Triad formation: organization and function of the sarcoplasmic reticulum calcium release channel and triadin in normal and dysgenic muscle in vitro - PubMed (original) (raw)

Triad formation: organization and function of the sarcoplasmic reticulum calcium release channel and triadin in normal and dysgenic muscle in vitro

B E Flucher et al. J Cell Biol. 1993 Dec.

Abstract

Excitation-contraction (E-C) coupling is thought to involve close interactions between the calcium release channel (ryanodine receptor; RyR) of the sarcoplasmic reticulum (SR) and the dihydropyridine receptor (DHPR) alpha 1 subunit in the T-tubule membrane. Triadin, a 95-kD protein isolated from heavy SR, binds both the RyR and DHPR and may thus participate in E-C coupling or in interactions responsible for the formation of SR/T-tubule junctions. Immunofluorescence labeling of normal mouse myotubes shows that the RyR and triadin co-aggregate with the DHPR in punctate clusters upon formation of functional junctions. Dysgenic myotubes with a deficiency in the alpha 1 subunit of the DHPR show reduced expression and clustering of RyR and triadin; however, both proteins are still capable of forming clusters and attaining mature cross-striated distributions. Thus, the molecular organization of the RyR and triadin in the terminal cisternae of SR as well as its association with the T-tubules are independent of interactions with the DHPR alpha 1 subunit. Analysis of calcium transients in dysgenic myotubes with fluorescent calcium indicators reveals spontaneous and caffeine-induced calcium release from intracellular stores similar to those of normal muscle; however, depolarization-induced calcium release is absent. Thus, characteristic calcium release properties of the RyR do not require interactions with the DHPR; neither do they require the normal organization of the RyR in the terminal SR cisternae. In hybrids of dysgenic myotubes fused with normal cells, both action potential-induced calcium transients and the normal clustered organization of the RyR are restored in regions expressing the DHPR alpha 1 subunit.

PubMed Disclaimer

Cited by

Formation of junctions involved in excitation-contraction coupling in skeletal and cardiac muscle.
Flucher BE, Franzini-Armstrong C. Flucher BE, et al. Proc Natl Acad Sci U S A. 1996 Jul 23;93(15):8101-6. doi: 10.1073/pnas.93.15.8101. Proc Natl Acad Sci U S A. 1996. PMID: 8755610 Free PMC article.
Acute RyR1 Ca2+ leak enhances NADH-linked mitochondrial respiratory capacity.
Zanou N, Dridi H, Reiken S, Imamura de Lima T, Donnelly C, De Marchi U, Ferrini M, Vidal J, Sittenfeld L, Feige JN, Garcia-Roves PM, Lopez-Mejia IC, Marks AR, Auwerx J, Kayser B, Place N. Zanou N, et al. Nat Commun. 2021 Dec 10;12(1):7219. doi: 10.1038/s41467-021-27422-1. Nat Commun. 2021. PMID: 34893614 Free PMC article.
The relationship between form and function throughout the history of excitation-contraction coupling.
Franzini-Armstrong C. Franzini-Armstrong C. J Gen Physiol. 2018 Feb 5;150(2):189-210. doi: 10.1085/jgp.201711889. Epub 2018 Jan 9. J Gen Physiol. 2018. PMID: 29317466 Free PMC article. Review.
Extraction of junctional complexes from triad junctions of rabbit skeletal muscle.
Motoike HK, Caswell AH, Smilowitz HM, Brandt NR. Motoike HK, et al. J Muscle Res Cell Motil. 1994 Oct;15(5):493-504. doi: 10.1007/BF00121156. J Muscle Res Cell Motil. 1994. PMID: 7860698
Cooperation of two-domain Ca(2+) channel fragments in triad targeting and restoration of excitation- contraction coupling in skeletal muscle.
Flucher BE, Weiss RG, Grabner M. Flucher BE, et al. Proc Natl Acad Sci U S A. 2002 Jul 23;99(15):10167-72. doi: 10.1073/pnas.122345799. Epub 2002 Jul 15. Proc Natl Acad Sci U S A. 2002. PMID: 12119388 Free PMC article.

References

1. J Biol Chem. 1987 Sep 5;262(25):11904-7 - PubMed
1. J Cell Biol. 1989 Jul;109(1):135-47 - PubMed
1. J Neurochem. 1987 Nov;49(5):1498-506 - PubMed
1. Dev Biol. 1987 Dec;124(2):490-503 - PubMed
1. Nature. 1988 Jan 28;331(6154):315-9 - PubMed

Triad formation: organization and function of the sarcoplasmic reticulum calcium release channel and triadin in normal and dysgenic muscle in vitro - PubMed (original) (raw)