Cardiac troponin T is essential in sarcomere assembly and cardiac contractility
Mutations of the gene ( TNNT2 ) encoding the thin-filament contractile protein cardiac troponin T are responsible for 15% of all cases of familial hypertrophic cardiomyopathy, the leading cause of sudden death in young athletes 1 , 2 . Mutant proteins are thought to act through a dominant-negative m...
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| Published in | Nature genetics Vol. 31; no. 1; pp. 106 - 110 |
|---|---|
| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
New York
Nature Publishing Group US
01.05.2002
Nature Publishing Group |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Mutations of the gene (
TNNT2
) encoding the thin-filament contractile protein cardiac troponin T are responsible for 15% of all cases of familial hypertrophic cardiomyopathy, the leading cause of sudden death in young athletes
1
,
2
. Mutant proteins are thought to act through a dominant-negative mode that impairs function of heart muscle
3
.
TNNT2
mutations can also lead to dilated cardiomyopathy, a leading cause of heart failure
4
. Despite the importance of cardiac troponin T in human disease, its loss-of-function phenotype has not been described. We show that the zebrafish
silent heart
(
sih
) mutation affects the gene
tnnt2
. We characterize two mutated alleles of
sih
that severely reduce
tnnt2
expression: one affects mRNA splicing, and the other affects gene transcription. Tnnt2, together with α-tropomyosin (Tpma) and cardiac troponins C and I (Tnni3), forms a calcium-sensitive regulatory complex within sarcomeres
5
. Unexpectedly, in addition to loss of Tnnt2 expression in
sih
mutant hearts, we observed a significant reduction in Tpma and Tnni3, and consequently, severe sarcomere defects. This interdependence of thin-filament protein expression led us to postulate that some mutations in
tnnt2
may trigger misregulation of thin-filament protein expression, resulting in sarcomere loss and myocyte disarray, the life-threatening hallmarks of
TNNT2
mutations in mice and humans
6
,
7
. |
|---|---|
| AbstractList | Mutations of the gene (
TNNT2
) encoding the thin-filament contractile protein cardiac troponin T are responsible for 15% of all cases of familial hypertrophic cardiomyopathy, the leading cause of sudden death in young athletes
1
,
2
. Mutant proteins are thought to act through a dominant-negative mode that impairs function of heart muscle
3
.
TNNT2
mutations can also lead to dilated cardiomyopathy, a leading cause of heart failure
4
. Despite the importance of cardiac troponin T in human disease, its loss-of-function phenotype has not been described. We show that the zebrafish
silent heart
(
sih
) mutation affects the gene
tnnt2
. We characterize two mutated alleles of
sih
that severely reduce
tnnt2
expression: one affects mRNA splicing, and the other affects gene transcription. Tnnt2, together with α-tropomyosin (Tpma) and cardiac troponins C and I (Tnni3), forms a calcium-sensitive regulatory complex within sarcomeres
5
. Unexpectedly, in addition to loss of Tnnt2 expression in
sih
mutant hearts, we observed a significant reduction in Tpma and Tnni3, and consequently, severe sarcomere defects. This interdependence of thin-filament protein expression led us to postulate that some mutations in
tnnt2
may trigger misregulation of thin-filament protein expression, resulting in sarcomere loss and myocyte disarray, the life-threatening hallmarks of
TNNT2
mutations in mice and humans
6
,
7
. Mutations of the gene (TNNT2) encoding the thin-filament contractile protein cardiac troponin T are responsible for 15% of all cases of familial hypertrophic cardiomyopathy, the leading cause of sudden death in young athletes. Mutant proteins are thought to act through a dominant-negative mode that impairs function of heart muscle. TNNT2 mutations can also lead to dilated cardiomyopathy, a leading cause of heart failure. Despite the importance of cardiac troponin T in human disease, its loss-of-function phenotype has not been described. We show that the zebrafish silent heart (sih) mutation affects the gene tnnt2. We characterize two mutated alleles of