scholarly journals Repression of an activity-dependent autocrine insulin signal is required for sensory neuron development in C. elegans

2018 ◽  
Author(s):  
Lauren Bayer Horowitz ◽  
Julia P. Brandt ◽  
Niels Ringstad
Keyword(s):  
Nervous System ◽  
System Development ◽  
Nervous System Development ◽  
P38 Map Kinase ◽  
Dependent Manner ◽  
Neuron Development ◽  
C Elegans ◽  
Chemosensory Neuron ◽  
Insulin Receptor Signaling ◽  
Activity Dependent

AbstractNervous system development is instructed both by genetic programs and activity-dependent refinement of gene expression and connectivity. How these mechanisms are integrated remains poorly understood. Here, we report that the regulated release of insulin-like peptides (ILPs) during development of the C. elegans nervous system accomplishes such an integration. We find that the p38 MAP kinase PMK-3, which is required for the differentiation of chemosensory BAG neurons, functions by limiting expression of an autocrine ILP signal that represses a chemosensory-neuron fate. ILPs are released from BAGs in an activity-dependent manner during embryonic development, and regulate neurodifferentiation through a non-canonical insulin receptor signaling pathway. The differentiation of a specialized neuron-type is, therefore, coordinately regulated by a genetic program that controls ILP expression and by neural activity, which regulates ILP release. Autocrine signals of this kind may have general and conserved functions as integrators of deterministic genetic programs with activity-dependent mechanisms during neurodevelopment.

scholarly journals sli is required for proper morphology and migration of sensory neurons in the Drosophila PNS

2019 ◽  
Vol 14 (1) ◽  
Author(s):  
Madison Gonsior ◽  
Afshan Ismat
Keyword(s):  
Nervous System ◽  
Sensory Neurons ◽  
Glial Cells ◽  
System Development ◽  
Nervous System Development ◽  
Final Position ◽  
Neuron Development ◽  
Guidance Cues ◽  
And Migration

Abstract Neurons and glial cells coordinate with each other in many different aspects of nervous system development. Both types of cells are receiving multiple guidance cues to guide the neurons and glial cells to their proper final position. The lateral chordotonal organs (lch5) of the Drosophila peripheral nervous system (PNS) are composed of five sensory neurons surrounded by four different glial cells, scolopale cells, cap cells, attachment cells and ligament cells. During embryogenesis, the lch5 neurons go through a rotation and ventral migration to reach their final position in the lateral region of the abdomen. We show here that the extracellular ligand sli is required for the proper ventral migration and morphology of the lch5 neurons. We further show that mutations in the Sli receptors Robo and Robo2 also display similar defects as loss of sli, suggesting a role for Slit-Robo signaling in lch5 migration and positioning. Additionally, we demonstrate that the scolopale, cap and attachment cells follow the mis-migrated lch5 neurons in sli mutants, while the ventral stretching of the ligament cells seems to be independent of the lch5 neurons. This study sheds light on the role of Slit-Robo signaling in sensory neuron development.

scholarly journals Regulation of Gliogenesis by lin-32/Atoh1 in Caenorhabditis elegans

2020 ◽  
Vol 10 (9) ◽  
pp. 3271-3278 ◽  
Author(s):  
Albert Zhang ◽  
Kentaro Noma ◽  
Dong Yan
Keyword(s):  
Nervous System ◽  
Caenorhabditis Elegans ◽  
Embryonic Development ◽  
Molecular Mechanisms ◽  
System Development ◽  
Nervous System Development ◽  
Proneural Gene ◽  
C Elegans ◽  
Fundamental Process ◽  
Mutant Phenotypes

Abstract The regulation of gliogenesis is a fundamental process for nervous system development, as the appropriate glial number and identity is required for a functional nervous system. To investigate the molecular mechanisms involved in gliogenesis, we used C. elegans as a model and identified the function of the proneural gene lin-32/Atoh1 in gliogenesis. We found that lin-32 functions during embryonic development to negatively regulate the number of AMsh glia. The ectopic AMsh cells at least partially arise from cells originally fated to become CEPsh glia, suggesting that lin-32 is involved in the specification of specific glial subtypes. Moreover, we show that lin-32 acts in parallel with cnd-1/ NeuroD1 and ngn-1/ Neurog1 in negatively regulating an AMsh glia fate. Furthermore, expression of murine Atoh1 fully rescues lin-32 mutant phenotypes, suggesting lin-32/Atoh1 may have a conserved role in glial specification.

