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.

scholarly journals A screen for genetic loci required for body-wall muscle development during embryogenesis in Caenorhabditis elegans.

Genetics ◽  
1994 ◽  
Vol 137 (2) ◽  
pp. 483-498
Author(s):  
J Ahnn ◽  
A Fire
Keyword(s):  
Caenorhabditis Elegans ◽  
Myosin Heavy Chain ◽  
Muscle Cell ◽  
Heavy Chain ◽  
Body Wall ◽  
Muscle Development ◽  
Contractile Function ◽  
The Body ◽  
Body Wall Muscle ◽  
Genetic Loci

Abstract We have used available chromosomal deficiencies to screen for genetic loci whose zygotic expression is required for formation of body-wall muscle cells during embryogenesis in Caenorhabditis elegans. To test for muscle cell differentiation we have assayed for both contractile function and the expression of muscle-specific structural proteins. Monoclonal antibodies directed against two myosin heavy chain isoforms, the products of the unc-54 and myo-3 genes, were used to detect body-wall muscle differentiation. We have screened 77 deficiencies, covering approximately 72% of the genome. Deficiency homozygotes in most cases stain with antibodies to the body-wall muscle myosins and in many cases muscle contractile function is observed. We have identified two regions showing distinct defects in myosin heavy chain gene expression. Embryos homozygous for deficiencies removing the left tip of chromosome V fail to accumulate the myo-3 and unc-54 products, but express antigens characteristic of hypodermal, pharyngeal and neural development. Embryos lacking a large region on chromosome III accumulate the unc-54 product but not the myo-3 product. We conclude that there exist only a small number of loci whose zygotic expression is uniquely required for adoption of a muscle cell fate.

scholarly journals MUSCLE TENSION AND REFLEXES IN THE EARTHWORM

1923 ◽  
Vol 5 (3) ◽  
pp. 327-333 ◽  
Author(s):  
A. R. Moore
Keyword(s):  
Nerve Cord ◽  
Ventral Nerve Cord ◽  
Body Wall ◽  
Muscle Tension ◽  
Posterior Part ◽  
The Body ◽  
Entire Length ◽  
Sensory Cells ◽  
Ventral Region ◽  
Anterior Segments

1. By the use of preparations of earthworm in which the cutaneous receptors have been anesthetized with a solution of M/8 MgCl2, it is shown that peristalsis can be initiated by tension alone. 2. The receptors of the tension reflex are the intermyal sensory cells of the ventral region of the body wall. 3. It is concluded that Straub obtained the tension reflex because his preparations contained the intermyal receptors; Budington was unable to observe the tension reflex in any preparation from which the intermyal receptors had been removed. 4. Intermyal receptors are the receptors of the following reaction: Passive unilateral tension of the posterior part of an earthworm induces active homolateral tension of the musculature of the anterior segments, and results in the course of progress being brought into line with the enforced orientation of the tail. This reaction is termed the homostrophic reflex. 5. The receptors for the reaction are distributed throughout the entire length of the worm, the effectors are limited to the anterior 15 to 20 segments. The impulse is conducted by the ventral nerve cord. 6. The interaction of the homostrophic reflex and tropisms is considered.

scholarly journals Three-dimensional simulation of the Caenorhabditis elegans body and muscle cells in liquid and gel environments for behavioural analysis

2018 ◽  
Vol 373 (1758) ◽  
pp. 20170376 ◽  
Author(s):  
Andrey Palyanov ◽  
Sergey Khayrulin ◽  
Stephen D. Larson
Keyword(s):  
Caenorhabditis Elegans ◽  
Muscle Activation ◽  
Body Wall ◽  
Particle System ◽  
Three Dimensional ◽  
Muscle Cells ◽  
The Body ◽  
C Elegans ◽  
Muscle Activation Patterns ◽  
Simulation Engine

To better understand how a nervous system controls the movements of an organism, we have created a three-dimensional computational biomechanical model of the Caenorhabditis elegans body based on real anatomical structure. The body model is created with a particle system–based simulation engine known as Sibernetic, which implements the smoothed particle–hydrodynamics algorithm. The model includes an elastic body-wall cuticle subject to hydrostatic pressure. This cuticle is then driven by body-wall muscle cells that contract and relax, whose positions and shape are mapped from C. elegans anatomy, and determined from light microscopy and electron micrograph data. We show that by using different muscle activation patterns, this model is capable of producing C. elegans -like behaviours, including crawling and swimming locomotion in environments with different viscosities, while fitting multiple additional known biomechanical properties of the animal.  This article is part of a discussion meeting issue ‘Connectome to behaviour: modelling C. elegans at cellular resolution’.

