Role of autophagy, SQSTM1, SH3GLB1, and TRIM63 in the turnover of nicotinic acetylcholine receptors

Khan, Muzamil Majid; Strack, S.; Wild, Franziska; Hanashima, Akira; Gasch, Alexander; Brohm, Kathrin; Reischl, Markus; Carnio, Silvia; Labeit, D.; Sandri, Marco; Labeit, Siegfried; Rudolf, Rüdiger

doi:10.4161/auto.26841

Cited by 94 publications

(113 citation statements)

References 56 publications

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“…Rowland et al showed that acetylcholine receptors do not traffi c to autophagosomes in the non-innervated muscle cells of C. elegans [49] . In contrast, a recent report demonstrated that in mouse tibialis anterior muscles, autophagy contributes to the basal and atrophy-induced turnover of muscletype cholinergic receptors, nicotinic/nicotinic acetylcholine receptors in a tripartite motif containing 63 (TRIM63)-dependent manner [53] . Such a discrepancy might be due to the different species used in experiments.…”

Section: In Addition To Gabars Glutamatergic N-methyl-d-aspartate Rementioning

confidence: 88%

Autophagy in synaptic development, function, and pathology

et al. 2015

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In the nervous system, neurons contact each other to form neuronal circuits and drive behavior, relying heavily on synaptic connections. The proper development and growth of synapses allows functional transmission of electrical information between neurons or between neurons and muscle fi bers. Defects in synapse-formation or development lead to many diseases. Autophagy, a major determinant of protein turnover, is an essential process that takes place in developing synapses. During the induction of autophagy, proteins and cytoplasmic components are encapsulated in autophagosomes, which fuse with lysosomes to form autolysosomes. The cargoes are subsequently degraded and recycled. However, aberrant autophagic activity may lead to synaptic dysfunction, which is a common pathological characteristic in several disorders. Here, we review the current understanding of autophagy in regulating synaptic development and function. In addition, autophagy-related synaptic dysfunction in human diseases is also summarized.

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Section: In Addition To Gabars Glutamatergic N-methyl-d-aspartate Rementioning

confidence: 88%

Autophagy in synaptic development, function, and pathology

et al. 2015

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“…Several genome-wide screens, albeit not aimed at studying TRIMs, indicate that a number of additional TRIMs (TRIM29, TRIM51 and TRIM69) modulate autophagy (Lipinski et al, 2010;McKnight et al, 2012). Furthermore, TRIM13, TRIM28, TRIM55, TRIM56 and TRIM63 have been reported in separate studies to affect autophagy (Tomar et al, 2012;Barde et al, 2013;Pizon et al, 2013;Yang et al, 2013;Khan et al, 2014;Kimura et al, 2015;Pineda et al, 2015).…”

Section: Trims As Autophagy Regulatorsmentioning

confidence: 99%

“…TRIMs affect autophagy as a whole process (Lipinski et al, 2010;Perera et al, 2011;McKnight et al, 2012;Tomar et al, 2012;Barde et al, 2013;Pizon et al, 2013;Khan et al, 2014;Pineda et al, 2015) and interact with ATG factors (Behrends et al, 2010;Yang et al, 2013;Mandell et al, 2014;Kimura et al, 2015). Of the 82 human TRIMs, 49 TRIMs have an effect on autophagy (Table S1).…”

Section: Trims As Autophagy Regulatorsmentioning

confidence: 99%

“…2C; Table S1) (Lipinski et al, 2010;Niida et al, 2010;Perera et al, 2011;McKnight et al, 2012;Tomar et al, 2012;Barde et al, 2013;Pizon et al, 2013;Yang et al, 2013;Khan et al, 2014;Mandell et al, 2014;Choi et al, 2015;Kimura et al, 2015). TRIMs act as autophagy receptor regulators (meaning that they act as both receptors and platforms for assembly of autophagosome machinery) by two means.…”

