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A 5′ duplication of the alpha‐cardiac actin gene in BALB/c mice is associated with abnormal levels of alpha‐cardiac and alpha‐skeletal actin mRNAs in adult cardiac tissue.
Author(s) -
Garner I.,
Minty A.J.,
Alonso S.,
Barton P.J.,
Buckingham M.E.
Publication year - 1986
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1002/j.1460-2075.1986.tb04535.x
Subject(s) - biology , gene duplication , microbiology and biotechnology , gene , exon , actin , promoter , alpha (finance) , gene expression , genetics , medicine , construct validity , nursing , patient satisfaction
We describe the structure and transcriptional activity of the 5′ portion of the alpha‐cardiac actin gene of BALB/c mice. Southern blotting and DNA sequencing reveal that the promoter and first three exons of the gene are present as perfect repeats in a direct duplication of 9.5 kbp situated immediately upstream of the gene. Both promoters are active in adult cardiac tissue. Transcripts from the partial gene duplication give rise to novel RNAs that are spliced correctly in the actin region and polyadenylated. The level of mature alpha‐cardiac actin mRNA is only 16.5% that found in mice that do not possess the duplication. This is due, at least in part, to interference at the transcriptional level. Transcripts from the alpha‐skeletal actin gene accumulate to abnormally high levels in the hearts of such mutant mice. This result suggests tight regulatory coupling for this actin gene pair.