title: An intronic enhancer essential for tissue-specific expression of the aldolase B transgenes.
abstract: Expression in mice of transgenes directed by regulatory regions of the rat aldolase B gene requires the presence of a B element located in the first intron, while constructs devoid of this intronic enhancer are silent. Histo- and immunochemical staining of transgenic tissue sections showed that the longer transgene was expressed in the proximal tubular cells of the kidney, enterocytes located in small intestine villi and liver parenchymal cells. In the liver, a maximal expression was observed in perivenous hepatocytes, while the transgene was weakly active in periportal hepatocytes, which reproduced the pattern of functional zonation already reported for other glycolytic and gluconeogenic genes in the liver. We also established that the transgene retained the necessary elements for a correct chronological expression during development but was lacking elements necessary for activation by high carbohydrate diet. Instead, transgene expression was paradoxically stimulated in fasted animals, suggesting that the endogenous gene, which must be active under both glycolytic and gluconeogenic conditions, could possess distinct elements activating it in fasted as well as in carbohydrate-fed animals; the former element might be conserved in the transgene and the latter one might be lost.
authors.affiliation: Laboratoire de Biologie Moléculaire Morphologique, Centre Hospitalo Universitaire Saint Antoine, 27, rue de Chaligny, 75012 Paris, France.
authors.forename: J C
authors.initials: JC
authors.lastname: Sabourin
authors.forename: A S
authors.initials: AS
authors.lastname: Kern
authors.forename: C
authors.initials: C
authors.lastname: Grégori
authors.forename: A
authors.initials: A
authors.lastname: Porteu
authors.forename: C
authors.initials: C
authors.lastname: Cywiner
authors.forename: F P
authors.initials: FP
authors.lastname: Châtelet
authors.forename: A
authors.initials: A
authors.lastname: Kahn
authors.forename: A L
authors.initials: AL
authors.lastname: Pichard
mesh_terms: D000375:Aging / Q000378:metabolism; D000818:Animals; D000831:Animals, Newborn; D015152:Blotting, Northern; D001921:Brain / Q000201:enzymology; D015500:Chloramphenicol O-Acetyltransferase / Q000096:biosynthesis; D005314:Embryonic and Fetal Development; D004742:Enhancer Elements, Genetic; D005260:Female; D005634:Fructose-Bisphosphate Aldolase / Q000096:biosynthesis* / Q000235:genetics; D015971:Gene Expression Regulation, Enzymologic; D005865:Gestational Age; D005943:Gluconeogenesis; D006019:Glycolysis; D007150:Immunohistochemistry; D007422:Intestines / Q000201:enzymology; D007438:Introns; D007687:Kidney Tubules, Proximal / Q000201:enzymology; D008099:Liver / Q000166:cytology / Q000196:embryology / Q000201:enzymology; D051379:Mice; D008822:Mice, Transgenic; D009928:Organ Specificity; D011247:Pregnancy; D051381:Rats; D011994:Recombinant Proteins / Q000096:biosynthesis; D013154:Spleen / Q000201:enzymology
chemical_list: D011994:Recombinant Proteins; D015500:Chloramphenicol O-Acetyltransferase; D005634:Fructose-Bisphosphate Aldolase