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Centre de Recherche en Reproduction Animale, Department of Veterinary Biomedicine, Faculty of Veterinary Medicine, University of Montreal, St. Hyacinthe, Quebec, Canada J2S 7C6
Address all correspondence and requests for reprints to: Dr. David W. Silversides, Centre de Recherche en Reproduction Animale, Faculty of Veterinary Medicine, University of Montreal, St. Hyacinthe, Quebec, Canada J2S 7C6. E-mail: silverdw{at}ere.umontreal.ca
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Abstract |
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Introduction |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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Steroids required for male sex differentiation are produced by the fetal testes shortly after sex determination, which in the mouse occurs between embryonic day 10.5 (e10.5) and e12 and in the pig occurs between e21 and e26 (3, 4). In the male fetus, the developing Leydig cells produce and secrete testosterone, which is required for the retention and growth of the Wolffian duct, the anlagen of the male internal reproductive tract, as well as for the growth of external male structures. In the female, the lack of testosterone results in regression of the Wolffian duct. Partial or complete deprivation of testosterone to the male fetus during gestation, whether via surgical (5), pharmaceutical (6), or genetic (7, 8) means, will result in developmental anomalies in secondary male sex structures, which in extreme cases can produce genetic males displaying female secondary sex characteristics.
The molecular biology of steroid hormone synthesis is now relatively well characterized (9, 10, 11). The rate-limiting enzymatic step in gonadal and adrenal steroidogenesis is the conversion of cholesterol to pregnenolone by the cytochrome P450 enzyme complex for cholesterol side-chain cleavage (P450SCC), which is situated on the inner side of the mitochondrial membrane. The acutely regulated step in steroidogenesis in these organs, however, is the delivery of cholesterol from cellular stores across the mitochondrial membrane for presentation to the P450SCC enzymatic complex. Extensive studies of several steroidogenic cell systems have identified a number of protein molecules potentially implicated in the acute regulation of steroidogenesis (for review, see Ref.12). In particular, a class of 30-kDa proteins, localized to mitochondria, is induced by trophic hormone stimulation and has been implicated in the transport of cholesterol across the mitochondrial membrane. These proteins have been described in rat and mouse Leydig cell lines (13, 14), rat adrenal cortex and CL primary cell cultures, and bovine adrenal and granulosa cell cultures (15). Because of their acute hormone responsiveness and their ability to stimulate steroid production in the absence of hormone stimulation, these proteins have been named steroidogenic acute regulatory proteins (StAR) (12, 14). The mouse Leydig tumor cell line MA10 proved useful for the purification and microsequencing of peptides derived from these proteins; this information, in turn, allowed the design of degenerate nucleotide primers and the PCR amplification of partial complementary DNA (cDNA) sequences for the mouse StAR gene (14). These sequences were used to screen a phage mouse Leydig tumor cell cDNA library, and full-length StAR cDNA sequences were derived (14). Mouse StAR genomic organization was described (16), human cDNA and genomic sequences were generated (17, 18), and partial ovine cDNA sequences were reported (19). Independently, human StAR cDNA was cloned as an orphan sequence identified via chimeric association with human p220 translation initiation factor (20), and bovine StAR cDNA was cloned as an orphan sequence identified via differential cDNA expression studies of CL cells taken from early and late in the bovine estrous cycle (21). More recently, the rat StAR cDNA has been reported (22).
Recently, we proposed the pig as a useful model for studying mammalian sex determination and differentiation at the molecular level (4). To examine the expression of StAR gene for both fetal sex differentiation and maternal maintenance of pregnancy in the pig, we have cloned StAR cDNA sequences from this species. In a parallel study, bovine StAR cDNA sequences were cloned, and the expression of bovine StAR was studied in fetal and adult tissues from this species.
