Mutations in the Caenorhabditis elegans unc–4 gene alter the synaptic input to ventral cord motor neurons

Nature ◽  
1992 ◽  
Vol 355 (6363) ◽  
pp. 838-841 ◽  
Author(s):  
J. G. White ◽  
E. Southgate ◽  
J. N. Thomson
Keyword(s):  
Caenorhabditis Elegans ◽  
Motor Neurons ◽  
Synaptic Input ◽  
Ventral Cord

scholarly journals Dominant unc-37 mutations suppress the movement defect of a homeodomain mutation in unc-4, a neural specificity gene in Caenorhabditis elegans.

Genetics ◽  
1993 ◽  
Vol 135 (3) ◽  
pp. 741-753 ◽  
Author(s):  
D M Miller ◽  
C J Niemeyer ◽  
P Chitkara
Keyword(s):  
Caenorhabditis Elegans ◽  
Motor Neurons ◽  
Synaptic Input ◽  
Neuronal Morphology ◽  
Axonal Guidance ◽  
Temperature Sensitive ◽  
Homeodomain Protein ◽  
Loss Of Function ◽  
Selection Scheme ◽  
Synaptic Specificity

Abstract The unc-4 gene of Caenorhabditis elegans encodes a homeodomain protein that defines synaptic input to ventral cord motor neurons. unc-4 mutants are unable to crawl backward because VA motor neurons are miswired with synaptic connections normally reserved for their sister cells, the VB motor neurons. These changes in connectivity are not accompanied by any visible effects upon neuronal morphology, which suggests that unc-4 regulates synaptic specificity but not axonal guidance or outgrowth. In an effort to identify other genes in the unc-4 pathway, we have devised a selection scheme for rare mutations that suppress the Unc-4 phenotype. We have isolated four, dominant, extragenic, allele-specific suppressors of unc-4(e2322ts), a temperature sensitive allele with a point mutation in the unc-4 homeodomain. Our data indicate that these suppressors are gain-of-function mutations in the previously identified unc-37 gene. We show that the loss-of-function mutation unc-37(e262) phenocopies the Unc-4 movement defect but does not prevent unc-4 expression or alter VA motor neuron morphology. These findings suggest that unc-37 functions with unc-4 to specify synaptic input to the VA motor neurons. We propose that unc-37 may be regulated by unc-4. Alternatively, unc-37 may encode a gene product that interacts with the unc-4 homeodomain.

scholarly journals Caenorhabditis elegans excitatory ventral cord motor neurons derive rhythm for body undulation

2018 ◽  
Vol 373 (1758) ◽  
pp. 20170370 ◽  
Author(s):  
Quan Wen ◽  
Shangbang Gao ◽  
Mei Zhen
Keyword(s):  
Caenorhabditis Elegans ◽  
Motor Neurons ◽  
Central Pattern Generators ◽  
Oscillatory Activity ◽  
C Elegans ◽  
Ventral Cord ◽  
Small Neuron ◽  
Motor Rhythm ◽  
Pattern Generators

The intrinsic oscillatory activity of central pattern generators underlies motor rhythm. We review and discuss recent findings that address the origin of Caenorhabditis elegans motor rhythm. These studies propose that the A- and mid-body B-class excitatory motor neurons at the ventral cord function as non-bursting intrinsic oscillators to underlie body undulation during reversal and forward movements, respectively. Proprioception entrains their intrinsic activities, allows phase-coupling between members of the same class motor neurons, and thereby facilitates directional propagation of undulations. Distinct pools of premotor interneurons project along the ventral nerve cord to innervate all members of the A- and B-class motor neurons, modulating their oscillations, as well as promoting their bi-directional coupling. The two motor sub-circuits, which consist of oscillators and descending inputs with distinct properties, form the structural base of dynamic rhythmicity and flexible partition of the forward and backward motor states. These results contribute to a continuous effort to establish a mechanistic and dynamic model of the C. elegans sensorimotor system. C. elegans exhibits rich sensorimotor functions despite a small neuron number. These findings implicate a circuit-level functional compression. By integrating the role of rhythm generation and proprioception into motor neurons, and the role of descending regulation of oscillators into premotor interneurons, this numerically simple nervous system can achieve a circuit infrastructure analogous to that of anatomically complex systems. C. elegans has manifested itself as a compact model to search for general principles of sensorimotor behaviours. This article is part of a discussion meeting issue ‘Connectome to behaviour: modelling C. elegans at cellular resolution’.

