PMID- 10570158
OWN - NLM
STAT- MEDLINE
DCOM- 20000106
LR  - 20190501
IS  - 0027-8424 (Print)
IS  - 0027-8424 (Linking)
VI  - 96
IP  - 24
DP  - 1999 Nov 23
TI  - Transcriptional regulation of the rat Mullerian inhibiting substance type II
      receptor in rodent Leydig cells.
PG  - 13831-8
AB  - Mullerian inhibiting substance (MIS) causes regression of the fetal Mullerian
      duct on binding a heteromeric complex of types I and II cell-surface receptors in
      the fetal urogenital ridge. The MIS type II receptor (MISRII), which provides
      specificity for MIS, is also expressed in the adult testis, ovary, and uterus.
      The rat MISRII promoter was cloned to study the molecular mechanisms underlying
      its temporal and cell-specific expression. The 1.6-kilobase (kb) promoter
      contained no recognizable TATA or CAAT box, but there was a consensus Sp1 site
      upstream of the transcription initiation site. Two binding sites for the orphan
      nuclear receptor steroidogenic factor-1 (SF-1) are occupied in vitro by using
      nuclear extracts from R2C cells, an MIS-responsive rat Leydig cell line that
      expresses endogenous MISRII, with differing affinities, indicating that the
      distal SF-1 site is bound more avidly than is the proximal SF-1 site. R2C cells
      transfected with MISRII promoter/luciferase reporter constructs show a 12-fold
      induction with the 1.6-kb fragment and deletion of sequences upstream of -282-bp 
      lowered luciferase expression to one-third. Mutation of both SF-1 sites greatly
      inhibited luciferase expression, whereas mutation of either site alone resulted
      in continuing activation by endogenous SF-1, indicating redundancy. In vitro
      binding and transcriptional analyses suggest that a proximal potential
      Smad-responsive element and an uncharacterized element also contribute to
      activation of the MISRII gene. R2C cells and MISRII promoter regulation can now
      be used to uncover endogenous transcription factors responsible for receptor
      expression or repression.
FAU - Teixeira, J
AU  - Teixeira J
AD  - Pediatric Surgical Research Laboratories, Massachusetts General Hospital, Harvard
      Medical School, Boston, MA 02114, USA. teixeira@helix.mgh.harvard.edu
FAU - Kehas, D J
AU  - Kehas DJ
FAU - Antun, R
AU  - Antun R
FAU - Donahoe, P K
AU  - Donahoe PK
LA  - eng
SI  - GENBANK/AF092445
GR  - F32 HD007954/HD/NICHD NIH HHS/United States
GR  - R29-CA79459/CA/NCI NIH HHS/United States
GR  - R01-HD32112/HD/NICHD NIH HHS/United States
GR  - F32-HD07954/HD/NICHD NIH HHS/United States
GR  - R01 HD032112/HD/NICHD NIH HHS/United States
GR  - F32 HD007954-03/HD/NICHD NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Proc Natl Acad Sci U S A
JT  - Proceedings of the National Academy of Sciences of the United States of America
JID - 7505876
RN  - 0 (DNA, Complementary)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Fushi Tarazu Transcription Factors)
RN  - 0 (Homeodomain Proteins)
RN  - 0 (Receptors, Cytoplasmic and Nuclear)
RN  - 0 (Receptors, Peptide)
RN  - 0 (Receptors, Transforming Growth Factor beta)
RN  - 0 (Steroidogenic Factor 1)
RN  - 0 (Transcription Factors)
RN  - 0 (anti-Mullerian hormone receptor)
RN  - 0 (steroidogenic factor 1, rat)
RN  - EC 1.13.12.- (Luciferases)
SB  - IM
MH  - Amino Acid Sequence
MH  - Animals
MH  - Base Sequence
MH  - Binding Sites
MH  - Cloning, Molecular
MH  - DNA, Complementary
MH  - DNA-Binding Proteins/metabolism
MH  - Fushi Tarazu Transcription Factors
MH  - *Gene Expression Regulation
MH  - Genes, Reporter
MH  - Homeodomain Proteins
MH  - Leydig Cells/cytology/*metabolism
MH  - Luciferases/genetics
MH  - Male
MH  - Molecular Sequence Data
MH  - Promoter Regions, Genetic
MH  - Rats
MH  - Receptors, Cytoplasmic and Nuclear
MH  - Receptors, Peptide/*genetics
MH  - Receptors, Transforming Growth Factor beta
MH  - Sequence Analysis, DNA
MH  - Steroidogenic Factor 1
MH  - Transcription Factors/metabolism
MH  - Transcription, Genetic
MH  - Tumor Cells, Cultured
PMC - PMC24150
EDAT- 1999/11/26 00:00
MHDA- 1999/11/26 00:01
CRDT- 1999/11/26 00:00
PHST- 1999/11/26 00:00 [pubmed]
PHST- 1999/11/26 00:01 [medline]
PHST- 1999/11/26 00:00 [entrez]
AID - 10.1073/pnas.96.24.13831 [doi]
PST - ppublish
SO  - Proc Natl Acad Sci U S A. 1999 Nov 23;96(24):13831-8. doi:
      10.1073/pnas.96.24.13831.