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Materials and Methods |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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Rapid amplification of 3'-cDNA ends (3'RACE) cloning porcine
StAR
To identify a useful source of RNA for subsequent 3'RACE and
5'RACE cloning of porcine StAR cDNA sequences, the cDNA
fragment represented by primers pStAR.A and pStAR.1 was amplified and
cloned via reverse transcription-PCR from pig ovarian polyadenylated
[poly(A)+] RNA to give clone pStAR.A1(cDNA). Based on
coding sequences of the porcine StAR gene derived from
preliminary genomic and cDNA cloning, homologous sense and antisense
primers were designed for cDNA cloning via 3'RACE and 5'RACE PCR
methods. Ovarian total RNA was recovered via the acid phenol method
(23). Poly(A)+ RNA was derived using magnetic bead
technology (Magnetobeads, Dynal Corp., Great Neck, NY), as previously
described (24). To generate the 3'-end of porcine StAR cDNA,
2 µg poly(A)+ RNA were reverse transcribed using a
poly(deoxythymidine) adapter-primer, AD/T7T17
(5'-GGATCCAAGCTTGAATTCTAATACGACTCACTATAGGGTTT-TTTTTTTTTTTTTT),
and reverse transcriptase enzyme according to the supplier’s
instructions (Superscript RT, Life Technologies, Grand Island, NY). Of
the 30-µl total volume of first strand synthesis reaction, 2 µl
were used in a primary PCR reaction of 40 cycles using specific sense
primer 3'A (5'-GACCAGCCCATGGAGAGGCTT) and nonspecific primer AD/BHE
(5'-GGATCCAAGCTTGAATTCTAATACG) and the following cycling conditions:
45-sec denaturation at 95 C, 45-sec annealing at 64 C, and 2-min
elongation at 72 C. One microliter of this first PCR was used to seed a
nested PCR involving specific sense primer 3'B
(5'-AGCGCATGGAGGCCATGGGC) and nonspecific primer AD/ET7
(5'-GAATTCTAATACGACTCACTATAGGG), with the same cycling conditions as
mentioned. An amplified band of 800 bp was identified on a 1% agarose
gel, cloned into PCRII vector (Invitrogen), and upon preliminary
sequencing was shown to represent the 3'-end of porcine StAR
gene. Complete sequencing of this clone, named pStAR.3'RACE AD/ET7.3'B,
was performed in house via the dideoxy method and via commercially
available automated sequencing methods (Regional DNA Synthesis
Laboratory, University of Calgary, Calgary, Canada).
5'RACE cDNA cloning porcine StAR
To derive 5' cDNA sequences for porcine StAR gene, a
RACE 5' method was used as previously described (25) with minor
modifications. Briefly, 2 µg porcine ovarian poly(A)+ RNA
were reverse transcribed using the heterologous StAR
antisense primer 1. The RNA was then hydrolyzed via incubation with 0.4
N NaOH for 30 min at 65 C, and first stranded cDNA was
recovered and purified via centrifugal filtration (Microcon-100
microconcentrator, Amicon, Lexington, MA). The cDNA was then
precipitated via incubation with 2 vol ethanol, 0.2 M
sodium acetate, and 15 µg glycogen at -20 C for 1 h. Single
stranded DNA ligation was performed between the first strand cDNA and a
primer designed for this purpose (ANCH.PRIM:
5'-GCAGGATCCTGAAGCTTGAATTC, with the 5'-end phosphorylated and the
3'-end modified with an amino group). The ligation reaction was
performed in a volume of 10 µl at room temperature for 24 h in a
hexamine chloride buffer (25) using T4 RNA ligase (New England Biolabs,
Beverley, CA). A first PCR reaction was performed using a specific
antisense primer 5'1 (5'-GCGCTCCACAAGCTCTTCATAA) and the nonspecific
primer ANCH.SEQ (5'-GAATTCAAGCTTCAGGATCCTGC) with 40 cycles of 45-sec
denaturation at 95 C, 45 sec of annealing at 66 C, and 2 min of
elongation at 72 C. A second, nested PCR reaction was then performed
using the specific antisense primer 5'2 (5'-TGGTCCACCACCACCTCCAGC) and
the primer ANCH.SEQ, seeded with 1 µl of the first PCR reaction.
Amplification reactions were size-fractionated on a 1% agarose gel,
and a band of about 700 bp was identified, gel purified, and cloned
into PCRII vector. Sequencing confirmed that this clone, identified as
pStAR.5'RACE ANCH.SEQ.5'2, represented 5'-cDNA sequences for the
porcine StAR gene.
