scholarly journals Role of GPR55 during Axon Growth and Target Innervation

eNeuro ◽  
2015 ◽  
Vol 2 (5) ◽  
pp. ENEURO.0011-15.2015 ◽  
Author(s):  
Hosni Cherif ◽  
Anteneh Argaw ◽  
Bruno Cécyre ◽  
Alex Bouchard ◽  
Jonathan Gagnon ◽  
...  
Keyword(s):  
Axon Growth ◽  
Target Innervation

scholarly journals The Role of Lipids, Lipid Metabolism and Ectopic Lipid Accumulation in Axon Growth, Regeneration and Repair after CNS Injury and Disease

Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 1078
Author(s):  
Debasish Roy ◽  
Andrea Tedeschi
Keyword(s):  
Nervous System ◽  
Lipid Metabolism ◽  
Lipid Accumulation ◽  
Axon Regeneration ◽  
Axon Growth ◽  
The Body ◽  
Cns Repair ◽  
Cord Injury ◽  
Cns Trauma

Axons in the adult mammalian nervous system can extend over formidable distances, up to one meter or more in humans. During development, axonal and dendritic growth requires continuous addition of new membrane. Of the three major kinds of membrane lipids, phospholipids are the most abundant in all cell membranes, including neurons. Not only immature axons, but also severed axons in the adult require large amounts of lipids for axon regeneration to occur. Lipids also serve as energy storage, signaling molecules and they contribute to tissue physiology, as demonstrated by a variety of metabolic disorders in which harmful amounts of lipids accumulate in various tissues through the body. Detrimental changes in lipid metabolism and excess accumulation of lipids contribute to a lack of axon regeneration, poor neurological outcome and complications after a variety of central nervous system (CNS) trauma including brain and spinal cord injury. Recent evidence indicates that rewiring lipid metabolism can be manipulated for therapeutic gain, as it favors conditions for axon regeneration and CNS repair. Here, we review the role of lipids, lipid metabolism and ectopic lipid accumulation in axon growth, regeneration and CNS repair. In addition, we outline molecular and pharmacological strategies to fine-tune lipid composition and energy metabolism in neurons and non-neuronal cells that can be exploited to improve neurological recovery after CNS trauma and disease.

scholarly journals The role of microtubules in growth cone turning at substrate boundaries.

1995 ◽  
Vol 128 (1) ◽  
pp. 127-137 ◽  
Author(s):  
E Tanaka ◽  
M W Kirschner
Keyword(s):  
Growth Cone ◽  
Collagen Type ◽  
Axon Growth ◽  
Growth Cones ◽  
Collagen Type Iv ◽  
Early Step ◽  
Growth Cone Collapse ◽  
Type Iv ◽  
And Behaviors

To understand the role of microtubules in growth cone turning, we observed fluorescently labeled microtubules in neurons as they encountered a substrate boundary. Neurons growing on a laminin-rich substrate avoided growing onto collagen type IV. Turning growth cones assumed heterogeneous morphologies and behaviors that depended primarily in their extent of adhesion to the substrate. We grouped these behaviors into three categories-sidestepping, motility, and growth-mediated reorientation. In sidestepping and motility-mediated reorientation, the growth cone and parts of the axon were not well attached to the substrate so the acquisition of an adherent lamella caused the entire growth cone to move away from the border and consequently reoriented the axon. In these cases, since the motility of the growth cone dominates its reorientation, the microtubules were passive, and reorientation occurred without significant axon growth. In growth-mediated reorientation, the growth cone and axon were attached to the substrate. In this case, microtubules reoriented within the growth cone to stabilize a lamella. Bundling of the reoriented microtubules was followed by growth cone collapse to form new axon, and further, polarized lamellipodial extension. These observations indicate that when the growth cone remains adherent to the substrate during turning, the reorientation and bundling of microtubules is an important, early step in growth cone turning.

scholarly journals Role of Drosophila Rap/Fzr (DCdh1) in Retinal Axon Targeting and its Interactions with Loco and Liprin-alpha

2020 ◽  
Author(s):  
Marta Grońska-Pęski ◽  
Tadmiri R. Venkatesh
Keyword(s):  
Cell Cycle ◽  
Ubiquitin Ligase ◽  
Axon Growth ◽  
Scaffolding Protein ◽  
List Type ◽  
Axon Targeting ◽  
The Third ◽  
Retinal Axon ◽  
Third Instar Larvae

AbstractThe development of the wild type Drosophila compound eye involves stereotypical targeting of photoreceptor axons to the specific layers of the optic ganglion, medulla and lamina, in the third instar larvae. To test the hypothesis that ubiquitin ligases play an important role during retinal axon targeting we have examined the patterns of axon targeting in the developing eye of the retina aberrant in pattern (rap/fzr) mutants. Rap/Fzr is a homolog of mammalian Cdh1, an activator of anaphase promoting complex (APC), a multi-subunit E3 ubiquitin ligase, regulating the cell cycle progression. Previous work has shown that Rap/Fzr is required during eye development for proper cell cycle regulation, glia differentiation and pattern formation. It was also necessary for proper neuromuscular junction development and circadian rhythms. Our results show that Rap/Fzr is required for proper retinal axon targeting in the developing eye. Using ro-tau-lacZ, we show that the R2-R5 axons fail to stop in the lamina and mis-target to the medulla levels. Also, mosaic analyses experiments using FLP-FRT and GAL4-UAS techniques show that Rap/Fzr functions in a cell autonomous manner. To test for possible role of other signalling molecules and interactions with Rap/Fzr, we have examined rap/fzr axon projection phenotypes in double mutant combinations with the RGS protein, locomotion defective (loco) mutants and a scaffolding protein, Liprin-α. Our studies suggest that Rap/Fzr is required for proper axon targeting during Drosophila visual system development, and the phenotype is enhanced in double mutants with either loco or Liprin-α. These results are consistent with other mammalian studies reporting a role of Cdh1 in axon growth and targeting and provides further insights into neuronal functions of the ubiquitin ligase APC/CCdh1.HighlightsLoss of rap/fzr in the third instar Drosophila eye disc leads to photoreceptor axon overgrowthOverexpression of rap/fzr leads to photoreceptor axon leads to axon shortening and clumpingLoss of LocoP452 leads to photoreceptor overgrowthDouble mutants of rap and loco or rap and Liprin-α show axon enhancement of the axon targeting defects in the Drosophila third instar larvae eye imaginal discs.