Section: Trims Function As Autophagic 'Receptor Regulators'mentioning

confidence: 99%

“…These and additional roles are linked to a variety of health conditions. For instance, TRIMs have been implicated in autoimmune and inflammatory disorders (Jefferies et al, 2011;Kawai and Akira, 2011;Kimura et al, 2015) that are associated with genetic polymorphisms (French FMF Consortium, 1997;The International FMF Consortium Guido, 1997), as well as in insulin resistance (Karlberg et al, 2005;Song et al, 2013), urate metabolism (Köttgen et al, 2013), cancer (Hatakeyama, 2011), asthma (Shin et al, 2011;Collison et al, 2013), and neurodegenerative and neuromuscular diseases (Leonhardt et al, 1994;Khan et al, 2014). Among the best-studied roles for TRIMs is their role in cell-autonomous antiviral defense, a trend partially driven by intense research focusing on human immunodeficiency virus (HIV) (Stremlau et al, 2004;Nisole et al, 2005;Pertel et al, 2011;Versteeg et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

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Precision autophagy directed by receptor regulators – emerging examples within the TRIM family

Kimura

Mandell

Deretić

2016

Journal of Cell Science

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Selective autophagy entails cooperation between target recognition and assembly of the autophagic apparatus. Target recognition is conducted by receptors that often recognize tags, such as ubiquitin and galectins, although examples of selective autophagy independent of these tags are emerging. It is less known how receptors cooperate with the upstream autophagic regulators, beyond the well-characterized association of receptors with Atg8 or its homologs, such as LC3B (encoded by MAP1LC3B), on autophagic membranes. The molecular details of the emerging role in autophagy of the family of proteins called TRIMs shed light on the coordination between cargo recognition and the assembly and activation of the principal autophagy regulators. In their autophagy roles, TRIMs act both as receptors and as platforms ('receptor regulators') for the assembly of the core autophagy regulators, such as ULK1 and Beclin 1 in their activated state. As autophagic receptors, TRIMs can directly recognize endogenous or exogenous targets, obviating a need for intermediary autophagic tags, such as ubiquitin and galectins. The receptor and regulatory features embodied within the same entity allow TRIMs to govern cargo degradation in a highly exact process termed 'precision autophagy'.

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Progressive resistance exercise prevents muscle strength loss due to muscle atrophy induced by methylmercury systemic intoxication

Gouvêa

Silva

Cabral

et al. 2021

JCSM Clinical Reports

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BackgroundThis study investigated the effects of methylmercury intoxication on mice skeletal muscle subjected or not to progressive resistance training (RT).MethodsFour experimental groups were formed. Control and Con + RT received water and methylmercury (MeHg) and MeHg + RT groups received methylmercury (5 mg/kg/day), via gavage for 14 days. The Con + RT and MeHg + RT animals performed weighted ladder climbing RT, three times a week for 4 weeks. Animal muscle strength and gastrocnemius and soleus cross‐section area, fibrosis, myosin heavy chains (MyHCs), E3‐ligases MAFbx and MuRF1, 20S proteasome (P20S) and LC3‐II content were analysed. In addition, P20S chymotrypsin‐like activity was evaluated.ResultsResistance training protected MeHg + RT mice against strength loss but not against muscle atrophy. The latter appeared to be associated with MyHCs significant content reductions observed in the MeHg and MeHg + RT groups. In soleus muscle, there was an increase in E3‐ligases and P20S levels and P20S activity in both methylmercury groups compared with control ones. This pattern was also observed for gastrocnemius muscle, except for P20S content and activity that decreased. The P‐AKT content decreased in the soleus and gastrocnemius of the MeHg animals while significant elevation of LC3‐II content levels occurred.ConclusionsThe accumulation of methylmercury caused an increase in skeletal muscle MyHCs degradation, resulting in muscle atrophy that was reinforced by the elevated fibrosis area. Although RT did not reverse this condition, maintenance of muscle strength levels in animals submitted to MeHg + RT was detected. We believe that RT somewhat protected MeHg from damage to neural muscle structures, to be further investigated.

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Role of autophagy, SQSTM1, SH3GLB1, and TRIM63 in the turnover of nicotinic acetylcholine receptors

Cited by 94 publications

References 56 publications

Autophagy in synaptic development, function, and pathology

Autophagy in synaptic development, function, and pathology

Precision autophagy directed by receptor regulators – emerging examples within the TRIM family

Progressive resistance exercise prevents muscle strength loss due to muscle atrophy induced by methylmercury systemic intoxication

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