Open reading frame (ORF) StAR porcine cDNA
To provide complete coding sequences of porcine StAR
for subsequent Northern expression analysis, primers were designed to
PCR amplify the ORF (sense primer Exp A:
5'-GGATCCATGCTCCTAGCGACGTTTAAGCTGT, where GGATCC is an exogenous
BamHI site; antisense primer Exp1:
5'-AAGCTTAGCTTTAACACCTGGCTTCCAGAG, where AAGCTT is an exogenous
HindIII site). Ovarian poly(A)+ RNA was reverse
transcribed as described above for the 3' RACE methods, and a PCR
amplification was performed using standard methods. The resulting band
was cloned into PCRII vector to give pStAR.EXP.A1.
Northern analysis porcine StAR and P-450 SCC
To study the developmental expression of porcine StAR
gene during gonadal sex differentiation, fetal ovaries and testes were
dissected from fetuses taken from pregnant sows at a local abattoir.
Gestational length was estimated by measuring the embryonic crown-rump
length (26). At the same time, samples of placenta, adult ovaries, and
fetal kidneys as well as adolescent and adult testes were taken. Total
RNA was extracted via the acid-phenol method or, for the adrenal glands
and adult tissues, via pelleting over a cesium chloride gradient (27).
RNA (10 µg total/tissue type) was size-fractionated on a 1%
formaldehyde-1% agarose gel and transferred via capillarity to a nylon
membrane (Hybond-N, Amersham Corp., Arlington Heights, IL). To
estimate the relative RNA loading per well, the membrane was stained
with methylene blue via standard methods (28), and the gel image was
digitized (Foto/Eclipse, Fotodyne). A radioactive double stranded probe
was generated using porcine pStAR.EXP.A1 clone. In addition, 518 bp of
cDNA sequences for the porcine P-450 side-chain cleavage
(P-450SCC) gene were generated via reverse
transcription-PCR amplification of porcine ovarian RNA. Primers were
designed based on published sequences (29) to give 518 bp of cDNA
sequences including the steroid binding sequence (sense: pSCC.A,
5'-CAATGTTACCGAGATGCT; antisense: pSCC.1, 5'-CTGGAGTGGATCCTGATTG).
Membranes were hybridized overnight with radioactive probes for porcine
StAR or porcine P-450SCC generated
via the random priming method (Quick Prime, Pharmacia) using
[
-32P]CTP (DuPont, Wilmington, DE). Membranes were
then washed at high stringency and exposed to photographic film
(BioMax, Eastman Kodak, Rochester, NY) at -70 C overnight and for
6–24 h (see figure legends).
cDNA cloning bovine StAR
To test the clonal representation of a bovine CL cDNA library
(30) made in Lambda Zap Express (Stratagene) as well as to derive
bovine StAR sequences for physiological studies in this
species, 500,000 plaque-forming units were hybridized with a probe (A1)
derived from porcine partial cDNA StAR sequences. After the
initial screening, approximately 50 plaques hybridized strongly; 12 of
these were purified via replating at serial dilutions and rehybridized.
Two clones were selected for in vivo excision of the insert
containing pBK plasmid, and upon restriction analysis revealed an
insert of approximately 2.5 kb. Sequencing and comparisons with
previously published sequences (21) confirmed that these clones,
labeled pBK.bStAR(cDNA), represented bovine StAR cDNA
sequences.
Northern analysis bovine StAR
Representative bovine tissues were analyzed for StAR
gene expression using the homologous bovine probe derived via phage
cloning. Total RNA was generated via the acid-phenol method or via
cesium chloride gradient pelleting (27), and 10 µg/tissue were loaded
per lane for Northern analysis. The following tissues were analyzed:
adult epididymus, adult testicles, testicles from a 7-month-old fetus,
ovaries from a 5-month-old fetus, superovulated adult follicles, CL,
adult oviducts, uterus, cotyledons (placenta), and adrenal gland. A
radioactive probe was generated with the 2.5-kb pBK.bStAR(cDNA)
sequence using the random priming method (Quick Prime, Pharmacia) and
[-32P]deoxy-CTP (DuPont). Size-fractionated bands were
transferred via capillarity to nylon membrane and hybridized overnight
to the bovine StAR probe. The hybridized blot was exposed to
photographic film (BioMax, Kodak) for 1 week at -70 C with an
intensifying screen.
