Control of mitochondrial transport and localization in neurons

MacAskill, Andrew F.; Kittler, Josef T.

doi:10.1016/j.tcb.2009.11.002

Cited by 315 publications

(335 citation statements)

References 104 publications

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“…It has been reported that Arm motifs of p115 protein bind the Rab1 GTPase controlling ER to Golgi trafficking and regulate vesicle tethering 42 . Mitochondrial aggregating phenotypes have been observed after dysfunction of Miro and Trak2 proteins, suggesting that alteration of transport results in aggregation 43,44 . In neurons, mitochondrial aggregation and tethering is believed to serve to capture these organelles at specific locations requiring high-energy and Ca 2 + buffering conditions 43,45 .…”

Section: Discussionmentioning

confidence: 99%

The Eutherian Armcx genes regulate mitochondrial trafficking in neurons and interact with Miro and Trak2

et al. 2012

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Brain function requires neuronal activity-dependent energy consumption. neuronal energy supply is controlled by molecular mechanisms that regulate mitochondrial dynamics, including Kinesin motors and mitofusins, miro1-2 and Trak2 proteins. Here we show a new protein family that localizes to the mitochondria and controls mitochondrial dynamics. This family of proteins is encoded by an array of armadillo (Arm) repeat-containing genes located on the X chromosome. The Armcx cluster is unique to Eutherian mammals and evolved from a single ancestor gene (Armc10). We show that these genes are highly expressed in the developing and adult nervous system. Furthermore, we demonstrate that Armcx3 expression levels regulate mitochondrial dynamics and trafficking in neurons, and that Alex3 interacts with the Kinesin/miro/Trak2 complex in a Ca 2 + -dependent manner. our data provide evidence of a new Eutherian-specific family of mitochondrial proteins that controls mitochondrial dynamics and indicate that this key process is differentially regulated in the brain of higher vertebrates.

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Section: Discussionmentioning

confidence: 99%

The Eutherian Armcx genes regulate mitochondrial trafficking in neurons and interact with Miro and Trak2

et al. 2012

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“…This morphology has been demonstrated to increase metabolic demands and the risk of oxidative stress in A9 cells compared to other dopaminergic cell populations (128)(129)(130). Long axons require more energy to accommodate transport machinery to and from soma, while the low diameter impairs motility and further increases the metabolic demands (131,132). Further, lack of nodes of Ranvier elevates Na + /K + activity due to a less efficient action potential mechanism (133).…”

Section: Selective Vulnerability Of Dopaminergic Neurons In the Snpc:mentioning

confidence: 99%

“…Further, lack of nodes of Ranvier elevates Na + /K + activity due to a less efficient action potential mechanism (133). Massive arborization with many synapses is energy demanding, as mitochondria are concentrated around voltage gated Ca 2+ sites (132,134). Taken together, these cells require a highly dispersed mitochondrial network with an increased metabolic demand associated with production of reactive oxygen species (ROS), while having reduced transportation mechanisms for mitophagy.…”

Section: Selective Vulnerability Of Dopaminergic Neurons In the Snpc:mentioning

confidence: 99%

“…A9 cells further lack calbindin, a protective Ca 2+ buffering protein (135). Hence, these cells rely heavily on mitochondria to supply energy for Ca 2+ pumps and buffer high levels of cytosolic Ca 2+ directly, with an increased risk to stress the mitochondrial system due to calcium overloading (132). Although a link between calbindin and neuroprotection is reported (136), other studies have demonstrated that it is not causally related to the vulnerability of these cells (137).…”

Section: Selective Vulnerability Of Dopaminergic Neurons In the Snpc:mentioning

confidence: 99%

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Cytoprotective effects of growth factors: BDNF more potent than GDNF in an organotypic culture model of Parkinson's disease

et al. 2011

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“…KIF1B encodes a motor protein that transports mitochondria and synaptic vesicle precursors, through two alternatively spliced isoforms (i.e., KIF1Bα and KIF1Bβ) with distinct C-terminal cargo-binding domains [14]. KIF1Bα is one of microtubule-dependent molecular motors involved in important intracellular functions such as organelle transport and cell division [15].…”

Section: Introductionmentioning

confidence: 99%

Polymorphisms in the kinesin-like factor 1 B gene and risk of epithelial ovarian cancer in Eastern Chinese women

Shi

Jiang

et al. 2015

Tumor Biol.

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The kinesin-like factor 1 B (KIF1B) gene plays an important role in the process of apoptosis and the transformation and progression of malignant cells. Genetic variations in KIF1B may contribute to risk of epithelial ovarian cancer (EOC). In this study of 1,324 EOC patients and 1,386 cancer-free female controls, we investigated associations between two potentially functional single nucleotide polymorphisms in KIF1B and EOC risk by the conditional logistic regression analysis. General linear regression model was used to evaluate the correlation between the number of variant alleles and KIF1B mRNA expression levels. We found that the rs17401966 variant AG/GG genotypes were significantly associated with a decreased risk of EOC (adjusted odds ratio (OR)=0.81, 95 % confidence interval (CI)=0.68-0.97), compared with the AA genotype, but no associations were observed for rs1002076. Women who carried both rs17401966 AG/GG and rs1002076 AG/AA genotypes of KIF1B had a 0.82-fold decreased risk (adjusted 95 % CI=0.69-0.97), compared with others. Additionally, there was no evidence of possible interactions between about-mentioned co-variants. Further genotype-phenotype correlation analysis indicated that the number of rs17401966 variant G allele was significantly associated with KIF1B mRNA expression levels (P for GLM= 0.003 and 0.001 in all and Chinese subjects, respectively), with GG carriers having the lowest level of KIF1B mRNA expression. Taken together, the rs17401966 polymorphism likely regulates KIF1B mRNA expression and thus may be associated with EOC risk in Eastern Chinese women. Larger, independent studies are warranted to validate our findings.

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Control of mitochondrial transport and localization in neurons

Cited by 315 publications

References 104 publications

The Eutherian Armcx genes regulate mitochondrial trafficking in neurons and interact with Miro and Trak2

The Eutherian Armcx genes regulate mitochondrial trafficking in neurons and interact with Miro and Trak2

Cytoprotective effects of growth factors: BDNF more potent than GDNF in an organotypic culture model of Parkinson's disease

Polymorphisms in the kinesin-like factor 1 B gene and risk of epithelial ovarian cancer in Eastern Chinese women

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