You are not currently logged in.
Access your personal account or get JSTOR access through your library or other institution:
If You Use a Screen ReaderThis content is available through Read Online (Free) program, which relies on page scans. Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Expression of the Differentiation-Induced Gene for Fatty Acid-Binding Protein is Activated by Glucocorticoid and cAMP
Jonathan S. Cook, John J. Lucas, Eric Sibley, Mark A. Bolanowski, Robert J. Christy, Thomas J. Kelly and M. Daniel Lane
Proceedings of the National Academy of Sciences of the United States of America
Vol. 85, No. 9 (May 1, 1988), pp. 2949-2953
Published by: National Academy of Sciences
Stable URL: http://www.jstor.org/stable/31921
Page Count: 5
Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Preview not available
We have isolated and characterized a fragment of the gene encoding adipose fatty acid-binding protein (gene 422) from a 3T3-L1 adipocyte genomic library. The 5′-flanking sequence of the 422 gene contains potential regulatory regions for adipose-specific expression. At position -120 there is a fat-specific element that occurs in several genes expressed as preadipocytes differentiate, and at position -393 there is a glucocorticoid regulatory element core sequence. Chimeric constructs were prepared by ligating 858 base pairs or 248 base pairs of 5′-flanking sequence and 22 nucleotides of 5′-untranslated sequence of the 422 gene to the bacterial gene encoding chloramphenicol acetyltransferase (CAT); these constructs (Δ 858.CAT and Δ 248.CAT) were transfected into 3T3-L1 preadipocytes. When differentiation was initiated by the adipogenic agents methylisobutylxanthine (a cAMP phosphodiesterase inhibitor), dexamethasone, and insulin, expression of both constructs increased, reaching maximal levels within 24 hr. Both constructs were maximally induced 48 hr before appreciable accumulation of the endogenous 422 mRNA. Expression of Δ 858.CAT, but not of Δ 248.CAT, was induced by dexamethasone, which correlates with deletion of the potential glucocorticoid regulatory element. Expression of both constructs was induced by 8-bromoadenosine 3′,5′-cyclic monophosphate, thus implicating the first 248 base pairs of 5′-flanking sequence of the 422 gene in the response to cAMP. Indirect effects by the adipogenic factors on CAT protein or mRNA synthesis and turnover were ruled out, since replacing the 5′-flanking region of the 422 gene constructs with viral promoters abolished the effects of dexamethasone and 8-bromoadenosine 3′,5′-cyclic monophosphate on CAT expression. We conclude that the first 858 base pairs of 5′-flanking sequence of the 422 gene contains elements that mediate activation by dexamethasone and cAMP.
Proceedings of the National Academy of Sciences of the United States of America © 1988 National Academy of Sciences