scholarly journals Lola regulates glutamate receptor expression at the Drosophila neuromuscular junction

Biology Open ◽  
2012 ◽  
Vol 1 (4) ◽  
pp. 362-375 ◽  
Author(s):  
A. Fukui ◽  
M. Inaki ◽  
G. Tonoe ◽  
H. Hamatani ◽  
M. Homma ◽  
...  
Keyword(s):  
Neuromuscular Junction ◽  
Glutamate Receptor ◽  
Receptor Expression

scholarly journals Drosophila Mon1 and Rab7 interact to regulate glutamate receptor levels at the neuromuscular junction

2020 ◽  
Vol 64 (4-5-6) ◽  
pp. 289-297
Author(s):  
Anagha Basargekar ◽  
Shweta Yogi ◽  
Zeeshan Mushtaq ◽  
Senthilkumar Deivasigamani ◽  
Vimlesh Kumar ◽  
...  
Keyword(s):  
Neuromuscular Junction ◽  
Glutamate Receptor ◽  
Receptor Expression ◽  
Strong Increase ◽  
Short Life Span ◽  
Early Endosomes ◽  
Severe Motor ◽  
Strength And Plasticity ◽  
Larval Neuromuscular Junction

Regulation of post-synaptic receptors plays an important role in determining synaptic strength and plasticity. The Drosophila larval neuromuscular junction (nmj) has been used extensively as a model to understand some of these processes. In this context, we are interested in the role of Drosophila Monensin sensitivity protein 1 (DMon1) in regulating glutamate receptor (GluRIIA) levels at the nmj. DMon1 is an evolutionarily conserved protein which, in complex with calcium caffeine zinc sensitivity1 (CCZ1), regulates the conversion of early endosomes to late endosomes through recruitment of Rab7. C-terminal deletion mutants of Dmon1 (Dmon1Δ181) exhibit lethality. The escapers have a short life span and exhibit severe motor defects. At the nmj, these mutants show defects in synaptic morphology and a strong increase in GluRIIA levels. The mechanism by which Dmon1 regulates GluRIIA is unclear. In this study, we have characterized an EMS mutant referred to as pog 1 and demonstrate it to be an allele of Dmon1. Further, we have examined the role of rab7 in regulating GluRIIA. We show that similar to Dmon1, knock-down of rab7 using RNAi in neurons, but not muscles, leads to an increase in GluRIIA. Loss of one copy each of Dmon1 and rab7 leads to a synergistic increase in receptor expression. Further, overexpression of an activated Rab7 can rescue the GluRIIA phenotype observed in Dmon1Δ181 mutants. Together, these results highlight a neuronal role for Rab7 in GluRIIA regulation and underscore the importance of the endo-lysosomal pathway in this process.

scholarly journals Dmon1 and rab7 interact to regulate glutamate receptor GluRIIA levels at the larval Drosophila neuromuscular junction

2020 ◽  
Author(s):  
Anagha Basargekar ◽  
Shweta Yogi ◽  
Zeeshan Mushtaq ◽  
Senthil Deivasigamani ◽  
Vimlesh Kumar ◽  
...  
Keyword(s):  
Neuromuscular Junction ◽  
Glutamate Receptor ◽  
Receptor Expression ◽  
Strong Increase ◽  
Short Life Span ◽  
Early Endosomes ◽  
Severe Motor ◽  
Strength And Plasticity ◽  
Larval Neuromuscular Junction

AbstractRegulation of post-synaptic receptors plays an important role in determining synaptic strength and plasticity. The Drosophila larval neuromuscular junction (nmj) has been used extensively as a model to understand some of these processes. In this context, we are interested in the role of Drosophila Monensin sensitive protein 1 (DMon1) in regulating glutamate receptor (GluRIIA) levels at the nmj. Dmon1 is an evolutionarily conserved protein which, in complex with CCZ1, regulates the conversion of early endosomes to late endosomes through recruitment of Rab7. C-terminal deletion mutants of Dmon1 (Dmon1Δ181) exhibit lethality. The escapers have a short life span and exhibit severe motor defects. At the nmj, these mutants show a defects in synaptic morphology and a strong increase in glutamate receptor GluRIIA levels. The mechanism by which Dmon1 regulates GluRIIA is unclear.In this study, we have described the characterization the mutation in an EMS mutant referred to as pog1 and demonstrate this mutant to be an allele of Dmon1. Further, we have examined the role of rab7 in regulation the of GluRIIA. We show that similar to Dmon1, knock-down of rab7 using RNAi in neurons, and not muscles, leads to an increase in GluRIIA. Loss of one copy each of Dmon1 with rab7 leads to a synergistic increase in receptor expression. Further, overexpression of an activated Rab7 can rescue the GluRIIA phenotype observed in Dmon1Δ181 mutants. Together, these results highlight a neuronal role for Rab7 in GluRIIA regulation and underscores the important of the endo-lysosomal pathway in this process.

scholarly journals Glial Wingless/Wnt Regulates Glutamate Receptor Clustering and Synaptic Physiology at the Drosophila Neuromuscular Junction

2014 ◽  
Vol 34 (8) ◽  
pp. 2910-2920 ◽  
Author(s):  
K. S. Kerr ◽  
Y. Fuentes-Medel ◽  
C. Brewer ◽  
R. Barria ◽  
J. Ashley ◽  
...  
Keyword(s):  
Neuromuscular Junction ◽  
Glutamate Receptor ◽  
Receptor Clustering ◽  
Synaptic Physiology

scholarly journals Glutamate Receptor Expression in Multiple Sclerosis Lesions

2008 ◽  
Vol 18 (1) ◽  
pp. 52-61 ◽  
Author(s):  
Jia Newcombe ◽  
Alim Uddin ◽  
Rosamund Dove ◽  
Bela Patel ◽  
Lechoslaw Turski ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Glutamate Receptor ◽  
Receptor Expression

TRPC1 and metabotropic glutamate receptor expression in rat auditory midbrain neurons

2015 ◽  
Vol 93 (6) ◽  
pp. 964-972 ◽  
Author(s):  
Maria Ll. Valero ◽  
Elena Caminos ◽  
Jose M. Juiz ◽  
Juan R. Martinez-Galan
Keyword(s):  
Glutamate Receptor ◽  
Metabotropic Glutamate Receptor ◽  
Receptor Expression ◽  
Auditory Midbrain ◽  
Metabotropic Glutamate ◽  
Midbrain Neurons
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