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The complete sequence of the mouse skeletal alpha-actin gene reveals several conserved and inverted repeat sequences outside of the protein-coding region

Hu, Mickey Chien-Tsung and Sharp, Sandra B. and Davidson, Norman (1986) The complete sequence of the mouse skeletal alpha-actin gene reveals several conserved and inverted repeat sequences outside of the protein-coding region. Molecular and Cellular Biology, 6 (1). pp. 15-25. ISSN 0270-7306.

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The complete nucleotide sequence of a genomic clone encoding the mouse skeletal alpha-actin gene has been determined. This single-copy gene codes for a protein identical in primary sequence to the rabbit skeletal alpha-actin. It has a large intron in the 5'-untranslated region 12 nucleotides upstream from the initiator ATG and five small introns in the coding region at codons specifying amino acids 41/42, 150, 204, 267, and 327/328. These intron positions are identical to those for the corresponding genes of chickens and rats. Similar to other skeletal alpha-actin genes, the nucleotide sequence codes for two amino acids, Met-Cys, preceding the known N-terminal Asp of the mature protein. Comparison of the nucleotide sequences of rat, mouse, chicken, and human skeletal muscle alpha-actin genes reveals conserved sequences (some not previously noted) outside of the protein-coding region. Furthermore, several inverted repeat sequences, partially within these conserved regions, have been identified. These sequences are not present in the vertebrate cytoskeletal beta-actin genes. The strong conservation of the inverted repeat sequences suggests that they may have a role in the tissue-specific expression of skeletal alpha-actin genes.

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Additional Information:Copyright © 1986 by the American Society for Microbiology. Received 17 June 1985/Accepted 24 September 1985. We are grateful to Michael Steinmetz for generously providing a BALB/c genomic cosmid library, to Charles P. Ordahl for the chicken skeletal α-actin genomic clone, to Leonard I. Garfinkel for a rat α-actin cDNA, to Beverley J. Bond for the Drosophila actin DmA2 genomic clone, and to Tim Hunkapiller for BALB/c genomic DNA and help with the computer analyses. We also thank Joan Steitz for valuable discussions and David Solnick, Bruce J. Nicholson, Terry P. Snutch, Robert Little, and Nevis L. Fregien for their helpful comments on this manuscript. This work was supported by a Public Health Service research grant from the National Institutes of Health.
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Deposited On:16 Jun 2008
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