title: Characterization of the mouse prostaglandin F receptor gene: a transgenic mouse study of a regulatory region that controls its expression in the stomach and kidney but not in the ovary.
abstract: BACKGROUND
  The actions of prostaglandin F2alpha are mediated by a cell-surface receptor (FP), but little is known about the regulation of FP gene expression. To clarify the mechanisms underlying tissue specific transcription of the mouse FP gene, we isolated and characterized mouse genomic DNA clones encoding FP.
  
  
  RESULTS
  Structural analysis revealed that the mouse FP gene is composed of three exons and two introns, and spans more than 11 kilobases. By primer extension and PCR analyses, the major transcription start site was identified as a cytosine nucleotide, but additional sites of transcription initiation were found in the ovary. There was no apparent difference in the FP gene transcription initiation site between the ovary, kidney and stomach. Sequence analysis of the putative promoter region showed only two potential SP-1 binding sites, but no other typical well-known consensus sequences. We generated transgenic mice with the potential promoter region of the FP gene connected to the lacZ reporter gene. Northern blot analysis showed that the pattern of expression of the transgene corresponded to that of FP expression, except in the ovary. Upon analysis by in situ hybridization, the lacZ gene transcripts were found to be expressed in the fundic glands in the stomach, and the cortical tubules in the kidney, in which endogenous FP transcripts were also expressed. On the contrary, expression of lacZ transcripts was not detected in the corpora lutea, where the highest expression of FP mRNA was observed.
  
  
  CONCLUSIONS
  These studies suggest that a separate control mechanism exists for FP expression in the ovary, distinct from the expression in the stomach and kidney.
authors.affiliation: Department of Physiological Chemistry, Faculty of Pharmaceutical Sciences, Kyoto University, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Hasumoto
authors.forename: Y
authors.initials: Y
authors.lastname: Sugimoto
authors.forename: M
authors.initials: M
authors.lastname: Gotoh
authors.forename: E
authors.initials: E
authors.lastname: Segi
authors.forename: A
authors.initials: A
authors.lastname: Yamasaki
authors.forename: M
authors.initials: M
authors.lastname: Yamaguchi
authors.forename: H
authors.initials: H
authors.lastname: Honda
authors.forename: H
authors.initials: H
authors.lastname: Hirai
authors.forename: M
authors.initials: M
authors.lastname: Negishi
authors.forename: A
authors.initials: A
authors.lastname: Kakizuka
authors.forename: A
authors.initials: A
authors.lastname: Ichikawa
mesh_terms: D000595:Amino Acid Sequence; D000818:Animals; D001483:Base Sequence; D015237:Dinoprost / Q000378:metabolism; D005260:Female; D005753:Gastric Mucosa / Q000378:metabolism; D005786:Gene Expression Regulation; D007668:Kidney / Q000378:metabolism; D051379:Mice; D008822:Mice, Transgenic; D008969:Molecular Sequence Data; D009928:Organ Specificity; D010053:Ovary / Q000378:metabolism; D011982:Receptors, Prostaglandin / Q000235:genetics* / Q000378:metabolism
chemical_list: D011982:Receptors, Prostaglandin; C034671:prostaglandin F2alpha receptor; D015237:Dinoprost