Arginine Kinase Expression and Localization in Growth Cone Migration

Wang, Yu-mei E.; Esbensen, Pia; Bentley, David

doi:10.1523/jneurosci.18-03-00987.1998

Cited by 47 publications

(30 citation statements)

References 75 publications

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“…This difference in vulnerability of the brain is also found clinically, because hyperammonemia causes irreversible CNS symptoms compatible with axonal loss in neonates and infants but not in adults (Brusilow and Horwich, 2001). Evidence for direct coupling of the Cr/PCr/CK system to growth cone activity and axonal growth (Wang et al, 1998) and Cr and PCr age dependency of the CNS in the first weeks of postnatal life (Tsuji et al, 1995) also supports the difference we found between developing and mature aggregates. It suggests a higher CNS sensitivity to Cr variations in young children than in adulthood.…”

Section: Nh 4 CL Exposure Does Not Alter Axonal Morphology In Mature supporting

confidence: 85%

“…There is substantial evidence that creatine (Cr) and the Cr/phosphocreatine (PCr)/creatine kinase (CK) system are involved in neuronal growth cone activity and axonal elongation (Wang et al, 1998). In addition, the CNS is the main affected target in infants with a creatine deficiency syndrome attributable to guanidinoacetate methyltransferase, arginine:glycine amidinotransferase, or Cr transporter deficiencies.…”

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confidence: 99%

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Ammonium-Induced Impairment of Axonal Growth Is Prevented through Glial Creatine

Braissant¹,

Henry²,

Villard³

et al. 2002

J. Neurosci.

100

137

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Hyperammonemia in neonates and infants affects brain development and causes mental retardation. We report that ammonium impaired cholinergic axonal growth and altered localization and phosphorylation of intermediate neurofilament protein in rat reaggregated brain cell primary cultures. This effect was restricted to the phase of early maturation but did not occur after synaptogenesis. Exposure to NH 4 Cl decreased intracellular creatine, phosphocreatine, and ADP. We demonstrate that creatine cotreatment protected axons from ammonium toxic effects, although this did not restore high-energy phosphates. The protection by creatine was glial cell-dependent. Our findings suggest that the means to efficiently sustain CNS creatine concentration in hyperammonemic neonates and infants should be assessed to prevent impairment of axonogenesis and irreversible brain damage.

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Section: Nh 4 CL Exposure Does Not Alter Axonal Morphology In Mature supporting

confidence: 85%

mentioning

confidence: 99%

Ammonium-Induced Impairment of Axonal Growth Is Prevented through Glial Creatine

Braissant¹,

Henry²,

Villard³

et al. 2002

J. Neurosci.

100

137

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“…The literature on phosphoenolpyruvate phosphomutase is scarce and its possible involvement in DUI unclear. Of the proteins with multiple occurrences, arginine kinase is a phosphotransferase involved in supplying ATP to cellular processes including growth and motility (79). It has been reported in sea-urchin Paracentrotus lividus eggs (80) and high levels observed during oocyte development of a penaeid shrimp suggests an important role in meeting energy demands for cell growth and proliferation (81).…”

Section: Discussionmentioning

confidence: 99%

Proteomic Analysis of Eggs from Mytilus edulis Females Differing in Mitochondrial DNA Transmission Mode

Diz

Dudley

Cogswell

et al. 2013

Molecular & Cellular Proteomics

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Many bivalves have an unusual mechanism of mitochondrial DNA (mtDNA) inheritance called doubly uniparental inheritance (DUI) in which distinctly different genomes are inherited through the female (F genome) and male (M genome) lineages. In fertilized eggs that will develop into male embryos, the sperm mitochondria remain in an aggregation, which is believed to be delivered to the primordial germ cells and passed to the next generation through the sperm. In fertilized eggs that will develop into female embryos, the sperm mitochondria are dispersed throughout the developing embryo and make little if any contribution to the next generation. The frequency of embryos with the aggregated or dispersed mitochondrial type varies among females. Previous models of DUI have predicted that maternal nuclear factors cause molecular differences among unfertilized eggs from females producing embryos with predominantly dispersed or aggregated mitochondria. We test this hypothesis using females of each of the two types from a natural population. We have found small, yet detectable, differences of the predicted type at the proteome level. We also provide evidence that eggs of females giving the dispersed pattern have consistently lower expression for different proteasome subunits than eggs of females giving the aggregated pattern. These results, combined with those of an earlier study in which we used hatchery lines of Mytilus, and with a transcriptomic study in a clam that has the DUI system of mtDNA transmission, reinforce the hypothesis that the ubiquitinproteasome system plays a key role in the mechanism of DUI and sex determination in bivalves. We also report that eggs of females giving the dispersed pattern have higher expression for arginine kinase and enolase, enzymes involved in energy production, whereas ferritin, which is involved in iron homeostasis, has lower expression. We discuss these results in the context of genetic models for DUI and suggest experimental methods for further understanding the role of these proteins in DUI. Proteomics has made a rapid progress when applied to model species where genomic databases are well developed, but recent reviews have pointed to the growing interest in applying proteomics to nonmodel species in areas such as evolutionary ecology (1), aquatic toxicology (2), aquatic pollution (3), aquaculture (4), and marine biology (5). In the marine mussel genus Mytilus, an unusual system of mtDNA inheritance occurs characterized by the presence of two mitochondrial genomes (called F and M) one of which is inherited maternally and the other paternally (6 -9). This phenomenon, called doubly uniparental inheritance of mtDNA (DUI), 1 suggests a connection between mtDNA inheritance and sex determination. DUI also occurs in other species belonging to three bivalve orders (10, 11). Since the 1990s, DUI has been under intensive investigation, but the molecular mechanism for DUI and how it relates to sex determination, is still to be elucidated (for review, see 12-15).Cytological studies of fertilize...

