Loss of Protein Kinase Csnk2b/CK2 beta at Neuromuscular Junctions Affects Morphology and Dynamics of Aggregated Nicotinic Acetylcholine Receptors, Neuromuscular Transmission, and Synaptic Gene Expression
Eiber N, Rehman M, Kravic B, Rudolf R, Sandri M, Hashemolhosseini S (2019)
Publication Type: Journal article
Publication year: 2019
Journal
Book Volume: 8
Journal Issue: 8
DOI: 10.3390/cells8080940
Abstract
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 beta-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 CK2 beta regarding the clustering of AChRs and downstream signaling at NMJs is unknown. Here, we compared conditional CK2 beta-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.
Authors with CRIS profile
Nane Eiber
Lehrstuhl für Biochemie und Pathobiochemie
Bojana Kravic
Lehrstuhl für Biochemie und Pathobiochemie
Said Hashemolhosseini
Lehrstuhl für Biochemie und Pathobiochemie
Involved external institutions
University of Padua / Universita degli Studi di Padova
Italy (IT)
Hochschule Mannheim University of Applied Sciences
Germany (DE)
Italy (IT)
Hochschule Mannheim University of Applied Sciences
Germany (DE)
How to cite
APA:
Eiber, N., Rehman, M., Kravic, B., Rudolf, R., Sandri, M., & Hashemolhosseini, S. (2019). Loss of Protein Kinase Csnk2b/CK2 beta at Neuromuscular Junctions Affects Morphology and Dynamics of Aggregated Nicotinic Acetylcholine Receptors, Neuromuscular Transmission, and Synaptic Gene Expression. Cells, 8(8). https://dx.doi.org/10.3390/cells8080940
MLA:
Eiber, Nane, et al. "Loss of Protein Kinase Csnk2b/CK2 beta at Neuromuscular Junctions Affects Morphology and Dynamics of Aggregated Nicotinic Acetylcholine Receptors, Neuromuscular Transmission, and Synaptic Gene Expression." Cells 8.8 (2019).
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