Association of hepatic β 2 ‐adrenergic receptor gene transcript destabilization during postnatal development in the sprague‐dawley rat with a M r 85,000 protein that binds selectively to the β 2 ‐adrenergic receptor mRNA 3′‐untranslated region

In the liver, transcript destabilization contributes to the decrease in steady‐state levels of β 2 ‐adrenergic receptor mRNA that occurs during early postnatal development in the rat. From genomic DNA, polymerase chain reaction (PCR) was used to amplify a 718‐basepair (bp) fragment of the β 2 ‐adrenergic receptor gene including the entire 3′‐untranslated region. Results from SDS‐gel electrophoresis and autoradiography demonstrated a M r 85,000 cellular factor present in postnatal day 60, but not fetal day 18 rat liver that was ultraviolet (UV) light‐crosslinked to in vitro transcribed β 2 ‐adrenergic receptor RNA 3′‐untranslated region. Unlabeled β 2 ‐adrenergic receptor RNA 3′‐untranslated region, but not mouse β‐actin RNA, competed with labeled β 2 ‐adrenergic receptor RNA 3′‐untranslated region for binding to the M r 85,000 protein. Cross‐linking of the β 2 ‐adrenergic receptor RNA 3′‐untranslated region to the M r 85,000 protein was inhibited by the ribohomopolymer poly(U), with poly(A), poly(C) and poly(G) having little or no effect. Thus, a M r 85,000 protein has been identified in adult male rat liver that may interact with U‐rich sequences in the 3′‐untranslated region of the β 2 ‐adrenergic receptor mRNA and may account for the decreased stability of hepatic β 2 ‐adrenergic receptor gene transcripts that occurs during development. © 1995 Wiley‐Liss, Inc.