scholarly journals Genome-Wide Activity-Dependent MeCP2 Phosphorylation Regulates Nervous System Development and Function

Neuron ◽  
2011 ◽  
Vol 72 (1) ◽  
pp. 72-85 ◽  
Author(s):  
Sonia Cohen ◽  
Harrison W. Gabel ◽  
Martin Hemberg ◽  
Ashley N. Hutchinson ◽  
L. Amanda Sadacca ◽  
...  
Keyword(s):  
Nervous System ◽  
System Development ◽  
Nervous System Development ◽  
Genome Wide ◽  
And Function ◽  
Activity Dependent

scholarly journals Characterization of RQ1, a mutant involved in nervous system development in C. Elegans

2021 ◽  
Author(s):  
Matthew M Bueno de Mesquita
Keyword(s):  
Nervous System ◽  
System Development ◽  
Nervous System Development ◽  
Wild Type ◽  
Directional Information ◽  
Double Stranded Rna ◽  
Knock Out ◽  
C Elegans ◽  
Strong Candidate

During the development of the nervous system, guidance cues provide directional information to the growth cones of migrating axons. In C. elegans, ventral to dorsal migration is in part mediated by the ligand UNC-6 and its receptor UNC-5. In an UNC-5 null mutant the DA and DB motor neuron axons fail to migrate in a wild type manner to the dorsal cord, despite initial dorsalward outgrowth from the cell bodies. A genetic enhancer screen was conducted in an UNC-5 null strain and one mutant, rq1, was found to have increased axon guidance defects. To identify the mutated gene in rq1, microinjection experiments were performed and were able to rescue two rq1 phontypes. RNAi experiments were performed where double stranded RNA corresponding to all the genes in the region were used individually to knock out the transcripts. Several of these were able to phenocopy the defects of rq1. The rq1 mutation could be located in any one of five genes known to be present on the rescuing cosmid while combined results implicate three strong candidate genes, M03C11.8, H04D03.1 and H04D03.4.

scholarly journals TheC. elegansephrin EFN-4 functions non-cell autonomously with heparan sulfate proteoglycans to promote axon outgrowth and branching

2015 ◽  
Author(s):  
Alicia A Schwieterman ◽  
Alyse N Steves ◽  
Vivian Yee ◽  
Cory J Donelson ◽  
Aaron Pital ◽  
...  
Keyword(s):  
Nervous System ◽  
Neurite Outgrowth ◽  
Motor Neurons ◽  
System Development ◽  
Nervous System Development ◽  
The Body ◽  
Tissue Type ◽  
Eph Receptors ◽  
C Elegans ◽  
Core Proteins

The Eph receptors and their cognate ephrin ligands play key roles in many aspects of nervous system development. These interactions typically occur within an individual tissue type, serving either to guide axons to their terminal targets or to define boundaries between the rhombomeres of the hindbrain. We have identified a novel role for theCaenorhabditis elegansephrin EFN-4 in promoting primary neurite outgrowth in AIY interneurons and D-class motor neurons. Rescue experiments reveal that EFN-4 functions non-cell autonomously in the epidermis to promote primary neurite outgrowth. We also find that EFN-4 plays a role in promoting ectopic axon branching in aC. elegansmodel of X-linked Kallmann syndrome. In this context, EFN-4 functions non-cell autonomously in the body wall muscle, and in parallel with HS biosynthesis genes and HSPG core proteins, which function cell autonomously in the AIY neurons. This is the first report of an epidermal ephrin providing a developmental cue to the nervous system.

scholarly journals Multiple conserved cell adhesion protein interactions mediate neural wiring of a sensory circuit in C. elegans

2017 ◽  
Author(s):  
Byunghyuk Kim ◽  
Scott W. Emmons
Keyword(s):  
Nervous System ◽  
Cell Adhesion ◽  
Sensory Neuron ◽  
Protein Interactions ◽  
Synapse Formation ◽  
System Development ◽  
Nervous System Development ◽  
Surface Proteins ◽  
C Elegans ◽  
Nervous System Function