The Caenorhabditis elegans odr-2 Gene Encodes a Novel Ly-6-Related Protein Required for Olfaction

Genetics ◽  
2001 ◽  
Vol 157 (1) ◽  
pp. 211-224 ◽  
Author(s):  
Joseph H Chou ◽  
Cornelia I Bargmann ◽  
Piali Sengupta
Keyword(s):  
Caenorhabditis Elegans ◽  
Motor Neurons ◽  
Amino Terminus ◽  
Signaling Proteins ◽  
Related Protein ◽  
Olfactory Neurons ◽  
Unique Role ◽  
C Elegans ◽  
Founding Member ◽  
High Concentrations

Abstract Caenorhabditis elegans odr-2 mutants are defective in the ability to chemotax to odorants that are recognized by the two AWC olfactory neurons. Like many other olfactory mutants, they retain responses to high concentrations of AWC-sensed odors; we show here that these residual responses are caused by the ability of other olfactory neurons (the AWA neurons) to be recruited at high odor concentrations. odr-2 encodes a membrane-associated protein related to the Ly-6 superfamily of GPI-linked signaling proteins and is the founding member of a C. elegans gene family with at least seven other members. Alternative splicing of odr-2 yields three predicted proteins that differ only at the extreme amino terminus. The three isoforms have different promoters, and one isoform may have a unique role in olfaction. An epitope-tagged ODR-2 protein is expressed at high levels in sensory neurons, motor neurons, and interneurons and is enriched in axons. The AWC neurons are superficially normal in their development and structure in odr-2 mutants, but their function is impaired. Our results suggest that ODR-2 may regulate AWC signaling within the neuronal network required for chemotaxis.

scholarly journals Mutations Affecting Nerve Attachment of Caenorhabditis elegans

Genetics ◽  
2001 ◽  
Vol 157 (4) ◽  
pp. 1611-1622 ◽  
Author(s):  
Go Shioi ◽  
Michinari Shoji ◽  
Masashi Nakamura ◽  
Takeshi Ishihara ◽  
Isao Katsura ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Nerve Cord ◽  
Ventral Nerve Cord ◽  
Body Wall ◽  
The Body ◽  
Genetic Loci ◽  
Muscle Attachment ◽  
C Elegans ◽  
Ventral Cord ◽  
Excretory Canal

Abstract Using a pan-neuronal GFP marker, a morphological screen was performed to detect Caenorhabditis elegans larval lethal mutants with severely disorganized major nerve cords. We recovered and characterized 21 mutants that displayed displacement or detachment of the ventral nerve cord from the body wall (Ven: ventral cord abnormal). Six mutations defined three novel genetic loci: ven-1, ven-2, and ven-3. Fifteen mutations proved to be alleles of previously identified muscle attachment/positioning genes, mup-4, mua-1, mua-5, and mua-6. All the mutants also displayed muscle attachment/positioning defects characteristic of mua/mup mutants. The pan-neuronal GFP marker also revealed that mutants of other mua/mup loci, such as mup-1, mup-2, and mua-2, exhibited the Ven defect. The hypodermis, the excretory canal, and the gonad were morphologically abnormal in some of the mutants. The pleiotropic nature of the defects indicates that ven and mua/mup genes are required generally for the maintenance of attachment of tissues to the body wall in C. elegans.

Cellular studies of peripheral neurons in siphon skin of Aplysia californica

1979 ◽  
Vol 42 (2) ◽  
pp. 530-557 ◽  
Author(s):  
C. H. Bailey ◽  
V. F. Castellucci ◽  
J. Koester ◽  
E. R. Kandel
Keyword(s):  
Motor Neurons ◽  
Synaptic Input ◽  
Firing Pattern ◽  
White Cell ◽  
Type I ◽  
Type Ii ◽  
Peripheral Neurons ◽  
Peripheral Neuron ◽  
Type I Neuron ◽  
Kinetics Of

1. To account for the similarity in the kinetics of habituation between the central and peripheral components of siphon withdrawal, we have tested the idea (52) that each centrally located mechanoreceptor sensory neuron sends two branches to siphon motor neurons; one to centrally located siphon motor neurons and a collateral branch that remains in the periphery and innervates the peripheral siphon motor neurons. 2. We have found a group of peripheral siphon motor neurons and tested the connection onto these cells by central mechanoreceptors. In addition, we have defined by various electrophysiological and morphological criteria two general classes of peripheral neurons that lie along the course of the siphon nerve. 3. One class (type I) consists of only a single cell in each animal. This peripheral neuron typically has the largest cell body found lying along the siphon nerve and is the only peripheral nerve cell that appears white when viewed under epi-illumination. The type I neuron often has a highly regular firing pattern, which occurs in the absence of spontaneous synaptic input. The three-dimensional morphology of this neuron suggests a paucity of fine processes, most of which do not arborize and may terminate in the connective tissue sheath. Fine structural observations of the peripheral white cell have revealed the presence of large densecore granules. The peripheral type I neuron is similar in most of its electrophysiological and morphological properties to central neurons postulated to be neurosecretory. The peripheral white cell is, at present, the only peripheral neuron we can identify with certainty as a unique individual. 4. The second class (type II) of peripheral neurons are siphon motor neurons for the peripheral component of the siphon-withdrawal reflex. In contrast to the type I neurons, members of the second class of peripheral neurons possess smaller, more spherical cell bodies that have varying amounts of orange pigmentation and which give rise to a relatively well-developed and arborized dendritic tree. Type II neurons feature an irregular spontaneous firing pattern that is occasionally modulated by a rich spontaneous synaptic input. Peripheral siphon motor neurons have restricted motor fields that produce contraction of the mantle floor and the base of the siphon. Most of the type II neurons were found to be electrically coupled to one another. 5. The peripheral siphon motor neurons resemble the central siphon motor neurons in that they receive a collateral synapse from centrally located mechanoreceptor sensory neurons. This peripheral sensory-to-motor synapse exhibits the same kinetics of decrement as its central counterpart, both of which parallel behavioral habituation. 6. The rich mechanoreceptor input onto the relatively isolated dendritic trees of the peripheral siphon motor neurons provide a uniquely restricted neuropil to study the sensory-to-motor synapse. The peripheral motor neurons may, therefore, be a useful simple preparation for the cellular study of behavioral plasticity.

