min™! Sterol retention times were: 14.5 min, 5o-

cholestane (M* = 372); 18.2 min, cholesterol (M* = 368); 18.3 min, C27A*"* (M~ = 426); 18.5 min, 5øœ-cholesta- 8(9)-en-3B-ol (C27A®, M* = 428)

A14-SR activity was evaluated on the basis of peak area ratios between m/z 426 and m/z 372 ions (C27A*"4/5o- cholestane) or m/z 428 and m/z 372 ions (C27AŸ/5a- cholestane) at the expected retention time

RESULTS AND DISCUSSION

Isolation of sterol A14-reductase During the preparation and delipidation of a bovine liver 38-kDa protein exhibiting EPT activity [25], a protein co- migrating in SDS/PAGE was revealed by amino-acid sequence analysis The determined N-terminal sequence of the protein, APPQGSRAPLEFGGPLGAAALML, was 87% identical to residues 2-24 of human SR-1 (GenBank accession no AF096304) [18] The digestion of the 38-kDa band with S aureus V8 protease produced three major fragments with molecular masses of ~27, 19.5, and 9.5 kDa The 27- and 9.5-kDa fragments confirmed the N-terminal sequence, whereas the sequence of the 19.5-kDa fragment was AVLTTMDITHDGFGFMLAF, 95% iden- tical to residues 243-261 of human SR-1 and 440-458 of human LBR (GenBank accession no L25931) Human SR-1 has been reported to be a sterol reductase, based on similarities with sterol reductases from yeast, fungi, and plants, although its catalytic activity has not been identified [18] Moreover, human SR-1 exhibits 58% identity with the C-terminal domain (residues 197-615) of human LBR [18], which possesses Al4-SR activity [17] For this reason we hypothesized that the purified 38-kDa bovine protein is a

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™ 1

hibri97 197 -F EVTPIRAKDLEFGGVPGVFLIMFGLPVFLFLLLLMCK - QK

Ae 8 Se SSE Sete Bella Sa Sie eee Slee S m6: Bì S m HÔI GÀ 672V 12 sikaiie sisike G3 íŒ6 Am.sE L É

TM 2

ati4ga 1 - - - MLLDMDLGVL|LỊPSLQSVYVLVFYFVYLAVAGELLPGKỆV! RịG|V LỊL

TM 3

bi4s 187 ATLTAFIFSLLLYILKALLAPASA - LAPGGNISGNI|L !I Y|DIF F LỊG hSRE1 137 ATLTAFIFSLFLIY|MKAQVAPVSA- - - - LAPGGNSGN/PI YIDIFFLIG hibri97 333 ATVFCVVLSVYLIYIMRSLKAPRND - LSPAS -ISGNAVY|DIFF I/G at14q 92 TFIFCVLVTLAL]Y|VTGRSSSNKGS- - - SLKPHVISGNL VHIDIWWFIG

™ 5

b1i4sK 22 E QL LỊY|V 6e[D|A L W Y[E E|A V L T TMÍD !ÌI HDGFÍG F ML|A[F GD T Lịa hSR-1 225 |LƒVNGFQL L|Y|V G|DỊA L W HỊE E{A VL T TMID I|THDGFIG FML|AIFGD T Lịa hlbr187 422 |LỊVN SF QL L|Y|V V|DÍA L WN|E E|A LL T TMID I|I HDGF|IG F ML|AIFGD | FIQ at14srẽ 179 |L[Y Q1 ECA LỊY|! L|D|Y F V HỊE ElY MT STWD I|I AERLIG F ML|VỊF GDL LW IỊP FỊT F|S|I|Q

sc 14sr 249 |L]VN F LQG F|Y| I F|DIG V L N|E El|G VL T MMID I|TTDGF|G F ML|AIFGD T Lịa

TM8

ati4a 229 GWWLILHNKVELTVPAIVVNCLVF GIA NIKIQ KIH | |/FIKKN- - - PKTP scl4sr 209 ARYILISVSPVELGWVKVVGILAIM SIA N|KÌQ KỊS EF|RQG - - - -KLE

bi4sr 325

hSR1 325

hlbr197 522

at14sq 276

bi4s 375

hSR-1 375

hlbr187 572

at14 329

Fig 1 Amino-acid sequence alignment of sterol A14-reductase and related sterol reductases Alignment was performed using the om1ca 2.0 program run with the default parameters Positions with consensus residues present in all sequences are boxed Positions with consensus residues present in at least three sequences are shaded Bovine A14-SR (b 14 sr); human SR-1 (h SR-1); residues 197-615 of human lamin B receptor (h Ibr197);

A thaliana A\4-SR (at 14 sr) (GenBank accession no AF256535); S cerevisiae A14-SR (sc 14 sr) (GenBank accession no $69420) For bovine AI4-SR, regions of the deduced amino-acid sequence corresponding to the N-terminal and V8 peptide sequences determined in the sequencing experiments of the protein purified from bovine liver are underlined TmpRED program (ExPASy Molecular Biology Server, http://www.expasy.ch/) was used to predict transmembrane domains, indicated by thick lines on top.