Nucleotide and amino acid comparisons
Comparisons of nucleotide and deduced amino acid sequences
were performed via a Lipman and Person type olgarithm (31)
using MacDNASIS software (Hitachi, Hialeah, FL).
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Results |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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. Porcine StAR
cDNA shows an ORF of 855 bp representing a transcribed protein of 285
amino acids, a 5'-untranslated region of 122 bp, and a 3'-untranslated
region of 234 bp, to give a total size of 1211 bp. Percent homologies
of porcine StAR cDNA at the nucleotide and deduced amino
acid levels (in parentheses) with StAR cDNA from
other species are as follows: bovine, 90.2% (89.1%); human, 87.3%
(88.8%); mouse, 84.3% (86.7%); and rat, 83.9% (86.3%).
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and 3). Our cloned porcine StAR cDNA sequence, at
1211 bp, suggests that the lower band may, in fact, be slightly larger
than the Northern estimates.
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. Porcine
StAR expression was detected in all testicular tissue
tested, including fetal testes (weeks 12 and 13 of gestation),
perinatal testes, and adult testes. In contrast, StAR
expression was not detected in fetal ovaries, consistent with an
absence of steroidogenesis in the fetal ovary, but was very weakly
present in adult ovaries (taken from slaughterhouse material, age and
stage of cycle unknown; compare these results with ovary in Fig. 3).
Porcine StAR expression was also seen in the adult adrenal
gland.
To further our understanding of the steroidogenic relationship between
the pig placenta and CL during gestation, we compared the expression of
the porcine StAR and P450SCC genes
within these tissues. Porcine StAR expression was relatively
weak, but was readily detected, in the placenta at 7 and 13 weeks
gestation, while StAR was strongly expressed in the CL at
these times. A porcine ovary (different sample from Fig. 3, again stage
of cycle undetermined) displays relatively strong StAR
expression, whereas adult kidney does not show StAR
expression.
We have also cloned and sequenced bovine StAR cDNA and find
our sequences in agreement with previously reported sequences (21),
with the following changes at the deduced amino acid level: 75H=Y,
102Q=H, 103A=P, 273K=N, and 274R=G. In our Northern studies of bovine
StAR expression, we found hybridizing bands of about 1.4 and
2.4 kb (Fig. 4). We demonstrate positive hybridization
of a bovine StAR cDNA probe to bovine fetal and adult
testes, superovulated ovary, CL, placentomes, and adrenal gland. Very
faint hybridization was seen in the fetal bovine ovary at 5 months
gestation; the significance of this is not known.
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Discussion |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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The transcript sizes seen on our Northern analysis of porcine StAR expression include a major band at 1.8 kb and a minor band at 1.1 kb. We have most likely cloned the lower band, which, via sequencing, is 1.2 kb. These findings are in general agreement with transcript sizes seen for StAR in other species: in the mouse, two major bands are seen at 3.4 and 1.6 kb (with a minor and inconsistent band at 2.7 kb) (16); in humans, a major transcript of 1.6 kb and minor transcripts of 4.4 and 7.5 kb are described (17, 20). In the cow, two transcript sizes are reported at 1.8 and 3.0 kb (21); our cloned bovine sequences at 2.7 kb correspond to the higher mol wt transcript. To date, no differential splicing has been described for the StAR gene, so it is probable that different transcript sizes represent differential use of polyadenylation signals. Expression of porcine P450SCC mirrored StAR expression, suggesting that porcine StAR expression is involved in steroidogenesis in these tissues.
During pregnancy, the relative contribution and importance of the CL and placenta for steroidogenesis and the maintenance of pregnancy varies between species (1). Also, major qualitative and quantitative differences exist in the steroidogenic capacity of placentas between species and even within species at different stages throughout pregnancy (1, 2, 34). For example, in humans, sheep, and horses, after a certain point in gestation the placenta can maintain pregnancy in the absence of the CL. In contrast in the pig the CL is required for the duration of pregnancy, and removal of the CL at any time throughout gestation will result in termination of the pregnancy.