ABSTRACTNervous system function relies on precise synaptic connections. A number of widely-conserved cell adhesion proteins are implicated in cell recognition between synaptic partners, but how these proteins act as a group to specify a complex neural network is poorly understood. Taking advantage of known connectivity in C. elegans, we identified and studied cell adhesion genes expressed in three interacting neurons in the mating circuits of the adult male. Two interacting pairs of cell surface proteins independently promote fasciculation between sensory neuron HOA and its postsynaptic target interneuron AVG: BAM-2/neurexin-related in HOA binds to CASY-1/calsyntenin in AVG; SAX-7/L1CAM in sensory neuron PHC binds to RIG-6/contactin in AVG. A third, basal pathway results in considerable HOA-AVG fasciculation and synapse formation in the absence of the other two. The features of this multiplexed mechanism help to explain how complex connectivity is encoded and robustly established during nervous system development.

scholarly journals Multiple conserved cell adhesion protein interactions mediate neural wiring of a sensory circuit in C. elegans

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Byunghyuk Kim ◽  
Scott W Emmons
Keyword(s):  
Nervous System ◽  
Cell Adhesion ◽  
Sensory Neuron ◽  
Protein Interactions ◽  
Synapse Formation ◽  
System Development ◽  
Nervous System Development ◽  
Surface Proteins ◽  
C Elegans ◽  
Nervous System Function

Nervous system function relies on precise synaptic connections. A number of widely-conserved cell adhesion proteins are implicated in cell recognition between synaptic partners, but how these proteins act as a group to specify a complex neural network is poorly understood. Taking advantage of known connectivity in C. elegans, we identified and studied cell adhesion genes expressed in three interacting neurons in the mating circuits of the adult male. Two interacting pairs of cell surface proteins independently promote fasciculation between sensory neuron HOA and its postsynaptic target interneuron AVG: BAM-2/neurexin-related in HOA binds to CASY-1/calsyntenin in AVG; SAX-7/L1CAM in sensory neuron PHC binds to RIG-6/contactin in AVG. A third, basal pathway results in considerable HOA-AVG fasciculation and synapse formation in the absence of the other two. The features of this multiplexed mechanism help to explain how complex connectivity is encoded and robustly established during nervous system development.

scholarly journals Functional Requirements for Heparan Sulfate Biosynthesis in Morphogenesis and Nervous System Development in C. elegans

PLoS Genetics ◽  
2017 ◽  
Vol 13 (1) ◽  
pp. e1006525 ◽  
Author(s):  
Cassandra R. Blanchette ◽  
Andrea Thackeray ◽  
Paola N. Perrat ◽  
Siegfried Hekimi ◽  
Claire Y. Bénard
Keyword(s):  
Nervous System ◽  
Heparan Sulfate ◽  
System Development ◽  
Nervous System Development ◽  
Functional Requirements ◽  
C Elegans

Genes that guide growth cones along the C. elegans ventral nerve cord

Development ◽  
1997 ◽  
Vol 124 (13) ◽  
pp. 2571-2580 ◽  
Author(s):  
B. Wightman ◽  
R. Baran ◽  
G. Garriga
Keyword(s):  
Nervous System ◽  
Growth Cone ◽  
Nerve Cord ◽  
Ventral Nerve Cord ◽  
System Development ◽  
Growth Cones ◽  
Nervous System Development ◽  
Nerve Bundle ◽  
C Elegans ◽  
Bundle Structure

During nervous system development, growth cone pioneering and fasciculation contribute to nerve bundle structure. Pioneer growth cones initially navigate along neuroglia to establish an axon scaffold that guides later extending growth cones. In C. elegans, the growth cone of the PVPR neuron pioneers the left ventral nerve cord bundle, providing a path for the embryonic extensions of the PVQL and AVKR growth cones. Later during larval development, the HSNL growth cone follows cues in the left ventral nerve cord bundle provided by the PVPR and PVQL axons. Here we show that mutations in the genes enu-1, fax-1, unc-3, unc-30, unc-42 and unc-115 disrupt pathfinding of growth cones along the left ventral nerve cord bundle. Our results indicate that unc-3 and unc-30 function in ventral nerve cord pioneering and that enu-1, fax-1, unc-42 and unc-115 function in recognition of the PVPR and PVQL axons by the AVKR and HSNL growth cones.

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