Actin genes in Xenopus and their developmental control

Development ◽  
1985 ◽  
Vol 89 (Supplement) ◽  
pp. 125-136
Author(s):  
J. B. Gurdon ◽  
T. J. Mohun ◽  
S. Brennan ◽  
S. Cascio
Keyword(s):  
Skeletal Muscle ◽  
Early Development ◽  
Actin Gene ◽  
Muscle Actin ◽  
Cell Type ◽  
Developmental Control ◽  
Normal Contact ◽  
Actin Genes ◽  
Cardiac Actin ◽  
Cell Type Specific

The results summarized here have established the temporal and regional activation of three kinds of Xenopus actin genes. The cardiac and skeletal muscle actin genes are among the first cell-type-specific genes to be expressed in early development. The first transcripts to be synthesized by these genes appear to be correctly initiated, spliced, and at once translated into proteins. Both cardiac and skeletal actin genes are strongly transcribed in the axial skeletal muscle of embryos. The mechanism by which the cardiac actin gene is first transcribed in only the somite region of an embryo depends, at least in part, on materials already localized in the subequatorial region of a fertilized but uncleaved egg. Cells which acquire this material seem able to activate their cardiac actin genes without requiring normal contact with other cells.

scholarly journals alpha-skeletal and alpha-cardiac actin genes are coexpressed in adult human skeletal muscle and heart.

1983 ◽  
Vol 3 (11) ◽  
pp. 1985-1995 ◽  
Author(s):  
P Gunning ◽  
P Ponte ◽  
H Blau ◽  
L Kedes
Keyword(s):  
Skeletal Muscle ◽  
Smooth Muscle ◽  
Human Skeletal Muscle ◽  
Cdna Clones ◽  
Actin Gene ◽  
Adult Heart ◽  
Adult Human ◽  
Actin Genes ◽  
Cardiac Actin ◽  
Actin Mrna

We determined the actin isotypes encoded by 30 actin cDNA clones previously isolated from an adult human muscle cDNA library. Using 3' untranslated region probes derived from alpha-skeletal, beta- and gamma-actin cDNAs and from an alpha-cardiac actin genomic clone, we showed that 28 of the cDNAs correspond to alpha-skeletal actin transcripts. Unexpectedly, however, the remaining two cDNA clones proved to derive from alpha-cardiac actin mRNA. Sequence analysis confirmed that the two skeletal muscle alpha-cardiac actin cDNAs are derived from transcripts of the cloned alpha-cardiac actin gene. Direct measurements of actin isotype mRNA expression in human skeletal muscle showed that alpha-cardiac actin mRNA is expressed at 5% the level of alpha-skeletal actin. Furthermore, the alpha-cardiac actin gene expressed in skeletal muscle is the same gene which produces alpha-cardiac actin mRNA in the human heart. Of equal surprise, we found that alpha-skeletal actin mRNA accounts for about half of the total actin mRNA in adult heart. Comparison of total actin mRNA levels in adult skeletal muscle and adult heart revealed that the steady-state levels in skeletal muscle are about twofold greater, per microgram of total cellular RNA, than those in heart. Thus, in skeletal muscle and in heart, both of the sarcomeric actin mRNA isotypes are quite abundant transcripts. We conclude that alpha-skeletal and alpha-cardiac actin genes are coexpressed as an actin pair in human adult striated muscles. Since the smooth-muscle actins (aortic and stomach) and the cytoplasmic actins (beta and gamma) are known to be coexpressed in smooth muscle and nonmuscle cells, respectively, we postulate that coexpression of actin pairs may be a common feature of mammalian actin gene expression in all tissues.

alpha-skeletal and alpha-cardiac actin genes are coexpressed in adult human skeletal muscle and heart

1983 ◽  
Vol 3 (11) ◽  
pp. 1985-1995
Author(s):  
P Gunning ◽  
P Ponte ◽  
H Blau ◽  
L Kedes
Keyword(s):  
Skeletal Muscle ◽  
Smooth Muscle ◽  
Human Skeletal Muscle ◽  
Cdna Clones ◽  
Actin Gene ◽  
Adult Heart ◽  
Adult Human ◽  
Actin Genes ◽  
Cardiac Actin ◽  
Actin Mrna

