scholarly journals Harmonization of L1CAM Expression Facilitates Axon Outgrowth and Guidance of a Motor Neuron

2020 ◽  
Author(s):  
Tessa Sherry ◽  
Hannah R. Nicholas ◽  
Roger Pocock
Keyword(s):  
Motor Neurons ◽  
Single Neuron ◽  
Early Adulthood ◽  
Axon Outgrowth ◽  
Axonal Development ◽  
Axon Development ◽  
Axonal Defects ◽  
Multiple Signaling ◽  
L1 Cell Adhesion Molecule ◽  
L1cam Expression

ABSTRACTBrain development requires precise regulation of axon outgrowth, guidance and termination by multiple signaling and adhesion molecules. How the expression of these neurodevelopmental regulators is transcriptionally controlled is poorly understood. The Caenorhabditis elegans SMD motor neurons terminate axon outgrowth upon sexual maturity and partially retract their axons during early adulthood. Here we show that C-Terminal Binding Protein-1 (CTBP-1), a transcriptional corepressor, is required for correct SMD axonal development. Loss of CTBP-1 causes multiple defects in SMD axon development: premature outgrowth, defective guidance, delayed termination and absence of retraction. CTBP-1 controls SMD axon development by repressing the expression of SAX-7 – a L1 cell adhesion molecule (L1CAM). CTBP-1-regulated repression is crucial as deregulated SAX-7/L1CAM causes aberrant SMD axons. We found that axonal defects caused by SAX-7/L1CAM misexpression are dependent on a distinct L1CAM, called LAD-2, which itself plays a parallel role in SMD axon guidance. Our results reveal that harmonization of L1CAM expression controls the development and maturation of a single neuron.

scholarly journals Harmonization of L1CAM expression facilitates axon outgrowth and guidance of a motor neuron

Development ◽  
2020 ◽  
Vol 147 (20) ◽  
pp. dev193805
Author(s):  
Tessa Sherry ◽  
Ava Handley ◽  
Hannah R. Nicholas ◽  
Roger Pocock
Keyword(s):  
Axon Guidance ◽  
Motor Neurons ◽  
Early Adulthood ◽  
Axon Outgrowth ◽  
Axonal Development ◽  
Axon Development ◽  
Axonal Defects ◽  
Multiple Signaling ◽  
L1 Cell Adhesion Molecule ◽  
L1cam Expression

ABSTRACTBrain development requires precise regulation of axon outgrowth, guidance and termination by multiple signaling and adhesion molecules. How the expression of these neurodevelopmental regulators is transcriptionally controlled is poorly understood. The Caenorhabditis elegans SMD motor neurons terminate axon outgrowth upon sexual maturity and partially retract their axons during early adulthood. Here we show that C-terminal binding protein 1 (CTBP-1), a transcriptional corepressor, is required for correct SMD axonal development. Loss of CTBP-1 causes multiple defects in SMD axon development: premature outgrowth, defective guidance, delayed termination and absence of retraction. CTBP-1 controls SMD axon guidance by repressing the expression of SAX-7, an L1 cell adhesion molecule (L1CAM). CTBP-1-regulated repression is crucial because deregulated SAX-7/L1CAM causes severely aberrant SMD axons. We found that axonal defects caused by deregulated SAX-7/L1CAM are dependent on a distinct L1CAM, called LAD-2, which itself plays a parallel role in SMD axon guidance. Our results reveal that harmonization of L1CAM expression controls the development and maturation of a single neuron.

scholarly journals Hypergravity hinders axonal development of motor neurons inCaenorhabditis elegans

PeerJ ◽  
2016 ◽  
Vol 4 ◽  
pp. e2666 ◽  
Author(s):  
Saraswathi Subbammal Kalichamy ◽  
Tong Young Lee ◽  
Kyoung-hye Yoon ◽  
Jin Il Lee
Keyword(s):  
Motor Neurons ◽  
Model Organism ◽  
Dorsal Side ◽  
The Body ◽  
Body Region ◽  
Neuron Development ◽  
Axonal Development ◽  
Axonal Projections ◽  
Axonal Defects ◽  
And Control