sih that severely reduce tnnt2 expression: one affects mRNA splicing, and the other affects gene transcription. Tnnt2, together with alpha-tropomyosin (Tpma) and cardiac troponins C and I (Tnni3), forms a calcium-sensitive regulatory complex within sarcomeres. Unexpectedly, in addition to loss of Tnnt2 expression in sih mutant hearts, we observed a significant reduction in Tpma and Tnni3, and consequently, severe sarcomere defects. This interdependence of thin-filament protein expression led us to postulate that some mutations in tnnt2 may trigger misregulation of thin-filament protein expression, resulting in sarcomere loss and myocyte disarray, the life-threatening hallmarks of TNNT2 mutations in mice and humans. Mutations of the gene (TNNT2) encoding the thin-filament contractile protein cardiac troponin T are responsible for 15% of all cases of familial hypertrophic cardiomyopathy, the leading cause of sudden death in young athletes. Mutant proteins are thought to act through a dominant-negative mode that impairs function of heart muscle. TNNT2 mutations can also lead to dilated cardiomyopathy, a leading cause of heart failure. Despite the importance of cardiac troponin T in human disease, its loss-of-function phenotype has not been described. We show that the zebrafish silent heart (sih) mutation affects the gene tnnt2. We characterize two mutated alleles of sih that severely reduce tnnt2 expression: one affects mRNA splicing, and the other affects gene transcription. Tnnt2, together with alpha-tropomyosin (Tpma) and cardiac troponins C and I (Tnni3), forms a calcium-sensitive regulatory complex within sarcomeres. Unexpectedly, in addition to loss of Tnnt2 expression in sih mutant hearts, we observed a significant reduction in Tpma and Tnni3, and consequently, severe sarcomere defects. This interdependence of thin-filament protein expression led us to postulate that some mutations in tnnt2 may trigger misregulation of thin-filament protein expression, resulting in sarcomere loss and myocyte disarray, the life-threatening hallmarks of TNNT2 mutations in mice and humans.Mutations of the gene (TNNT2) encoding the thin-filament contractile protein cardiac troponin T are responsible for 15% of all cases of familial hypertrophic cardiomyopathy, the leading cause of sudden death in young athletes. Mutant proteins are thought to act through a dominant-negative mode that impairs function of heart muscle. TNNT2 mutations can also lead to dilated cardiomyopathy, a leading cause of heart failure. Despite the importance of cardiac troponin T in human disease, its loss-of-function phenotype has not been described. We show that the zebrafish silent heart (sih) mutation affects the gene tnnt2. We characterize two mutated alleles of sih that severely reduce tnnt2 expression: one affects mRNA splicing, and the other affects gene transcription. Tnnt2, together with alpha-tropomyosin (Tpma) and cardiac troponins C and I (Tnni3), forms a calcium-sensitive regulatory complex within sarcomeres. Unexpectedly, in addition to loss of Tnnt2 expression in sih mutant hearts, we observed a significant reduction in Tpma and Tnni3, and consequently, severe sarcomere defects. This interdependence of thin-filament protein expression led us to postulate that some mutations in tnnt2 may trigger misregulation of thin-filament protein expression, resulting in sarcomere loss and myocyte disarray, the life-threatening hallmarks of TNNT2 mutations in mice and humans. Mutations of the gene (TNNT2) encoding the thin-filament contractile protein cardiac troponin T are responsible for 15% of all cases of familial hypertrophic cardiomyopathy, the leading cause of sudden death in young athletes. Mutant proteins are thought to act through a dominant-negative mode that impairs function of heart muscle. TNNT2 mutations can also lead to dilated cardiomyopathy, a leading cause of heart failure. Despite the importance of cardiac troponin T in human disease, its loss-of-function phenotype has not been described. We show that the zebrafish silent heart (sih) mutation affects the gene tnnt2. We characterize two mutated alleles of sih that severely reduce tnnt2 expression: one affects mRNA splicing, and the other affects gene transcription. Tnnt2, together with a-tropomyosin (Tpma) and cardiac troponins C and I (Tnni3), forms a calcium-sensitive regulatory complex within sarcomeres. Unexpectedly, in addition to loss of Tnnt2 expression in sih mutant hearts, we observed a significant reduction in Tpma and Tnni3, and consequently, severe sarcomere defects. This interdependence of thin-filament protein expression led us to postulate that some mutations in tnnt2 may trigger misregulation of thin-filament protein expression, resulting in sarcomere loss and myocyte disarray, the life-threatening hallmarks of TNNT2 mutations in mice and humans. |
| Author | Sehnert, Amy J. Weinstein, Brant M. Fishman, Mark Huq, Anja Stainier, Didier Y. R. Walker, Charline |
| Author_xml | – sequence: 1 givenname: Amy J. surname: Sehnert fullname: Sehnert, Amy J. organization: Department of Biochemistry and Biophysics, Programs in Developmental Biology, Genetics and Human Genetics, University of California at San Francisco, Department of Pediatrics, University of California at San Francisco – sequence: 2 givenname: Anja surname: Huq fullname: Huq, Anja organization: Department of Biochemistry and Biophysics, Programs in Developmental Biology, Genetics and Human Genetics, University of California at San Francisco – sequence: 3 givenname: Brant M. surname: Weinstein fullname: Weinstein, Brant M. organization: Laboratory of Molecular Genetics, National Institute of Child Health & Human Development, National Institutes of Health – sequence: 4 givenname: Charline surname: Walker fullname: Walker, Charline organization: Institute of Neuroscience, University of Oregon – sequence: 5 givenname: Mark surname: Fishman fullname: Fishman, Mark organization: Cardiovascular Research Center, Massachusetts General Hospital – sequence: 6 givenname: Didier Y. R. surname: Stainier fullname: Stainier, Didier Y. R. email: didier_stainier@biochem.ucsf.edu organization: Department of Biochemistry and Biophysics, Programs in Developmental Biology, Genetics and Human Genetics, University of California at San Francisco |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14184194$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/11967535$$D View this record in MEDLINE/PubMed |
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| CODEN | NGENEC |
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| Keywords | Heart Tropomyosin Contractility Cardiovascular disease Gene expression Myocardial disease Troponin T Vertebrata Brachydanio rerio Troponin I Molecular assembly Heart disease Pisces Hypertrophic cardiomyopathy Mutation Sarcomere |
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| Snippet | Mutations of the gene (
TNNT2
) encoding the thin-filament contractile protein cardiac troponin T are responsible for 15% of all cases of familial hypertrophic... Mutations of the gene (TNNT2) encoding the thin-filament contractile protein cardiac troponin T are responsible for 15% of all cases of familial hypertrophic... |
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| SubjectTerms | Agriculture Animal Genetics and Genomics Animals Athletes Base Sequence Biological and medical sciences Biomedical and Life Sciences Biomedicine Calcium Cancer Research Cardiomyocytes Cardiomyopathy Cardiomyopathy, Hypertrophic, Familial - genetics Classical genetics, quantitative genetics, hybrids Cloning, Molecular Danio rerio DNA - genetics Edema Embryos Fundamental and applied biological sciences. Psychology Gene Function Genetics of eukaryotes. Biological and molecular evolution Genotype & phenotype Human Genetics Humans letter Mice Microscopy Molecular Sequence Data Mutants Mutation Myocardial Contraction - genetics Myocardial Contraction - physiology Myocardium - metabolism Myocardium - pathology Phenotype Protein expression Proteins Sarcomeres - pathology Troponin T - deficiency Troponin T - genetics Troponin T - physiology Vertebrata Zebrafish - embryology Zebrafish - genetics Zebrafish - physiology |
| Title | Cardiac troponin T is essential in sarcomere assembly and cardiac contractility |
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