Growth cones stall and collapse during axon outgrowth in Caenorhabditis elegans

Development ◽  
1999 ◽  
Vol 126 (20) ◽  
pp. 4489-4498 ◽  
Author(s):  
K.M. Knobel ◽  
E.M. Jorgensen ◽  
M.J. Bastiani
Keyword(s):  
Caenorhabditis Elegans ◽  
Growth Cone ◽  
Nerve Cord ◽  
Body Wall ◽  
Growth Cones ◽  
The Body ◽  
Axon Outgrowth ◽  
Attachment Structures ◽  
Dorsal Nerve

During nervous system development, neurons form synaptic contacts with distant target cells. These connections are formed by the extension of axonal processes along predetermined pathways. Axon outgrowth is directed by growth cones located at the tips of these neuronal processes. Although the behavior of growth cones has been well-characterized in vitro, it is difficult to observe growth cones in vivo. We have observed motor neuron growth cones migrating in living Caenorhabditis elegans larvae using time-lapse confocal microscopy. Specifically, we observed the VD motor neurons extend axons from the ventral to dorsal nerve cord during the L2 stage. The growth cones of these neurons are round and migrate rapidly across the epidermis if they are unobstructed. When they contact axons of the lateral nerve fascicles, growth cones stall and spread out along the fascicle to form anvil-shaped structures. After pausing for a few minutes, they extend lamellipodia beyond the fascicle and resume migration toward the dorsal nerve cord. Growth cones stall again when they contact the body wall muscles. These muscles are tightly attached to the epidermis by narrowly spaced circumferential attachment structures. Stalled growth cones extend fingers dorsally between these hypodermal attachment structures. When a single finger has projected through the body wall muscle quadrant, the growth cone located on the ventral side of the muscle collapses and a new growth cone forms at the dorsal tip of the predominating finger. Thus, we observe that complete growth cone collapse occurs in vivo and not just in culture assays. In contrast to studies indicating that collapse occurs upon contact with repulsive substrata, collapse of the VD growth cones may result from an intrinsic signal that serves to maintain growth cone primacy and conserve cellular material.

scholarly journals Habituation of swimming activity in the medicinal leech

1985 ◽  
Vol 116 (1) ◽  
pp. 169-188
Author(s):  
E. A. Debski ◽  
W. O. Friesen
Keyword(s):  
Nerve Cord ◽  
Ventral Nerve Cord ◽  
Body Wall ◽  
Spontaneous Recovery ◽  
Medicinal Leech ◽  
The Body ◽  
Swimming Activity ◽  
Stimulus Generalization ◽  
Anterior Segments ◽  
Stimulation Of

Tactile stimulation (light stroking) of a body wall flap attached to the ventral nerve cord of the medicinal leech evokes episodes of swimming activity. This swimming response undergoes habituation, involving changes in swim initiation and swim maintenance. Repeated stimulation of the body wall flap evoked swimming activity between three and 39 times before this response failed. During repetitive stimulation, the length of swim episodes decreased by about 50%. The number of swim episodes which could be elicited was not correlated with swim episode length. Following habituation, swim initiation showed significant spontaneous recovery, but swim episode length returned only to 60% of control values. In preparations where spontaneous recovery was followed by rehabituation, the number of swim episodes elicited declined with each habituation-recovery sequence. Additional stimulation immediately following habituation trials had a dual effect: recovery of the swimming response was delayed, but the lengths of swim episodes following spontaneous recovery were increased. Pinching the body wall flap immediately restored the swimming response in an habituated preparation. Swim initiation habituated more rapidly during stimulation of anterior body wall flaps than during stimulation of mid-body or posterior flaps. However, swim length was independent of this regional variation in swim responsiveness. The number of swim episodes elicited by stimulation of body wall flaps attached to posterior or anterior segments depended upon whether this segment was stimulated before or after other flaps. In contrast, in mid-body segments there was no evidence for such stimulus generalization. The lengths of swim episodes elicited during sequential stimulation of several body wall flaps were independent of the stimulation sequence. We propose that separate processes control swim initiation and swim maintenance. These processes must be repeated in most, if not all, of the segmental ganglia of the leech ventral nerve cord.