As space flight becomes more accessible in the future, humans will be exposed to gravity conditions other than our 1G environment on Earth. Our bodies and physiology, however, are adapted for life at 1G gravity. Altering gravity can have profound effects on the body, particularly the development of muscles, but the reasons and biology behind gravity’s effect are not fully known. We asked whether increasing gravity had effects on the development of motor neurons that innervate and control muscle, a relatively unexplored area of gravity biology. Using the nematode model organismCaenorhabditis elegans, we examined changes in response to hypergravity in the development of the 19 GABAergic DD/VD motor neurons that innervate body muscle. We found that a high gravity force above 10G significantly increases the number of animals with defects in the development of axonal projections from the DD/VD neurons. We showed that a critical period of hypergravity exposure during the embryonic/early larval stage was sufficient to induce defects. While characterizing the nature of the axonal defects, we found that in normal 1G gravity conditions, DD/VD axonal defects occasionally occurred, with the majority of defects occurring on the dorsal side of the animal and in the mid-body region, and a significantly higher rate of error in the 13 VD axons than the 6 DD axons. Hypergravity exposure increased the rate of DD/VD axonal defects, but did not change the distribution or the characteristics of the defects. Our study demonstrates that altering gravity can impact motor neuron development.

IGF-I specifically enhances axon outgrowth of corticospinal motor neurons

2006 ◽  
Vol 9 (11) ◽  
pp. 1371-1381 ◽  
Author(s):  
P Hande Özdinler ◽  
Jeffrey D Macklis
Keyword(s):  
Motor Neurons ◽  
Axon Outgrowth ◽  
Igf I ◽  
Corticospinal Motor Neurons

scholarly journals GABAergic motor neurons bias locomotor decision-making in C. elegans

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Ping Liu ◽  
Bojun Chen ◽  
Zhao-Wen Wang
Keyword(s):  
Decision Making ◽  
Motor Neurons ◽  
Gaba Receptor ◽  
Single Neuron ◽  
Neural Circuit ◽  
Electrical Coupling ◽  
C Elegans ◽  
Sensory Modalities ◽  
Motor Information ◽  
Molecular Bases

Abstract Proper threat-reward decision-making is critical to animal survival. Emerging evidence indicates that the motor system may participate in decision-making but the neural circuit and molecular bases for these functions are little known. We found in C. elegans that GABAergic motor neurons (D-MNs) bias toward the reward behavior in threat-reward decision-making by retrogradely inhibiting a pair of premotor command interneurons, AVA, that control cholinergic motor neurons in the avoidance neural circuit. This function of D-MNs is mediated by a specific ionotropic GABA receptor (UNC-49) in AVA, and depends on electrical coupling between the two AVA interneurons. Our results suggest that AVA are hub neurons where sensory inputs from threat and reward sensory modalities and motor information from D-MNs are integrated. This study demonstrates at single-neuron resolution how motor neurons may help shape threat-reward choice behaviors through interacting with other neurons.

scholarly journals An autism-associated calcium channel variant causes defects in neuronal polarity and axon termination in the ALM neuron of C. elegans

2020 ◽  
Author(s):  
Tyler Buddell ◽  
Christopher C. Quinn
Keyword(s):  
Calcium Channel ◽  
Neurodevelopmental Disorders ◽  
Molecular Mechanisms ◽  
De Novo ◽  
Neuronal Polarity ◽  
Timothy Syndrome ◽  
C Elegans ◽  
Axon Development ◽  
Axon Termination ◽  
Axonal Defects

AbstractVariants of the CACNA1C voltage-gated calcium channel gene have been associated with autism and other neurodevelopmental disorders including bipolar disorder, schizophrenia, and ADHD. The Timothy syndrome mutation is a rare de novo gain-of-function variant in CACNA1C that causes autism with high penetrance, providing a powerful avenue into investigating the role of CACNA1C variants in neurodevelopmental disorders. In our previous work, we demonstrated that an egl-19(gof) mutation, that is equivalent to the Timothy syndrome mutation in the human homolog CACNA1C, can disrupt termination of the PLM axon in C. elegans. Here, we find that the egl-19(gof) mutation disrupts the polarity of process outgrowth in the ALM neuron of C. elegans. We also find that the egl-19(gof) mutation can disrupt termination of the ALM axon. These results suggest that the Timothy syndrome mutation can disrupt multiple steps of axon development. Further work exploring the molecular mechanisms that underlie these perturbations in neuronal polarity and axon termination will give us better understanding to how variants in CACNA1C contribute to the axonal defects that underlie autism.

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