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PMID: 7854355 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

Characterization of a corticotropin-releasing hormone-responsive element in the rat proopiomelanocortin gene promoter and molecular cloning of its binding protein.

Molecular endocrinology (Baltimore, Md.) ·Vol. 8 ·No. 10 ·1994-10-00 ·Pages 1377-88

Jin WD, Boutillier AL, Glucksman MJ, Salton SR, Loeffler JP, Roberts JL

Abstract

A corticotropin-releasing hormone (CRH) and cAMP-responsive region (-236/-133) in the rat POMC gene promoter previously reported to confer CRH/cAMP responsiveness to heterologous reporter constructs has been characterized. DNAse footprint analysis revealed that multiple elements in this region were bound by nuclear proteins from the POMC expressing AtT20 cells. When these individual DNA elements were separately tested in heterologous reporter constructs for CRH induction, only one element, designated PCRH-RE (POMC CRH responsive element, -171/-160) was found to give strong CRH stimulation (5- to 7-fold). This element appears novel as to the possible binding factors, although it has homology to the mouse metallothionein metal regulatory element. Gel shift analyses of the PCRH-RE with AtT20 cell nuclear extracts showed marked stimulation of retarded nucleoproteins following CRH stimulation, suggesting that the possible binding factor(s) may mediate transcriptional regulation at this site. The activity of PCRH-RE binding protein was inhibited by divalent cations, with Cu2+ and Cd2+ being most effective; Zn2+ had no effect, indicating that this binding factor(s) is functionally distinct from the metallothionein metal regulatory element binding protein. A 2.6 kilobase cDNA clone encoding a protein (PCRH-REB-1) binding to this element was isolated by Southwestern screening of an AtT20 expression library with radiolabeled PCRH-RE oligonucleotides. This clone was used to isolate several other cDNA clones to determine the sequence corresponding to the entire coding region of the protein (PCRH-REB), which proved to be identical to a recently described DNA binding protein of the replication factor C complex, mRFC140/Mouse Southwestern. Primer extension and Northern blot analysis revealed that the size of the full length mRNA is about 4.9 kilobases. PCRH-REB mRNA expression is not restricted to corticotrophs but is present in a broad tissue distribution as evaluated by reverse transcription polymerase chain reaction analysis. A bacterially expressed beta-galactosidase-PCRH-REB-1 fusion protein was shown to bind PCRH-RE efficiently. Furthermore, binding of the PCRH-REB-1 fusion protein to the POMC CRH-responsive element was inhibited by divalent cations with similar sensitivities to those observed using AtT20 nuclear extracts. The predicted PCHR-REB protein sequence presents several interesting motifs: one p-Loop motif (ATP binding site), nine protein kinase A phosphorylation sites (implying a possible role in responding to the CRH-induced cAMP signal), and regions of homology to proteins involved in DNA replication and repair. PCRH-REB is, therefore, a potential transacting factor binding to a major CRH-responsive element in the POMC promoter.

MeSH Terms
Animals Base Sequence Cations, Divalent Chloramphenicol O-Acetyltransferase/genetics Cloning, Molecular Corticotropin-Releasing Hormone/pharmacology Cyclic AMP/pharmacology DNA-Binding Proteins/genetics,metabolism Gene Expression Mice Molecular Sequence Data Nuclear Proteins/metabolism Pro-Opiomelanocortin/genetics Promoter Regions, Genetic RNA, Messenger/metabolism Rats Recombinant Fusion Proteins Regulatory Sequences, Nucleic Acid Sequence Analysis, DNA Thymidine Kinase/genetics Transcription Factors/genetics,metabolism Transfection
Chemicals
Cations, Divalent DNA-Binding Proteins Nuclear Proteins POMC CRH-responsive element binding protein, rat RNA, Messenger Recombinant Fusion Proteins Transcription Factors Pro-Opiomelanocortin Corticotropin-Releasing Hormone Cyclic AMP Chloramphenicol O-Acetyltransferase Thymidine Kinase
Authors & Affiliations
6 authors, click to expand affiliations / ORCID
Jin W D
Dr. Arthur M. Fishberg Research Center for Neurobiology, Mount Sinai School of Medicine, New York, New York 10029.
Boutillier A L
Glucksman M J
Salton S R
Loeffler J P
Roberts J L
Article Info
Journal
Molecular endocrinology (Baltimore, Md.)
Abbr.
Mol Endocrinol
ISSN
0888-8809
Published
1994-10-00
Pages
1377-88
Language
English
Region
United States
NLM ID
8801431
Subset
IM
Grants
NIDDK NIH HHS · DK-27484 · United States
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