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A14-SR To verify our hypothesis, bovine cDNA encoding

the 38-kDa protein was cloned to identify the catalytic

activity of the expressed protein

Cloning of the cDNA encoding bovine sterol

A14-reductase

Bovine cDNA clones, similar to human SR-/ (TM7SF2),

were retrieved by a BLASTN search in the EST database The

putative cDNA of the bovine Al4-SR was obtained by

aligning four different clones (GenBank accession nos

BE756766, BE756734, BE754556 and AW427392) [34] The

bovine cDNA was synthesized by RT-PCR using synthetic

primers based on the EST sequences, cloned into the

pCR2.1 vector, and sequenced on both strands The cloned

cDNA was 1370 bp long and contained an ORF of

1257 bp, encoding a protein of 418 amino acids with a

calculated molecular mass of 46 751 Da

The N-terminal amino-acid sequence of the protein

purified from liver and the amino-acid sequence of the 19.5-

kDa fragment generated by S aureus V8 protease digestion

corresponded to residues 2—24 and 243-261, respectively, of

the putative protein (Fig 1) In the purified protein, the

N-terminal methionine was cleaved out, as previously

described for most eukaryotic proteins [35] Moreover, the

sequenced 27- and 19.5-kDa fragments appeared to origi-

nate from cleavage of the protein in two parts (Fig 1),

which accounted for the calculated molecular mass of

46.7 kDa Therefore, the discrepancy between the appar-

ent molecular mass of 38 kDa estimated by SDS/PAGE

and the calculated molecular mass may be due to an

aberrant electrophoretic migration, as reported for other

structurally related proteins [19,36]

The putative protein was rich in leucine (19.1%) and

highly hydrophobic, with nine predicted membrane-span-

ning domains (Fig 1) The deduced amino-acid sequence

displayed similarity to putative human SR-1 (92%), the

197-615 domain of human LBR (71%), A thaliana Al4-SR

(59%), Saccharomyces cerevisiae Al4-SR (55%) (Fig 1),

and other sterol reductases [50% and 49% similarity to

human and 4A thaliana sterol A7-reductases, respectively,

and 44% to S cerevisiae sterol A24(28)-reductase]

The EFGGx(2)G signature of sterol A24(28)-reductase

and Al4-SR and the LLxSGWWGx(2)RH signature of

sterol reductases family [37] were present at positions 12-18

and 337-348 of the deduced amino-acid sequence, respec-

tively Ergosterol biosynthesis ERG4/ERG?24 family signa-

tures, Gx(2)[LIVM][YH]Dx[FYV]xGx(2)LNPR — and

[LIVM](2)HRx(2)Rpx(3)Cx(2)K YG [38] were found at

positions 167-182 and 383-399 of the deduced amino-acid

sequence, respectively A leucine-zipper region was present

at position 139-160

The presence of signature patterns conserved from yeast

Al4-SR (ERG24 gene) and sterol A24(28)-reductase (ERG4

gene), as well as the degree of similarity with human LBR

and Al4-SR from plants and yeast, strongly suggest that the

cloned cDNA corresponds to A/4-SR

Sterol A14-reductase mRNA expression in bovine tissues

Northern blot analysis of bovine tissues was performed with

Al4-SR cDNA A single transcript of ~ 1.8 kb was detected

in different tissues High levels of mRNA expression were

found in liver and brain (Fig 2) No transcript was detected

in the heart, contrary to TM7SF2, highly expressed in the human tissue [18]

Expression of sterol A14-reductase cDNA

in transfected COS-7 cells Western blot analysis Immunoblot analysis of the ex- pressed A/4-SR cDNA was performed using a polyclonal antibody raised against the bovine liver Al4-SR The antibody recognized a single band of ~38 kDa both in Al4-SR transfected cells and in bovine liver microsomes (Fig 3) No protein was detected in cells transfected with control vector The expressed myc-tag-A14-SR was detected

by both anti-(Al4-SR) Ig and anti-(c-myc) Ig as a protein of

=~ 56 kDa, consistent with the fusion of six myc epitopes (= 9.3 kDa) at the N-terminus of the protein (Fig 3) Cellular localization The cellular localization of myc-tag- Al4-SR was examined in transiently transfected COS-7 cells Double immunofluorescence analysis of cells showed a similar labelling pattern with anti-(myc-tag) Ig and anti- (A14-SR) Ig (Fig 4) The images showed that the newly formed protein was distributed throughout the ER in the proximity of the nucleus The same localization was observed in transfected cells over-expressing Al4-SR; no label was observed in control cells These results are consistent with the known subcellular localization of the enzymes involved in cholesterol biosynthesis and with the purification of the bovine protein from the ER