We determined the actin isotypes encoded by 30 actin cDNA clones previously isolated from an adult human muscle cDNA library. Using 3' untranslated region probes derived from alpha-skeletal, beta- and gamma-actin cDNAs and from an alpha-cardiac actin genomic clone, we showed that 28 of the cDNAs correspond to alpha-skeletal actin transcripts. Unexpectedly, however, the remaining two cDNA clones proved to derive from alpha-cardiac actin mRNA. Sequence analysis confirmed that the two skeletal muscle alpha-cardiac actin cDNAs are derived from transcripts of the cloned alpha-cardiac actin gene. Direct measurements of actin isotype mRNA expression in human skeletal muscle showed that alpha-cardiac actin mRNA is expressed at 5% the level of alpha-skeletal actin. Furthermore, the alpha-cardiac actin gene expressed in skeletal muscle is the same gene which produces alpha-cardiac actin mRNA in the human heart. Of equal surprise, we found that alpha-skeletal actin mRNA accounts for about half of the total actin mRNA in adult heart. Comparison of total actin mRNA levels in adult skeletal muscle and adult heart revealed that the steady-state levels in skeletal muscle are about twofold greater, per microgram of total cellular RNA, than those in heart. Thus, in skeletal muscle and in heart, both of the sarcomeric actin mRNA isotypes are quite abundant transcripts. We conclude that alpha-skeletal and alpha-cardiac actin genes are coexpressed as an actin pair in human adult striated muscles. Since the smooth-muscle actins (aortic and stomach) and the cytoplasmic actins (beta and gamma) are known to be coexpressed in smooth muscle and nonmuscle cells, respectively, we postulate that coexpression of actin pairs may be a common feature of mammalian actin gene expression in all tissues.

Isolation and characterization of six different chicken actin genes

1984 ◽  
Vol 4 (11) ◽  
pp. 2498-2508
Author(s):  
K S Chang ◽  
W E Zimmer ◽  
D J Bergsma ◽  
J B Dodgson ◽  
R J Schwartz
Keyword(s):  
Dna Sequences ◽  
Genomic Dna ◽  
Genomic Library ◽  
Smooth Muscle Actin ◽  
Actin Gene ◽  
Muscle Actin ◽  
Repeated Dna ◽  
Alpha Smooth Muscle Actin ◽  
Actin Genes ◽  
Actin Isoform

Genes representing six different actin isoforms were isolated from a chicken genomic library. Cloned actin cDNAs as well as tissue-specific mRNAs enriched in different actin species were used as hybridization probes to group individual actin genomic clones by their relative thermal stability. Restriction maps showed that these actin genes were derived from separate and nonoverlapping regions of genomic DNA. Of the six isolated genes, five included sequences from both the 5' and 3' ends of the actin-coding area. Amino acid sequence analysis from both the NH2- and COOH-terminal regions provided for the unequivocal identification of these genes. The striated isoforms were represented by the isolated alpha-skeletal, alpha-cardiac, and alpha-smooth muscle actin genes. The nonmuscle isoforms included the beta-cytoplasmic actin gene and an actin gene fragment which lacked the 5' coding and flanking sequence; presumably, this region of DNA was removed from this gene during construction of the genomic library. Unexpectedly, a third nonmuscle chicken actin gene was found which resembled the amphibian type 5 actin isoform (J. Vandekerckhove, W. W. Franke, and K. Weber, J. Mol. Biol., 152:413-426). This nonmuscle actin type has not been previously detected in warm-blooded vertebrates. We showed that interspersed, repeated DNA sequences closely flanked the alpha-skeletal, alpha-cardiac, beta-, and type 5-like actin genes. The repeated DNA sequences which surround the alpha-skeletal actin-coding regions were not related to repetitious DNA located on the other actin genes. Analysis of genomic DNA blots showed that the chicken actin multigene family was represented by 8 to 10 separate coding loci. The six isolated actin genes corresponded to 7 of 11 genomic EcoRI fragments. Only the alpha-smooth muscle actin gene was shown to be split by an EcoRI site. Thus, in the chicken genome each actin isoform appeared to be encoded by a single gene.

scholarly journals Regulation of the human cardiac/slow-twitch troponin C gene by multiple, cooperative, cell-type-specific, and MyoD-responsive elements.