Most interestingly, an absence of StAR transcription has been reported in the human placenta (17, 20); also, StAR protein was not seen in the mouse placenta (16). These observations support the hypothesis that within a mammalian species, mechanisms for steroidogenesis in the placenta need not be the same as those found in the gonads (1, 2). This may not be conceptually unreasonable, as the placenta is a composite fetal/maternal tissue, which is anatomically and developmentally distinct from the gonadal/adrenal tissues; as such, the placenta would not be subject to the same evolutionary pressures as other steroidogenic tissues. Indeed, the placenta contains some of the fastest evolving protein hormones described (35) and varies considerably in structure (36) as well as function (37) between mammalian species. In terms of placental function, care must be exercised not to extrapolate the findings in one mammalian species to others. In contrast to the lack of placental expression StAR seen in humans (order Primates) (17, 20), our data confirm that StAR is expressed by the placenta of at least two members of the order Artiodactyla, the pig and the cow.
Testosterone synthesis by the fetal testes is required for male sex differentiation, whereas fetal ovaries are not steroidogenically active. Consistent with this view, we detected strong expression of the porcine StAR gene in the developing testes during the time of sex differentiation, with an absence of StAR expression in the developing ovaries. StAR gene activity has also been reported in the human fetal kidney (20), although StAR protein has not been demonstrated. Neither StAR message nor protein was detected in mouse or rat kidney (16, 22). We looked for StAR gene expression in fetal and adult porcine kidneys and failed to detect any.
In the course of cloning porcine StAR cDNA sequences, we
have also cloned bovine StAR cDNA sequences from a 
library of bovine CL cDNA (30). Sequences for bovine StAR
cDNA have been described previously (21), and preliminary expression
studies have been presented. In contrast to these studies, which did
not show StAR expression in the endometrium of pregnancy, we
detected bovine StAR expression in placentomes (combined
cotyledons and caruncle tissue), indicating that StAR may
have a role in placental steroidogenesis in the bovine species (as
discussed above). Our findings of StAR expression in the cow
placenta via use of a homologous bovine probe confirm recent reports of
bovine StAR expression in the cotyledons and caruncles of
the cow placenta derived using a heterologous mouse probe (38). We
observed strong expression of bovine StAR in follicular
cells taken from superovulated ovaries and also expression in fetal and
adult bovine testes, tissues that where negative for expression in
original reports (21).
Analysis of the promoter region of the mouse StAR gene has revealed a recognition sequence for steroidogenic factor-1 (SF-1), an orphan nuclear receptor belonging to the steroid hormone receptor family (16). SF-1 was first described as a trans-acting factor for steroidogenesis in the gonads and adrenal gland, and SF-1 binding sites are found in promoter regions of steroidogenic enzyme genes, including P450SCC, P450c17, 3ßHSD (type II), and CYP19 (for cytochrome P450 aromatase) (39, 40, 41). More recently, SF-1 binding sites were described in the promoters of Dax-1, a dosage-sensitive gene believed to be involved in sex determination (42, 43); Mullerian inhibitory hormone (MIH), a protein hormone of the transforming growth factor-ß family involved in sex differentiation (44); as well as mouse and human StAR genes (16, 18). It is now apparent that SF-1 is implicated in the control of reproductive functions at numerous levels (45), including sex determination and differentiation as well as steroidogenesis. Expression of SF-1 precedes StAR and P450SCC gene expression in the developing mouse gonads, suggesting that SF-1 protein may be involved in the control of StAR expression (16, 43); recent functional studies in human tissue culture support this relationship (46). However, this relationship may be species and tissue dependent; in the rabbit CL, StAR protein levels have been shown to be responsive to estradiol (47), indicating that further comparative studies are warranted. Expression of SF-1, StAR, and P450SCC genes in the developing pig gonads, CL, and placenta as well as analysis of the promoter region of the porcine StAR gene await additional studies.
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Acknowledgments |
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Footnotes |
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Received October 8, 1996.
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