Abstract:
:In an earlier report, evidence was presented that the down-regulation of beta-actin mRNA during myogenesis was controlled by a region 3' to the promoter of the gene. In this paper we report the location of this regulatory sequence, determined by deletion analysis and the use of chimeric genes, transfected stably into the mouse myogenic cell line C2C12. The domain responsible for the reduction in beta-actin mRNA levels is at most 40 base pairs long and is located just 5' to the canonical polyadenylylation signal in the gene. Placement of this sequence in the corresponding 3' position both in the alpha-cardiac-actin gene and in the neomycin-resistance gene in pSV2-neo confers the beta-actin mRNA regulatory pattern when these constructs are stably introduced into C2C12 cells. Nuclear run-on experiments indicate that transcriptional control can account for the decrease observed in beta-actin mRNA levels during myogenesis for both the endogenous as well as the transfected beta-actin gene constructs. This 3' transcriptional control sequence is conserved in all of the vertebrate beta-actin genes sequenced and is not similar to any of the 3' processing-adenylylation or termination sequences described previously. This mode of gene regulation may reflect a more general mechanism involved in the process of gene suppression during development.
journal_name
Proc Natl Acad Sci U S Aauthors
DePonti-Zilli L,Seiler-Tuyns A,Paterson BMdoi
10.1073/pnas.85.5.1389subject
Has Abstractpub_date
1988-03-01 00:00:00pages
1389-93issue
5eissn
0027-8424issn
1091-6490journal_volume
85pub_type
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journal_title:Proceedings of the National Academy of Sciences of the United States of America
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