Characterization of synaptogyrin 3 as a new synaptic vesicle protein

Belizaire, Roger; Komanduri, Cheryl; Wooten, Kerry; Chen, Ming; Thaller, Christina; Janz, Roger

doi:10.1002/cne.20008

Cited by 41 publications

(46 citation statements)

References 65 publications

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“…Thus, synaptogyrin-3 is missorted in σ1B −/− synapses and accumulates, like SCAMP-1, in as yet unidentified membranes, which are not part of the SV recycling pool. In addition to its presence in the hippocampus, synaptogyrin-3 is also expressed in the substantia nigra, pars reticulata, pallidum and deep cerebellar nuclei, structures involved in the regulation of motor activities, and σ1B −/− mice have impaired motor coordination and are hypoactive [29,3]. Therefore, synaptogyrin-3 is a candidate for direct AP-1/σ1B-dependent Fig.…”

Section: Discussionmentioning

confidence: 93%

“…Synaptogyrin-1 and −3 can reside in the same SV, but while synaptogyrin-1 is ubiquitously expressed, synaptogyrin-3 expression is restricted to the hippocampal mossy fibres [29]. Synaptogyrin-1 distribution is hardly affected by the σ1B deficiency, but synaptogyrin-3 was reduced by 31 % in cortices and enriched by 50 % in synaptosomes.…”

Section: Sv Proteins Are Either Degraded Stored or Misroutedmentioning

confidence: 98%

“…We focused our WB analysis on SV proteins of the tetraspanin family (physin, gyrin and secretory carrierassociated membrane protein (SCAMP) families) because they can be used as markers for SV classes [29,30]. SCAMPs 1-5 are all found in early and late endosomes and are involved in the regulation of fusion pore opening/closure.…”

Section: Sv Proteins Are Either Degraded Stored or Misroutedmentioning

confidence: 99%

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AP-1/σ1B-Dependent SV Protein Recycling Is Regulated in Early Endosomes and Is Coupled to AP-2 Endocytosis

et al. 2014

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Adaptor protein (AP)-1/σ1B(-/-) mice have reduced synaptic-vesicle (SV) recycling and increased endosomes. Mutant mice have impaired spatial memory, and σ1B-deficient humans have a severe mental retardation. In order to define these σ1B(-/-) 'bulk' endosomes and to determine their functions in SV recycling, we developed a protocol to separate them from the majority of the neuronal endosomes. The σ1B(-/-) 'bulk' endosomes proved to be classic early endosomes with an increase in the phospholipid phosphatidylinositol 3-phosphate (PI-3-P), which recruits proteins mediating protein sorting out of early endosomes into different routes. σ1B deficiency induced alterations in the endosomal proteome reveals two major functions: SV protein storage and sorting into endolysosomes. Alternative endosomal recycling pathways are not up-regulated, but certain SV proteins are misrouted. Tetraspanins are enriched in σ1B(-/-) synaptosomes, but not in their endosomes or in their clathrin-coated-vesicles (CCVs), indicating AP-1/σ1B-dependent sorting. Synapses contain also more AP-2 CCV, although it is expected that they contain less due to reduced SV recycling. Coat composition of these AP-2 CCVs is altered, and thus, they represent a subpopulation of AP-2 CCVs. Association of calmodulin-dependent protein kinase (CaMK)-IIα, -δ and casein kinase (CK)-IIα with the endosome/SV pool is altered, as well as 14-3-3η, indicating changes in specific signalling pathways regulating synaptic plasticity. The accumulation of early endosomes and endocytotic AP-2 CCV indicates the regulation of SV recycling via early endosomes by the interdependent regulation of AP-2-mediated endocytosis and AP-1/σ1B-mediated SV reformation.

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Section: Discussionmentioning

confidence: 93%

Section: Sv Proteins Are Either Degraded Stored or Misroutedmentioning

confidence: 98%

Section: Sv Proteins Are Either Degraded Stored or Misroutedmentioning

confidence: 99%

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AP-1/σ1B-Dependent SV Protein Recycling Is Regulated in Early Endosomes and Is Coupled to AP-2 Endocytosis

et al. 2014

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“…Amysin (for which two transcripts were downregulated) regulates the assembly of the SNARE composite by forming stable complexes with the synaptic t-SNAREs syntaxin 1 and SNAP25, and inhibits exocytosis by interfering with synaptobrevin (Scales et al, 2002). Synaptogyrin 3 is a recently discovered brain-specific vesicular protein of unknown function (Belizaire et al, 2004). After identification of the many changes in this functional group by pairwise analysis, we conducted a post hoc group-wise analysis of other release-related genes represented on the microarray.…”

Section: Discussionmentioning

confidence: 99%

Distinctive Profiles of Gene Expression in the Human Nucleus Accumbens Associated with Cocaine and Heroin Abuse

