PUBLICATION
BCL2L13 at endoplasmic reticulum-mitochondria contact sites regulates calcium homeostasis to maintain skeletal muscle function
- Authors
- Grepper, D., Tabasso, C., Zanou, N., Aguettaz, A.K.F., Castro-Sepulveda, M., Ziegler, D.V., Lagarrigue, S., Arribat, Y., Martinotti, A., Ebrahimi, A., Daraspe, J., Fajas, L., Amati, F.
- ID
- ZDB-PUB-240823-1
- Date
- 2024
- Source
- iScience 27: 110510110510 (Journal)
- Registered Authors
- Aguettaz, Axel, Amati, Francesca, Ebrahimi, Ammar, Grepper, Dogan, Lagarrigue, Silviane, Martinotti, Adrien, Tabasso, Cassandra
- Keywords
- cell biology, pharmacology
- MeSH Terms
- none
- PubMed
- 39175772 Full text @ iScience
Citation
Grepper, D., Tabasso, C., Zanou, N., Aguettaz, A.K.F., Castro-Sepulveda, M., Ziegler, D.V., Lagarrigue, S., Arribat, Y., Martinotti, A., Ebrahimi, A., Daraspe, J., Fajas, L., Amati, F. (2024) BCL2L13 at endoplasmic reticulum-mitochondria contact sites regulates calcium homeostasis to maintain skeletal muscle function. iScience. 27:110510110510.
Abstract
The physical connection between mitochondria and endoplasmic reticulum (ER) is an essential signaling hub to ensure organelle and cellular functions. In skeletal muscle, ER-mitochondria calcium (Ca2+) signaling is crucial to maintain cellular homeostasis during physical activity. High expression of BCL2L13, a member of the BCL-2 family, was suggested as an adaptive response in endurance-trained human subjects. In adult zebrafish, we found that the loss of Bcl2l13 impairs skeletal muscle structure and function. Ca2+ signaling is altered in Bcl2l13 knockout animals and mitochondrial complexes activity is decreased. Organelle fractioning in mammalian cells shows BCL2L13 at mitochondria, ER, and mitochondria-associated membranes. ER-mitochondria contact sites number is not modified by BCL2L13 modulation, but knockdown of BCL2L13 in C2C12 cells changes cytosolic Ca2+ release and mitochondrial Ca2+ uptake. This suggests that BCL2L13 interaction with mitochondria and ER, and its role in Ca2+ signaling, contributes to proper skeletal muscle function.
Genes / Markers
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Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
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Orthology
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