Morphology of programmed cell death in the ventral nerve cord of Caenorhabditis elegans larvae

Development ◽  
1982 ◽  
Vol 67 (1) ◽  
pp. 89-100
Author(s):  
Alison M. G. Robertson ◽  
J. N. Thomson
Keyword(s):  
Cell Death ◽  
Caenorhabditis Elegans ◽  
Programmed Cell Death ◽  
Ultrastructural Study ◽  
Nerve Cord ◽  
Ventral Nerve Cord ◽  
Condensed Chromatin ◽  
C Elegans ◽  
Programmed Death ◽  
Selection Of

In the nematode C. elegans, cells undergoing programmed death in the developing ventral nerve cord were identified by Nomarski optics and prepared for ultrastructural study at various times after their birth in mitosis. The sequence of changes observed suggests that the hypodermis recognizes the dying cell before completion of telophase. The dying cell is engulfed and digestion then occurs until all that remains within the hypodermal cytoplasm is a collection of membranous whorls interspersed with condensed chromatin-like remnants. The process shares several features with apoptosis, the mode of programmed cell death observed in vertebrates and insects. The selection of cells for programmed death appears not to involve competition for peripheral targets.

Quantitative fluorescence imaging of mitochondria in body wall muscles of Caenorhabditis elegans under hyperglycemic conditions using a microfluidic chip

2020 ◽  
Vol 12 (6) ◽  
pp. 150-160 ◽  
Author(s):  
Samuel Sofela ◽  
Sarah Sahloul ◽  
Sukanta Bhattacharjee ◽  
Ambar Bose ◽  
Ushna Usman ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Fluorescence Imaging ◽  
Microfluidic Device ◽  
Microfluidic Chip ◽  
Body Wall ◽  
The Body ◽  
C Elegans ◽  
Technological Advantage ◽  
Body Wall Muscles ◽  
Quantitative Fluorescence

Abstract Type 2 diabetes is the most common metabolic disease, and insulin resistance plays a role in the pathogenesis of the disease. Because completely functional mitochondria are necessary to obtain glucose-stimulated insulin from pancreatic beta cells, dysfunction of mitochondrial oxidative pathway could be involved in the development of diabetes. As a simple animal model, Caenorhabditis elegans renders itself to investigate such metabolic mechanisms because it possesses insulin/insulin-like growth factor-1 signaling pathway similar to that in humans. Currently, the widely spread agarose pad-based immobilization technique for fluorescence imaging of the mitochondria in C. elegans is laborious, batchwise, and does not allow for facile handling of the worm. To overcome these technical challenges, we have developed a single-channel microfluidic device that can trap a C. elegans and allow to image the mitochondria in body wall muscles accurately and in higher throughput than the traditional approach. In specific, our microfluidic device took advantage of the proprioception of the worm to rotate its body in a microfluidic channel with an aspect ratio above one to gain more space for its undulation motion that was favorable for quantitative fluorescence imaging of mitochondria in the body wall muscles. Exploiting this unique feature of the microfluidic chip-based immobilization and fluorescence imaging, we observed a significant decrease in the mitochondrial fluorescence intensity under hyperglycemic conditions, whereas the agarose pad-based approach did not show any significant change under the same conditions. A machine learning model trained with these fluorescence images from the microfluidic device could classify healthy and hyperglycemic worms at high accuracy. Given this significant technological advantage, its easiness of use and low cost, our microfluidic imaging chip could become a useful immobilization tool for quantitative fluorescence imaging of the body wall muscles in C. elegans.

scholarly journals Functionally asymmetric motor neurons coordinate locomotion of Caenorhabditis elegans

2018 ◽  
Author(s):  
Oleg Tolstenkov ◽  
Petrus Van der Auwera ◽  
Jana F. Liewald ◽  
Wagner Steuer Costa ◽  
Olga Bazhanova ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Gap Junctions ◽  
Motor Neurons ◽  
Nerve Cord ◽  
Ventral Nerve Cord ◽  
Body Wave ◽  
Central Pattern Generators ◽  
Physiological Data ◽  
C Elegans ◽  
Pattern Generators

SummaryInvertebrate nervous systems are valuable models for fundamental principles of the control of behavior. Ventral nerve cord (VNC) motor neurons in Caenorhabditis elegans represent one of the best studied locomotor circuits, with known connectivity and functional information about most of the involved neuron classes. However, for one of those, the AS motor neurons (AS MNs), no physiological data is available. Combining specific expression and selective illumination, we precisely targeted AS MNs by optogenetics and addressed their role in the locomotion circuit. After photostimulation, AS MNs induce currents in post-synaptic body wall muscles (BWMs), exhibiting an initial asymmetry of excitatory output. This may facilitate complex regulatory motifs for adjusting direction during navigation. By behavioral and photo-inhibition experiments, we show that AS MNs contribute to propagation of the antero-posterior body wave during locomotion. By Ca2+-imaging in AS MNs and in their synaptic partners, we also reveal that AS MNs play a role in mediating forward and backward locomotion by integrating activity of premotor interneurons (PINs), as well as in coordination of the dorso-ventral body wave. AS MNs do not exhibit pacemaker properties, but potentially gate VNC central pattern generators (CPGs), as indicated by ceasing of locomotion when AS MNs are hyperpolarized. AS MNs provide positive feedback to the PIN AVA via gap junctions, a feature found also in other locomotion circuits. In sum, AS MNs have essential roles in coordinating locomotion, combining several functions, and emphasizing the compressed nature of the C. elegans nervous system in comparison to higher animals.HighlightsA class of motor neurons with unidentified function – AS cholinergic motor neurons - was characterized in C. elegans.AS neurons show asymmetry in both input and output and are specialized in coordination of dorso-ventral undulation bends.AS neurons mediate antero-posterior propagation of the undulatory body wave during locomotion.AS neurons integrate signals for forward and reverse locomotion from premotor interneurons and may gate ventral nerve cord central pattern generators (CPGs) via gap junctions.