1993 ◽  
Vol 13 (11) ◽  
pp. 6752-6765 ◽  
Author(s):  
T H Christensen ◽  
H Prentice ◽  
R Gahlmann ◽  
L Kedes
Keyword(s):  
Skeletal Muscle ◽  
Heart Muscle ◽  
Regulatory Elements ◽  
Troponin C ◽  
Cell Type ◽  
Promoter Elements ◽  
Specific Expression ◽  
First Intron ◽  
Cell Type Specific ◽  
Slow Twitch

The cardiac troponin C (cTnC) gene produces identical transcripts in slow-twitch skeletal muscle and in heart muscle (R. Gahlmann, R. Wade, P. Gunning, and L. Kedes, J. Mol. Biol. 201:379-391, 1988). A separate gene encodes the fast-twitch skeletal muscle troponin C and is not expressed in heart muscle. We have used transient transfection to characterize the regulatory elements responsible for skeletal and cardiac cell-type-specific expression of the human cTnC (HcTnC) gene. At least four separate elements cooperate to confer tissue-specific expression of this gene in differentiated myotubes; a basal promoter (between -61 and -13) augments transcription 9-fold, upstream major regulatory sequences (between -68 and -142 and between -1319 and -4500) augment transcription as much as 39-fold, and at least two enhancer-like elements in the first intron (between +58 and +1028 and between +1029 and +1523) independently augment transcription 4- to 5-fold. These enhancers in the first intron increase myotube-specific chloramphenicol acetyltransferase activity when linked to their own promoter elements or to the heterologous simian virus 40 promoter, and the effects are multiplicative rather than additive. Each of the major myotube regulatory regions is capable of responding directly or indirectly to the myogenic determination factor, MyoD.A MyoD expression vector in 10T1/2 cells induced constructs carrying either the upstream HcTnC promoter elements or the first intron of the gene 300- to 500-fold. Expression was inhibited by cotransfection with Id, a negative regulator of basic helix-loop-helix transcription factors. The basal promoter contains five tandem TGGGC repeats that interact with Sp1 or an Sp1-like factor in nuclear extracts. Mutational analysis of this element demonstrated that two of the five repeat sequences were sufficient to support basal level muscle cell-specific transcription. Whereas the basal promoter is also critical for expression in cardiac myocytes, the elements upstream of -67 appear to play little or no role. Major augmentation of expression in cardiomyocytes is also provided by sequences in the first intron, but these are upstream (between +58 and +1028). The downstream segment of the first intron has no enhancer activity in cardiomyocytes. A specific DNA-protein complex is formed by this C2 cell enhancer with extracts from C2 cells but not cardiomyocytes. These observations suggest that tissue-specific expression of the HcTnC gene is cooperatively regulated by the complex interactions of multiple regulatory elements and that different elements are used to regulate expression in myogenic and cardiac cells.

Heterogeneity of nemaline myopathy cases with skeletal muscle ?-actin gene mutations

2004 ◽  
Vol 56 (1) ◽  
pp. 86-96 ◽  
Author(s):  
Pankaj B. Agrawal ◽  
Corinne D. Strickland ◽  
Charles Midgett ◽  
Ana Morales ◽  
Daniel E. Newburger ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Gene Mutations ◽  
Nemaline Myopathy ◽  
Actin Gene ◽  
Muscle Actin ◽  
Muscle Actin Gene

scholarly journals Isolation and characterization of the mouse acetylcholine receptor delta subunit gene: identification of a 148-bp cis-acting region that confers myotube-specific expression.

1988 ◽  
Vol 107 (6) ◽  
pp. 2271-2279 ◽  
Author(s):  
T J Baldwin ◽  
S J Burden
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Acetylcholine Receptor ◽  
Subunit Gene ◽  
Cell Type ◽  
Cis Acting ◽  
Mouse Skeletal Muscle ◽  
Cell Type Specific ◽  
Delta Subunit ◽  
Cat Gene

We have isolated the gene encoding the delta subunit of the mouse skeletal muscle acetylcholine receptor (AChR) and have identified a 148-bp cis-acting region that controls cell type-specific and differentiation-dependent gene expression. The 5' flanking region of the delta subunit gene was fused to the protein-coding region of the chloramphenicol acetyltransferase (CAT) gene and gene fusions were transfected into C2 mouse skeletal muscle cells. Both transiently and stably transfected cells were assayed for CAT gene expression. Deletions from the 5' end of the mouse delta gene demonstrate that 148 bp of 5' flanking DNA is sufficient to confer cell type-specific and differentiation-dependent expression: CAT activity is present in transfected myotubes, but not in transfected 3T3 cells or 10T1/2 cells. Moreover, the level of CAT expression in myotubes transfected with constructs containing 148 bp of 5' flanking DNA from the delta subunit gene is identical to that in myotubes transfected with constructs containing 3.2 kb of 5' flanking DNA and similar to expression from the SV-40 early promoter. Increased CAT activity in myotubes is a result of an increased rate of transcription from the delta subunit promoter, since CAT RNA levels are also 35-fold more abundant in myotubes than myoblasts. In contrast, the SV-40 early promoter is similarly active in all cell types. Thus, 148 bp of 5' flanking DNA from the delta subunit gene contains all the information required for cell type-specific and differentiation-dependent expression of the AChR delta subunit.