Determination of Al4-SR activity To demonstrate that the cloned bovine liver cDNA encodes a protein with Al4-

SR activity, cDNA was cloned in the expression vector pMT2 and transfected into COS-7 cells Microsomes prepared from transfected cells were assayed for Al4-SR

adrenal skeletal

testis liver

E

se

xc 2 brain

:

Fig 2 Northern blot analysis of bovine tissues The RNAs (20 ug) extracted from different tissues were blotted onto a nitrocellulose filter and hybridized by *°P-labelled cDNA specific for bovine A14-SR (A) Hybridized A/4-SR transcript (arrow) (B) Nitrocellulose filter show- ing total RNA (288 and 18S rRNAs are indicated).

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A B C D kDa

Fig 3 Immunoblot analysis of bovine sterol A14-reductase expressed in

COS-7 cells Microsomal proteins were separated on a 12% (w/v) SDS

gel and transferred to PVDF membranes Lane A, bovine liver (40 pg

protein); lanes B and D, COS-7 cells transfected with myc-tag-A14-S'R

cDNA (5 ug protein); lane C, COS-7 cells transfected with 4/4-SR

cDNA (5 ug protein) Blots were probed with specific antibodies: anti-

(bovine liver Al4-SR) Ig danes A—-C) and anti-(myc-tag) Ig dane D)

Detection was performed by the enhanced chemiluminescence proce-

dure Molecular size markers are shown on the right

activity by incubation with C27A*"* sterol C27A® sterol was

undetectable at the beginning of incubation both in COS-7

cells and bovine liver microsomes Endogenous Al4-SR

activity of microsomes obtained from control COS-7 cells,

measured on the basis of C27A®* formation and C27A®*'*

disappearance, was much lower than that observed in

bovine liver microsomes (Fig 5) COS-7 cells expressing

Al4-SR cDNA exhibited Al4SR microsomal activity

sixfold to sevenfold higher than that of control cells and

comparable to that of bovine liver microsomes (Fig 5)

These results indicate that the cloned bovine cDNA encodes

a functional Al4-SR

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“control Al4SR liver

microsomes Fig 5 Sterol Al4reductase activity of transfected COS-7 cells Microsomes (0.24 mg protein), prepared from cells transfected with the empty pMT2 vector (control) or with 4/4-SR cDNA (A14-SR) and bovine liver microsomes (0.24 mg protein), were assayed for sterol Al4-reductase activity by incubation for 30 min with C27A*"* in the conditions described in Materials and methods Enzymatic activity was evaluated on the basis of peak area ratios between m/z 426 and m/z 372 ions (C27A*'*/5a-cholestane) or m/z 428 and m/z 372 ions (C27A*/Sa- cholestane) at the expected retention time At zero incubation time the C27A*'*/5a-cholestane peak area ratio determined for control cells, transfected cells, and liver microsomes was 4.23 + 0.56 Data shown are mean + SD (n = 3)

The present study describes the cloning and functional characterization of bovine Al4-SR, thus providing evi- dence that the previously cloned human T7M7SF?2 corre- sponds to A/4-SR Identification of TM7SF2 as the human gene encoding Al4-SR paves the way for studies

on molecular regulatory mechanisms of the 4/4-SR gene expression and its possible role in the metabolism of meiosis activating sterols Mutation analysis of TM7SF2 will clarify whether a defect in this gene underlies the Greenberg skeletal dysplasia

Fig 4 Cellular localization of sterol Al4-reductase (A) and (B) Immunofluorescence photomicrographs of transfected COS-7 cells expressing myc-tag-Al4-SR Cells were labelled with rabbit anti-(Al4-SR) Ig and secondary Cy3-conjugated sheep anti-(rabbit IgG) Ig (A) and then with monoclonal mouse anti-(myc-tag) Ig and secondary FITC-conjugated goat anti-(mouse IgG) Ig (B) (C) Immunoflurescence photomicro- graphs of transfected COS-7 cells expressing Al4-SR Cells were labelled with rabbit anti-(Al4-SR) Ig and secondary Cy3-conjugated sheep anti-(rabbit IgG) Ig.

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ACKNOWLEDGEMENTS

We are grateful to Prof D Barra and Prof L Binaglia for critical

reading of the manuscript and helpful suggestions Thanks are extended

to D Piobbico and A Toia for excellent technical assistance This study

was supported by grants from the University of Perugia, Italy

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