scholarly journals The AP2 clathrin adaptor protein complex regulates the abundance of GLR-1 glutamate receptors in the ventral nerve cord of Caenorhabditis elegans

2015 ◽  
Vol 26 (10) ◽  
pp. 1887-1900 ◽  
Author(s):  
Steven D. Garafalo ◽  
Eric S. Luth ◽  
Benjamin J. Moss ◽  
Michael I. Monteiro ◽  
Emily Malkin ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Nerve Cord ◽  
Ventral Nerve Cord ◽  
Secretory Pathway ◽  
Adaptor Protein ◽  
Intracellular Compartments ◽  
Clathrin Adaptor ◽  
Strength And Plasticity

Regulation of glutamate receptor (GluR) abundance at synapses by clathrin-mediated endocytosis can control synaptic strength and plasticity. We take advantage of viable, null mutations in subunits of the clathrin adaptor protein 2 (AP2) complex in Caenorhabditis elegans to characterize the in vivo role of AP2 in GluR trafficking. In contrast to our predictions for an endocytic adaptor, we found that levels of the GluR GLR-1 are decreased at synapses in the ventral nerve cord (VNC) of animals with mutations in the AP2 subunits APM-2/μ2, APA-2/α, or APS-2/σ2. Rescue experiments indicate that APM-2/μ2 functions in glr-1–expressing interneurons and the mature nervous system to promote GLR-1 levels in the VNC. Genetic analyses suggest that APM-2/μ2 acts upstream of GLR-1 endocytosis in the VNC. Consistent with this, GLR-1 accumulates in cell bodies of apm-2 mutants. However, GLR-1 does not appear to accumulate at the plasma membrane of the cell body as expected, but instead accumulates in intracellular compartments including Syntaxin-13– and RAB-14–labeled endosomes. This study reveals a novel role for the AP2 clathrin adaptor in promoting the abundance of GluRs at synapses in vivo, and implicates AP2 in the regulation of GluR trafficking at an early step in the secretory pathway.

scholarly journals Screening for Presenilin Inhibitors Using the Free-Living Nematode, Caenorhabditis elegans

2004 ◽  
Vol 9 (2) ◽  
pp. 147-152 ◽  
Author(s):  
Brenda R. Ellerbrock ◽  
Eileen M. Coscarelli ◽  
Mark E. Gurney ◽  
Timothy G. Geary
Keyword(s):  
Caenorhabditis Elegans ◽  
High Throughput Screening ◽  
Screening Method ◽  
Genetic System ◽  
Body Cavity ◽  
Egg Laying ◽  
The Body ◽  
Loss Of Function ◽  
C Elegans ◽  
Automated Method

Caenorhabditis elegans contains 3 homologs of presenilin genes that are associated with Alzheimer s disease. Loss-of-function mutations in C. elegans genes cause a defect in egg laying. In humans, loss of presenilin-1 (PS1) function reduces amyloid-beta peptide processing from the amyloid protein precursor. Worms were screened for compounds that block egg laying, phenocopying presenilin loss of function. To accommodate even relatively high throughput screening, a semi-automated method to quantify egg laying was devised by measuring the chitinase released into the culture medium. Chitinase is released by hatching eggs, but little is shed into the medium from the body cavity of a hermaphrodite with an egg laying deficient ( egl) phenotype. Assay validation involved measuring chitinase release from wild-type C. elegans (N2 strain), sel-12 presenilin loss-of-function mutants, and 2 strains of C. elegans with mutations in the egl-36K+ channel gene. Failure to find specific presenilin inhibitors in this collection likely reflects the small number of compounds tested, rather than a flaw in screening strategy. Absent defined biochemical pathways for presenilin, this screening method, which takes advantage of the genetic system available in C. elegans and its historical use for anthelminthic screening, permits an entry into mechanism-based discovery of drugs for Alzheimer s disease. ( Journal of Biomolecular Screening 2004:147-152)

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