Drosophila indirect flight muscle specific Act88F actin mutants as a model system for studying congenital myopathies of the human ACTA1 skeletal muscle actin gene

2010 ◽  
Vol 20 (6) ◽  
pp. 363-374 ◽  
Author(s):  
Sarah E. Haigh ◽  
Sheetal S. Salvi ◽  
Maria Sevdali ◽  
Meg Stark ◽  
David Goulding ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Flight Muscle ◽  
Model System ◽  
Indirect Flight Muscle ◽  
Actin Gene ◽  
Muscle Actin ◽  
Congenital Myopathies ◽  
Muscle Actin Gene

A third striated muscle actin gene is expressed during early development in the amphibian Xenopus laevis

1988 ◽  
Vol 202 (1) ◽  
pp. 67-76 ◽  
Author(s):  
Tim Mohun ◽  
Nigel Garrett ◽  
Francoise Stutz ◽  
George Spohr
Keyword(s):  
Xenopus Laevis ◽  
Early Development ◽  
Striated Muscle ◽  
Actin Gene ◽  
Muscle Actin ◽  
Muscle Actin Gene

Regulation of the human cardiac/slow-twitch troponin C gene by multiple, cooperative, cell-type-specific, and MyoD-responsive elements

1993 ◽  
Vol 13 (11) ◽  
pp. 6752-6765
Author(s):  
T H Christensen ◽  
H Prentice ◽  
R Gahlmann ◽  
L Kedes
Keyword(s):  
Skeletal Muscle ◽  
Heart Muscle ◽  
Regulatory Elements ◽  
Troponin C ◽  
Cell Type ◽  
Promoter Elements ◽  
Specific Expression ◽  
First Intron ◽  
Cell Type Specific ◽  
Slow Twitch

The cardiac troponin C (cTnC) gene produces identical transcripts in slow-twitch skeletal muscle and in heart muscle (R. Gahlmann, R. Wade, P. Gunning, and L. Kedes, J. Mol. Biol. 201:379-391, 1988). A separate gene encodes the fast-twitch skeletal muscle troponin C and is not expressed in heart muscle. We have used transient transfection to characterize the regulatory elements responsible for skeletal and cardiac cell-type-specific expression of the human cTnC (HcTnC) gene. At least four separate elements cooperate to confer tissue-specific expression of this gene in differentiated myotubes; a basal promoter (between -61 and -13) augments transcription 9-fold, upstream major regulatory sequences (between -68 and -142 and between -1319 and -4500) augment transcription as much as 39-fold, and at least two enhancer-like elements in the first intron (between +58 and +1028 and between +1029 and +1523) independently augment transcription 4- to 5-fold. These enhancers in the first intron increase myotube-specific chloramphenicol acetyltransferase activity when linked to their own promoter elements or to the heterologous simian virus 40 promoter, and the effects are multiplicative rather than additive. Each of the major myotube regulatory regions is capable of responding directly or indirectly to the myogenic determination factor, MyoD.A MyoD expression vector in 10T1/2 cells induced constructs carrying either the upstream HcTnC promoter elements or the first intron of the gene 300- to 500-fold. Expression was inhibited by cotransfection with Id, a negative regulator of basic helix-loop-helix transcription factors. The basal promoter contains five tandem TGGGC repeats that interact with Sp1 or an Sp1-like factor in nuclear extracts. Mutational analysis of this element demonstrated that two of the five repeat sequences were sufficient to support basal level muscle cell-specific transcription. Whereas the basal promoter is also critical for expression in cardiac myocytes, the elements upstream of -67 appear to play little or no role. Major augmentation of expression in cardiomyocytes is also provided by sequences in the first intron, but these are upstream (between +58 and +1028). The downstream segment of the first intron has no enhancer activity in cardiomyocytes. A specific DNA-protein complex is formed by this C2 cell enhancer with extracts from C2 cells but not cardiomyocytes. These observations suggest that tissue-specific expression of the HcTnC gene is cooperatively regulated by the complex interactions of multiple regulatory elements and that different elements are used to regulate expression in myogenic and cardiac cells.

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