ArticleThe Journal of biological chemistry2009
Proper restoration of excitation-contraction coupling in the dihydropyridine receptor beta1-null zebrafish relaxed is an exclusive function of the beta1a subunit.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 72 citations in OpenAlex.
- Interactive Role of the DHPR βBiomolecules · 2025Article
- In situ structural insights into the excitation-contraction coupling mechanism of skeletal muscle.Science advances · 2024Article
- Design and Applications of Genetically-Encoded Voltage-Dependent Calcium Channel Inhibitors.Handbook of experimental pharmacology · 2023Review
- CaHandbook of experimental pharmacology · 2023Article
- Selective posttranslational inhibition of CaNature communications · 2022Article
- The distal C terminus of the dihydropyridine receptor βProceedings of the National Academy of Sciences of the United States of America · 2022Article
- The Builders of the Junction: Roles of Junctophilin1 and Junctophilin2 in the Assembly of the Sarcoplasmic Reticulum-Plasma Membrane Junctions in Striated Muscle.Biomolecules · 2022Review
- Into the spotlight: RGK proteins in skeletal muscle.Cell calcium · 2021Review
- Physiological and Pathological Relevance of Selective and Nonselective CaAdvances in experimental medicine and biology · 2021Article
- Isoform-specific regulation of HCN4 channels by a family of endoplasmic reticulum proteins.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Skeletal muscle CaPflugers Archiv : European journal of physiology · 2020Review
- Excitation-contraction coupling in skeletal muscle: recent progress and unanswered questions.Biophysical reviews · 2020Review
- CaNature communications · 2019Article
- Duplex signaling by CaM and Stac3 enhances CaThe Journal of general physiology · 2018Article
- Voltage sensing mechanism in skeletal muscle excitation-contraction coupling: coming of age or midlife crisis?Skeletal muscle · 2018Review
- Stac proteins associate with the critical domain for excitation-contraction coupling in the II-III loop of CaThe Journal of general physiology · 2018Article
- De novo reconstitution reveals the proteins required for skeletal muscle voltage-induced CaProceedings of the National Academy of Sciences of the United States of America · 2017Article
- Transport of the alpha subunit of the voltage gated L-type calcium channel through the sarcoplasmic reticulum occurs prior to localization to triads and requires the beta subunit but not Stac3 in skeletal muscles.Traffic (Copenhagen, Denmark) · 2017Article
- Structural and biophysical analyses of the skeletal dihydropyridine receptor β subunit βThe Journal of biological chemistry · 2017Article
- Congenital myopathy results from misregulation of a muscle Ca2+ channel by mutant Stac3.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
The paralyzed zebrafish strain relaxed carries a null mutation for the skeletal muscle dihydropyridine receptor (DHPR) beta(1a) subunit. Lack of beta(1a) results in (i) reduced membrane expression of the pore forming DHPR alpha(1S) subunit, (ii) elimination of alpha(1S) charge movement, and (iii) impediment of arrangement of the DHPRs in groups of four (tetrads) opposing the ryanodine receptor (RyR1), a structural prerequisite for skeletal muscle-type excitation-contraction (EC) coupling. In this study we used relaxed larvae and isolated myotubes as expression systems to discriminate specific functions of beta(1a) from rather general functions of beta isoforms. Zebrafish and mammalian beta(1a) subunits quantitatively restored alpha(1S) triad targeting and charge movement as well as intracellular Ca(2+) release, allowed arrangement of DHPRs in tetrads, and most strikingly recovered a fully motile phenotype in relaxed larvae. Interestingly, the cardiac/neuronal beta(2a) as the phylogenetically closest, and the ancestral housefly beta(M) as the most distant isoform to beta(1a) also completely recovered alpha(1S) triad expression and charge movement. However, both revealed drastically impaired intracellular Ca(2+) transients and very limited tetrad formation compared with beta(1a). Consequently, larval motility was either only partially restored (beta(2a)-injected larvae) or not restored at all (beta(M)). Thus, our results indicate that triad expression and facilitation of 1,4-dihydropyridine receptor (DHPR) charge movement are common features of all tested beta subunits, whereas the efficient arrangement of DHPRs in tetrads and thus intact DHPR-RyR1 coupling is only promoted by the beta(1a) isoform. Consequently, we postulate a model that presents beta(1a) as an allosteric modifier of alpha(1S) conformation enabling skeletal muscle-type EC coupling.
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