Abstract
Homer represents a diversified family of scaffold and transduction proteins made up of several isoforms. Here, we present preliminary observations on skeletal muscle adaptation and plasticity in a transgenic model of Homer 2-/- mouse using a multifaceted approach entailing morphometry, quantitative RT-PCR (Reverse Transcription PCR), confocal immunofluorescence, and electrophysiology. Morphometry shows that Soleus muscle (SOL), at variance with Extensor digitorum longus muscle (EDL) and Flexor digitorum brevis muscle (FDB), displays sizable reduction of fibre cross-sectional area compared to the WT counterparts. In SOL of Homer 2-/- mice, quantitative RT-PCR indicated the upregulation of Atrogin-1 and Muscle ring finger protein 1 (MuRF1) genes, and confocal immunofluorescence showed the decrease of neuromuscular junction (NMJ) Homer content. Electrophysiological measurements of isolated FDB fibres from Homer 2-/- mice detected the exclusive presence of the adult ε-nAChR isoform excluding denervation. As for NMJ morphology, data were not conclusive, and further work is needed to ascertain whether the null Homer 2 phenotype induces any endplate remodelling. Within the context of adaptation and plasticity, the present data show that Homer 2 is a co-regulator of the normotrophic status in a muscle specific fashion.
Highlights
In Soleus muscle (SOL) muscles from Homer 2-/- mice, mean cross-sectional area (CSA) was decreased by about 24%, as compared to that of WT mice
No significant changes were detected in Extensor digitorum longus muscle (EDL) and Flexor digitorum brevis muscle (FDB)
The statistical analysis performed using one-way ANOVA and Changes in skeletal muscle mass may result from either changes in protein turnover, reflecting the balance between protein synthesis and protein degradation, or changes in cell turnover, reflecting the balance between myonuclear accretion and myonuclear loss
Summary
Homer proteins are scaffolds and transducers that play a central role in Ca2+ signalling, development, and adaptation in skeletal muscle [1,2,3,4,5]. Channels and regulates mechanotransduction in skeletal muscle [2]. Homer 1 proteins act as dynamic regulators of RyR1 activity, and the equilibrium between short and long Homer proteins at the receptor site defines the RyR1 channel activity [9]. Homer 1 expression is identical irrespective of the muscle type, whereas expression of Homer 2a/b appears to be characteristic of the slow-twitch phenotype. Distribution of Homer 2 in skeletal muscles appears to be species independent and fibre type-dependent [1,3]
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