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Neuromuscular Junction as an Entity of Nerve-Muscle Communication
Article

Loss of Protein Kinase Csnk2b/CK2β at Neuromuscular Junctions Affects Morphology and Dynamics of Aggregated Nicotinic Acetylcholine Receptors, Neuromuscular Transmission, and Synaptic Gene Expression

1
Institute of Biochemistry, Medical Faculty, Friedrich-Alexander-University of Erlangen-Nürnberg, 91054 Erlangen, Germany
2
Weill Cornell Medical College, Department of Medicine, New York, NY 10065, USA
3
Faculty of Biology, University of Duisburg-Essen, 45141 Essen, Germany
4
Institute of Molecular- and Cellular Biology, University of Applied Sciences Mannheim, 68163 Mannheim, Germany
5
Department of Biomedical Science, University of Padova, 35122 Padova, Italy
*
Author to whom correspondence should be addressed.
Cells 2019, 8(8), 940; https://doi.org/10.3390/cells8080940
Received: 28 June 2019 / Revised: 21 July 2019 / Accepted: 12 August 2019 / Published: 20 August 2019
The protein kinase Csnk2/CK2 is important for cell proliferation, differentiation, and survival. Previously, we showed that CK2 binds distinctive proteins at neuromuscular junctions (NMJs) of mice and phosphorylates some of them. CK2 likely stabilizes clustered nicotinic acetylcholine receptors (AChRs). In the absence of the β-subunit of CK2 in skeletal muscle fibers, mice develop an age-dependent decrease of grip strength accompanied by NMJ fragmentation and impairments of neuromuscular transmission. However, the precise role of CK2β regarding the clustering of AChRs and downstream signaling at NMJs is unknown. Here, we compared conditional CK2β-deficient mice with controls and found in the mutants (1) a lower decrement of endplate potentials after repetitive stimulation and decrements of nerve-evoked compound muscle action potentials decayed more rapidly after synaptic transmission was partially blocked, (2) that their muscle weakness was partially rescued by administration of an acetylcholine esterase inhibitor, (3) fragmented NMJs and impaired AChR clustering was detected in muscles and cultured muscle cells, (4) enlarged myonuclei, (5) impaired synaptic gene expression, and (6) a high turnover rate of their AChR clusters in vivo. Altogether, our data demonstrate a role for CK2 at the NMJ by maintaining a high density of AChRs and ensuring physiological synaptic gene expression. View Full-Text
Keywords: Csnk2b; Casein Kinase 2; acetylcholine receptor; neuromuscular junction Csnk2b; Casein Kinase 2; acetylcholine receptor; neuromuscular junction
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MDPI and ACS Style

Eiber, N.; Rehman, M.; Kravic, B.; Rudolf, R.; Sandri, M.; Hashemolhosseini, S. Loss of Protein Kinase Csnk2b/CK2β at Neuromuscular Junctions Affects Morphology and Dynamics of Aggregated Nicotinic Acetylcholine Receptors, Neuromuscular Transmission, and Synaptic Gene Expression. Cells 2019, 8, 940. https://doi.org/10.3390/cells8080940

AMA Style

Eiber N, Rehman M, Kravic B, Rudolf R, Sandri M, Hashemolhosseini S. Loss of Protein Kinase Csnk2b/CK2β at Neuromuscular Junctions Affects Morphology and Dynamics of Aggregated Nicotinic Acetylcholine Receptors, Neuromuscular Transmission, and Synaptic Gene Expression. Cells. 2019; 8(8):940. https://doi.org/10.3390/cells8080940

Chicago/Turabian Style

Eiber, Nane, Michael Rehman, Bojana Kravic, Rüdiger Rudolf, Marco Sandri, and Said Hashemolhosseini. 2019. "Loss of Protein Kinase Csnk2b/CK2β at Neuromuscular Junctions Affects Morphology and Dynamics of Aggregated Nicotinic Acetylcholine Receptors, Neuromuscular Transmission, and Synaptic Gene Expression" Cells 8, no. 8: 940. https://doi.org/10.3390/cells8080940

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