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“…The cytosolic muscle isoform localizes along the M-line to the myosin heads where it provides ATP during actomyosin contraction (24). The cytosolic brain isoform (CKB) and its insect homolog arginine kinase localize to the membranes of neurons and astrocytes and are concentrated along axons and moving lamellipodial edges of migrating glia, although the precise function of CKB is not known (25,26).We hypothesized that molecules necessary for the early stages of thrombin signaling might bind to the intracellular face of PAR-1. To examine this, we performed a yeast two-hybrid screen and discovered an interaction between the PAR-1 cytoplasmic tail (C-tail) and CKB.…”

mentioning

confidence: 99%

“…To examine this, we performed a yeast two-hybrid screen and discovered an interaction between the PAR-1 cytoplasmic tail (C-tail) and CKB. Because the muscle isoform of creatine kinase delivers a burst of compartmentalized ATP for contracting skeletal muscle and is linked to actomyosin function in various cells (22,26,27), we hypothesized that CKB may perform a similar function during PAR-1-directed cytoskeletal reorganization. Using three different methods to ablate CKB activity, we found that CKB was necessary for PAR-1 signal transduction to the cytoskeleton.…”

mentioning

confidence: 99%

Creatine kinase, an ATP-generating enzyme, is required for thrombin receptor signaling to the cytoskeleton

Mahajan

Pai²,

Lau³

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

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Thrombin orchestrates cellular events after injury to the vascular system and extravasation of blood into surrounding tissues. The pathophysiological response to thrombin is mediated by proteaseactivated receptor-1 (PAR-1), a seven-transmembrane G proteincoupled receptor expressed in the nervous system that is identical to the thrombin receptor in platelets, fibroblasts, and endothelial cells. Once activated by thrombin, PAR-1 induces rapid and dramatic changes in cell morphology, notably the retraction of growth cones, axons, and dendrites in neurons and processes in astrocytes. The signal is conveyed by a series of localized ATP-dependent reactions directed to the actin cytoskeleton. How cells meet the dynamic and localized energy demands during signal transmission is unknown. Using the yeast two-hybrid system, we identified an interaction between PAR-1 cytoplasmic tail and the brain isoform of creatine kinase, a key ATP-generating enzyme that regulates ATP within subcellular compartments. The interaction was confirmed in vitro and in vivo. Reducing creatine kinase levels or its ATP-generating potential inhibited PAR-1-mediated cellular shape changes as well as a PAR-1 signaling pathway involving the activation of RhoA, a small G protein that relays signals to the cytoskeleton. Thrombin-stimulated intracellular calcium release was not affected. Our results suggest that creatine kinase is bound to PAR-1 where it may be poised to provide bursts of site-specific high-energy phosphate necessary for efficient receptor signal transduction during cytoskeletal reorganization. P rotease activated receptor-1 (PAR-1) mediates the cellular responses to thrombin during blood coagulation, cell proliferation, vascular permeability changes, tumor metastasis, and nervous system injury (1-3). PAR-1 is a seven-transmembrane G protein-coupled receptor with a novel activation mechanism. Proteolysis at a thrombin cleavage site in the extracellular amino terminus exposes a new amino terminus containing the peptide ligand SFLLRN, which binds intramolecularly to initiate intracellular signals (4). Although originally detected in platelets, endothelial cells, and fibroblasts, PAR-1 is also expressed in the nervous system in a developmentally regulated manner and by specific subpopulations of neurons and astrocytes that are especially vulnerable to neurodegeneration and ischemic injury (1,5,6).In most cells expressing PAR-1, activation of the receptor transmits signals to the actin cytoskeleton that profoundly alter cell shape. Platelets, for example, convert from a spherical to disk shape and extend filopodia (7), endothelial cells contract (8), neurons retract axons, and astrocytes resorb processes and flatten their cell bodies (9-11). These signals also regulate changes in actin-related cell motility observed in neurons (10), fibroblasts (12), and tumor cells (3). The morphological response is mediated by a key signaling pathway that uses serine͞ threonine kinases, G␣12͞13, RhoA, and myosin light chain kinase; actomyosin contraction ...

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Arginine Kinase Expression and Localization in Growth Cone Migration

Cited by 47 publications

References 75 publications

Ammonium-Induced Impairment of Axonal Growth Is Prevented through Glial Creatine

Ammonium-Induced Impairment of Axonal Growth Is Prevented through Glial Creatine

Proteomic Analysis of Eggs from Mytilus edulis Females Differing in Mitochondrial DNA Transmission Mode

Creatine kinase, an ATP-generating enzyme, is required for thrombin receptor signaling to the cytoskeleton

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