Albertson

Schmidt

Kapatos

et al. 2006

Neuropsychopharmacol

126

125

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Drug abuse is thought to induce long-term cellular and behavioral adaptations as a result of alterations in gene expression. Understanding the molecular consequences of addiction may contribute to the development of better treatment strategies. This study utilized highthroughput Affymetrix microarrays to identify gene expression changes in the post-mortem nucleus accumbens of chronic heroin abusers. These data were analyzed independently and in relation to our previously reported data involving human cocaine abusers, in order to determine which expression changes were drug specific and which may be common to the phenomenon of addiction. A significant decrease in the expression of numerous genes encoding proteins involved in presynaptic release of neurotransmitter was seen in heroin abusers, a finding not seen in the cocaine-abusing cohort. Conversely, the striking decrease in myelin-related genes observed in cocaine abusers was not evident in our cohort of heroin subjects. Overall, little overlap in gene expression profiles was seen between the two drug-abusing cohorts: out of the approximately 39 000 transcripts investigated, the abundance of only 25 was significantly changed in both cocaine and heroin abusers, with nearly one-half of these being altered in opposite directions. These data suggest that the profiles of nucleus accumbens gene expression associated with chronic heroin or cocaine abuse are largely unique, despite what are thought to be common effects of these drugs on dopamine neurotransmission in this brain region. A re-examination of our current assumptions about the commonality of molecular mechanisms associated with substance abuse seems warranted.

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“…Twenty-three of the differentially expressed genes in regions of induced young adult neocortical neurogenesis are common to this developmental progenitor dataset (Figure 1F): ∼23% of our dataset of differentially expressed genes in regions of induced young adult neocortical neurogenesis. Of these, it is interesting to note that several genes are known to be involved in synaptogenesis and/or maintenance of synapses, e.g., Abca1 (Hirsch-Reinshagen et al, 2004; Kim et al, 2008; Karasinska et al, 2009); Apoe (Masliah et al, 1995; Hirsch-Reinshagen et al, 2004; Wahrle et al, 2004); C1qa , C1qb , and C1qc (Stevens et al, 2007); Ctsd (Mariani et al, 2006; Partanen et al, 2008); Syngr1 (Belizaire et al, 2004; Verma et al, 2004), and Tyrobp (a.k.a. Dap12/Karap ; Roumier et al, 2004; Nataf et al, 2005; Table 2).…”

Section: Resultsmentioning

confidence: 99%

Developmental Controls are Re-Expressed during Induction of Neurogenesis in the Neocortex of Young Adult Mice

Sohur¹,

Arlotta²,

Macklis³

2012

Front. Neurosci.

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Whether induction of low-level neurogenesis in normally non-neurogenic regions of the adult brain mimics aspects of developmental neurogenesis is currently unknown. Previously, we and others identified that biophysically induced, neuron subtype-specific apoptosis in mouse neocortex results in induction of neurogenesis of limited numbers of subtype-appropriate projection neurons with axonal projections to either thalamus or spinal cord, depending on the neuron subtype activated to undergo targeted apoptosis. Here, we test the hypothesis that developmental genes from embryonic corticogenesis are re-activated, and that some of these genes might underlie induction of low-level adult neocortical neurogenesis. We directly investigated this hypothesis via microarray analysis of microdissected regions of young adult mouse neocortex undergoing biophysically activated targeted apoptosis of neocortical callosal projection neurons. We compared the microarray results identifying differentially expressed genes with public databases of embryonic developmental genes. We find that, following activation of subtype-specific neuronal apoptosis, three distinct sets of normal developmental genes are selectively re-expressed in neocortical regions of induced neurogenesis in young adult mice: (1) genes expressed by subsets of progenitors and immature neurons in the developing ventricular and/or subventricular zones; (2) genes normally expressed by developmental radial glial progenitors; and (3) genes involved in synaptogenesis. Together with previous results, the data indicate that at least some developmental molecular controls over embryonic neurogenesis can be re-activated in the setting of induction of neurogenesis in the young adult neocortex, and suggest that some of these activate and initiate adult neuronal differentiation from endogenous progenitor populations. Understanding molecular mechanisms contributing to induced adult neurogenesis might enable directed CNS repair.

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Characterization of synaptogyrin 3 as a new synaptic vesicle protein

Cited by 41 publications

References 65 publications

AP-1/σ1B-Dependent SV Protein Recycling Is Regulated in Early Endosomes and Is Coupled to AP-2 Endocytosis

AP-1/σ1B-Dependent SV Protein Recycling Is Regulated in Early Endosomes and Is Coupled to AP-2 Endocytosis

Distinctive Profiles of Gene Expression in the Human Nucleus Accumbens Associated with Cocaine and Heroin Abuse

Developmental Controls are Re-Expressed during Induction of Neurogenesis in the Neocortex of Young Adult Mice

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