Role of Semaphorins during Axon Growth and Guidance

2008 ◽  
pp. 50-64 ◽  
Author(s):  
Eric Koncina ◽  
Lise Roth ◽  
Bertand Gonthier ◽  
Dominique Bagnard
Keyword(s):  
Axon Growth

The effects of protease inhibitors on axon growth through astrocytes

Development ◽  
1990 ◽  
Vol 109 (1) ◽  
pp. 59-66 ◽  
Author(s):  
J.W. Fawcett ◽  
E. Housden
Keyword(s):  
Protease Inhibitors ◽  
Dorsal Root Ganglia ◽  
Cell Invasion ◽  
Tumour Cell ◽  
Dorsal Root ◽  
Three Dimensional ◽  
Axon Growth ◽  
Tumour Cell Invasion ◽  
Effect On Growth

We have shown in a previous paper (Devl Biol. 135, 449, 1989) that axons regenerating from postnatal neurons are unable to penetrate three-dimensional cultures of mature astrocytes, while axons from embryonic dorsal root ganglia (DRGs) and retina will grow through such cultures for considerable distances. We have now investigated the role of proteases in the penetration of three-dimensional astrocyte cultures by axons from embryonic DRGs. Embryonic DRGs were grown in association with three-dimensional astrocyte cultures, with astrocyte monolayers, and with-air dried collagen. The effects of inhibitors of the three families of proteases that have been shown to be involved in tumour cell invasion were investigated. The serine protease inhibitors EACA and Trasylol both reduced growth in three-dimensional astrocyte cultures to around 50% of control, but had little effect on growth on astrocyte monolayers or on collagen. TIMP, which inhibits collagenases, had no effect on growth on two- or three-dimensional cultures. Cbz-gly-phen-amide, an inhibitor of enteroproteases, reduced growth in all three types of culture.

scholarly journals NGF-promoted axon growth and target innervation requires GITRL-GITR signaling

2008 ◽  
Vol 11 (2) ◽  
pp. 135-142 ◽  
Author(s):  
Gerard W O'Keeffe ◽  
Humberto Gutierrez ◽  
Pier Paolo Pandolfi ◽  
Carlo Riccardi ◽  
Alun M Davies
Keyword(s):  
Axon Growth ◽  
Target Innervation

scholarly journals Protective role of mRNA demethylase FTO on axon guiding molecules of nigro-striatal projection system in manganese-induced Parkinsonism

2021 ◽  
Author(s):  
Zhipeng Qi ◽  
Jiashuo Li ◽  
Ke Zhang ◽  
Yanan Liu ◽  
Xinxin Yang ◽  
...  
Keyword(s):  
Therapeutic Response ◽  
Axon Growth ◽  
Protective Role ◽  
Motor Dysfunction ◽  
Exposure Model ◽  
Domain Family ◽  
Projection System ◽  
Over Expression ◽  
Target Indicator

Abstract Background Parkinson's disease (PD) is a neurodegenerative disease caused by environmental and genetic factors. Manganese (Mn) exposure is a major environmental cause of PD. Cellular and molecular mechanism of Parkinsonism caused by Mn has not been explored clearly. In addition, patients with Mn-induced Parkinsonism show poor therapeutic response to levodopa. Therefore, there is need to explore the mechanisms underlying neurotoxicity of Mn exposure. Methods In short, we used SH-SY5Y cells and C57BL/6 mice to characterize Mn-induced Parkinsonism. We measured the behavioral, histological, ultrastructural and nigro-striatal projection system changes, cell viability, axon growth, and other target indicator levels, which led to the discovery of a novel mechanism of Mn-induced neurotoxicity. Results The findings of the current study showed that inhibition of fat mass and obesity-associated protein (FTO)-mediated demethylation of N6-methyladenosine (m6A) mRNA aggravates Mn-induced motor dysfunction. Notably, FTO level is low in Mn exposure model mice and enhances occurrence of dyskinesia in mice. Over-expression of FTO reduces m6A methylation in the key axon guiding molecules of nigro-striatal projection system, including ephrin-A5 and ephrin-B2. It increases ephrin-B2 mRNA decay through the m6A reader YT521-B homology domain family proteins 2 (YTHDF2). Conclusions The findings of this study show that FTO, a m6A demethylase, performs an indispensable function in Mn-induced Parkinsonism. Notably, re-expression of FTO and ephrin-B2 improved motor dysfunction after Mn exposure.

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