scholarly journals A Network of HSPG Core Proteins and HS Modifying Enzymes Regulates Netrin-Dependent Guidance of D-Type Motor Neurons in Caenorhabditis elegans

PLoS ONE ◽  
2013 ◽  
Vol 8 (9) ◽  
pp. e74908 ◽  
Author(s):  
Stephan Gysi ◽  
Christa Rhiner ◽  
Stephane Flibotte ◽  
Donald G. Moerman ◽  
Michael O. Hengartner
Keyword(s):  
Caenorhabditis Elegans ◽  
Motor Neurons ◽  
Core Proteins ◽  
Type Motor

scholarly journals The MADD-3 LAMMER Kinase Interacts with a p38 MAP Kinase Pathway to Regulate the Display of the EVA-1 Guidance Receptor in Caenorhabditis elegans

PLoS Genetics ◽  
2016 ◽  
Vol 12 (4) ◽  
pp. e1006010 ◽  
Author(s):  
Serena A. D’Souza ◽  
Luckshi Rajendran ◽  
Rachel Bagg ◽  
Louis Barbier ◽  
Derek M. van Pel ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Caenorhabditis Elegans ◽  
Map Kinase ◽  
Motor Neurons ◽  
Leading Edge ◽  
P38 Map Kinase ◽  
Endosomal Trafficking ◽  
Guidance Cue ◽  
Map Kinase Pathway ◽  
Kinase Pathway

The proper display of transmembrane receptors on the leading edge of migrating cells and cell extensions is essential for their response to guidance cues. We previously discovered that MADD-4, which is an ADAMTSL secreted by motor neurons in Caenorhabditis elegans, interacts with an UNC-40/EVA-1 co-receptor complex on muscles to attract plasma membrane extensions called muscle arms. In nematodes, the muscle arm termini harbor the post-synaptic elements of the neuromuscular junction. Through a forward genetic screen for mutants with disrupted muscle arm extension, we discovered that a LAMMER kinase, which we call MADD-3, is required for the proper display of the EVA-1 receptor on the muscle’s plasma membrane. Without MADD-3, EVA-1 levels decrease concomitantly with a reduction of the late-endosomal marker RAB-7. Through a genetic suppressor screen, we found that the levels of EVA-1 and RAB-7 can be restored in madd-3 mutants by eliminating the function of a p38 MAP kinase pathway. We also found that EVA-1 and RAB-7 will accumulate in madd-3 mutants upon disrupting CUP-5, which is a mucolipin ortholog required for proper lysosome function. Together, our data suggests that the MADD-3 LAMMER kinase antagonizes the p38-mediated endosomal trafficking of EVA-1 to the lysosome. In this way, MADD-3 ensures that sufficient levels of EVA-1 are present to guide muscle arm extension towards the source of the MADD-4 guidance cue.

Identification Of A Novel Gene Altered In The RQ1 Mutant Strain Affecting Motor Axon Migration In Caenorhabditis Elegans

2021 ◽  
Author(s):  
Haider Z. Naqvi
Keyword(s):  
Caenorhabditis Elegans ◽  
Axon Guidance ◽  
Motor Neurons ◽  
Genetic Background ◽  
Germ Line ◽  
Strong Indication ◽  
Wild Type ◽  
C Elegans ◽  
Novel Gene ◽  
Mutation Region

Novel genetic enhancer screens were conducted targeting mutants involved in the guidance of axons of the DA and DB classes of motor neurons in C. elegans. These mutations are expected in genes that function in parallel to the unc-g/Netrin pathway. The screen was conducted in an unc-5(e53) genetic background and enhancers of the axon guidance defects caused by the absence of UNC-5 were identified. Three mutants were previously identified in the screen called rq1, rq2 and rq3 and two additional mutants called H2-4 and M1-3, were isolated in this study. In order to identify the gene affected by the rq1 mutation, wild-type copies of genes in the mapped rq1 mutation region were injected into the mutants to rescue the phenotypic defects. This is a strong indication that the gene of interest is a novel gene called H04D03.1. Promising results indicate that the H04D03.1 protein also works in germ-line apoptosis.

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