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Articles in PresS, published online ahead of print February 13, 2002
Am J Physiol Cell Physiol, 10.1152/ajpcell.00541.2001
Submitted on November 13, 2001
Accepted on February 10, 2002
1 Division of Cardiovascular Medicine, Departments of Medicine and Pharmacology, Vanderbilt University Medical Center, Nashville, TN, USA
2 Department of Biological Sciences, Vanderbilt University, Nashville, TN, USA
* To whom correspondence should be addressed. E-mail: doug.vaughan{at}mcmail.vanderbilt.edu.
The BMAL2 gene encodes a member of the bHLH-PAS family of transcription factors, which control diverse physiological processes including circadian rhythms. We identified four novel human BMAL2 transcripts that differ by alternative splicing within their N-terminal regions. Divergent expression of these and previously reported transcripts was observed among human tissues. The functional consequences of alternative splicing for transcriptional activation by CLOCK:BMAL2 heterodimers were assessed using luciferase reporter gene constructs that contained one of three diurnally regulated promoters, namely those of the mouse period1, mouse vasopressin, and human plasminogen activator inhibitor-1 genes. These studies revealed that alternative splicing generates BMAL2 isoforms possessing high, medium, low, or no transcriptional activity. Similar results were obtained with each promoter, suggesting that alternative splicing may influence the amplitudes of both central and peripheral oscillators. Indeed, alternative splicing of BMAL2 may provide tissues with a rheostat capable of regulating CLOCK:BMAL2 heterodimer function across a broad continuum of potential transcriptional activities in order to accommodate varied metabolic demands and physiologic roles.
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