Genetics of cell and axon migrations in Caenorhabditis elegans

Development ◽  
1987 ◽  
Vol 100 (3) ◽  
pp. 365-382 ◽  
Author(s):  
E.M. Hedgecock ◽  
J.G. Culotti ◽  
D.H. Hall ◽  
B.D. Stern
Keyword(s):  
Caenorhabditis Elegans ◽  
Body Wall ◽  
Cell Layer ◽  
External Surface ◽  
Embryonic Cell ◽  
Epidermal Cells ◽  
The Body ◽  
Cell Lineages ◽  
Surface Molecules ◽  
Body Wall Muscles

The Caenorhabditis elegans epidermis comprises 78 cells which cover the external surface of the embryo as a single cell layer. These cells secrete the cuticle from their exterior faces and support the body wall muscles and most of the nervous system on their interior faces. The epidermal cells arise by autonomous embryonic cell lineages but show regulative interactions after their assembly into an epithelium. It is believed that the various epidermal cells express different kinds or amounts of surface molecules that govern their mutual assembly and also guide the attachments and migrations of the underlying body muscles and neurones. The first muscles and neurones may in turn express new surface molecules that refine later cell movements. Mutations in some 30 known genes disrupt the movements of cells or axons along the body wall.

scholarly journals Muscle cell attachment in Caenorhabditis elegans.

1991 ◽  
Vol 114 (3) ◽  
pp. 465-479 ◽  
Author(s):  
R Francis ◽  
R H Waterston
Keyword(s):  
Caenorhabditis Elegans ◽  
Basement Membrane ◽  
Muscle Cell ◽  
Body Wall ◽  
Cell Attachment ◽  
Muscle Cells ◽  
The Body ◽  
Nematode Caenorhabditis Elegans ◽  
Hypodermal Cell ◽  
Body Wall Muscles

In the nematode Caenorhabditis elegans, the body wall muscles exert their force on the cuticle to generate locomotion. Interposed between the muscle cells and the cuticle are a basement membrane and a thin hypodermal cell. The latter contains bundles of filaments attached to dense plaques in the hypodermal cell membranes, which together we have called a fibrous organelle. In an effort to define the chain of molecules that anchor the muscle cells to the cuticle we have isolated five mAbs using preparations enriched in these components. Two antibodies define a 200-kD muscle antigen likely to be part of the basement membrane at the muscle/hypodermal interface. Three other antibodies probably identify elements of the fibrous organelles in the adjacent hypodermis. The mAb IFA, which reacts with mammalian intermediate filaments, also recognizes these structures. We suggest that the components recognized by these antibodies are likely to be involved in the transmission of tension from the muscle cell to the cuticle.

Genetic defects in acetylcholine signalling promote protein degradation in muscle cells of Caenorhabditis elegans

2000 ◽  
Vol 113 (11) ◽  
pp. 2003-2010 ◽  
Author(s):  
N.J. Szewczyk ◽  
J.J. Hartman ◽  
S.J. Barmada ◽  
L.A. Jacobson
Keyword(s):  
Caenorhabditis Elegans ◽  
Body Wall ◽  
Muscle Protein ◽  
Muscle Cells ◽  
Negative Control ◽  
The Body ◽  
Reporter Protein ◽  
Release Of Acetylcholine ◽  
Body Wall Muscles ◽  
Ach Receptors

A myosin-lacZ fusion, expressed in 103 muscle cells of Caenorhabditis elegans, reports on how proteolysis in muscle is controlled by neural and intramuscular signals. Upon acute starvation, the fusion protein is degraded in the posterior 63 cells of the body-wall muscle, but remains stable in 32 anterior body-wall muscles and 8 vulval muscle cells. This distinction correlates with differences in the innervation of these cells. Reporter protein in the head and vulval muscles becomes labile upon genetic ‘denervation’ in mutants that have blocks in pre-synaptic synthesis or release of acetylcholine (ACh) or post-synaptic reception at nicotinic ACh receptors (nAChR), whereas protein in all 103 muscles is stabilized by the nicotinic agonist levamisole in the absence of ACh production. Levamisole does not stabilize muscle protein in nAChR mutants that are behaviorally resistant to levamisole. Neural inputs thus exert negative control over the proteolytic process in muscle by stimulating muscle nicotinic ACh receptors.

Observations on the epidermis of the miracidium and on the formation of the tegument of the sporocyst of Fasciola hepatica

Parasitology ◽  
1970 ◽  
Vol 61 (2) ◽  
pp. 177-190 ◽  
Author(s):  
V. R. Southgate
Keyword(s):  
Plasma Membrane ◽  
Basal Lamina ◽  
Body Wall ◽  
Fasciola Hepatica ◽  
Epidermal Cells ◽  
The Body ◽  
Transitional Epithelium ◽  
Dense Granules ◽  
Outer Covering ◽  
Body Wall Muscles

The relationship between the ciliated epidermal cells and the subepidermal layer of the miracidium of Fasciola hepatica has been described. Non-ciliated ridge-like extensions of the subepidermal layer separate the ciliated epidermal cells from each other. The sunken portions of the subepidermal layer, each containing a nucleus, lie below the outer body wall muscles of the miracidium and open into the ridge by narrow neck-like connexions. Elongate vesicles, which may be a source of stored plasma membrane similar to that which occurs in the transitional epithelium of other animals, fill most of the ridge. In addition, characteristic round electron dense granules are found in the ridge but the majority are found in the sunken portions of the subepidermal layer.The development and origins of the tegument of the sporocyst of F. hepatica have been described at the ultrastructural level. When the miracidium is in the process of penetrating the snail host, large vacuoles appear between the ciliated epidermal cells and the basal lamina which overlies the muscles of the body wall. These vacuoles have the effect of loosening the epidermal cells from the basal lamina of the body wall of the miracidium. Possible mechanisms involved in the formation of such vacuoles are suggested and discussed.During penetration of the snail the ciliated epidermal cells of the miracidium are lost; the ridge, a syncytial layer between the epidermal cells which is connected with the subepidermal layer, spreads over the basal lamina and exposed body wall muscles of the metamorphosing sporocyst to form the new outer covering of the sporocyst.Cytoplasm passes from the subtegumentary layer into the tegument during this stage of the development of the body wall of the sporocyst. Muscular contraction and microtubules may be involved in the outward movements of this cytoplasm. The nuclei of the subtegumentary layer remain below the muscles of the body wall.Twenty-four hours after penetration of the snail the outer plasma membrane of the tegument forms folds, which greatly increase the surface area.Sixty hours after penetration involutions between the folds, which may indicate pinocytosis, are present, and it is suggested that pinocytosis may play a role in food absorption.The fully formed tegument is a syncytial layer containing numerous electron dense granules, vacuoles, mitochondria and lipid droplets.The results on the formation of the tegument of the sporocyst have been discussed with reference to the controversy about the origins and terminology of the outer covering of the Platyhelminths.

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 Caenorhabditis elegans Unc-45 Is a Component of Muscle Thick Filaments and Colocalizes with Myosin Heavy Chain B, but Not Myosin Heavy Chain a

2000 ◽  
Vol 148 (2) ◽  
pp. 375-384 ◽  
Author(s):  
Wanyuan Ao ◽  
Dave Pilgrim
Keyword(s):  
Caenorhabditis Elegans ◽  
Myosin Heavy Chain ◽  
Heavy Chain ◽  
Body Wall ◽  
Thick Filament ◽  
The Body ◽  
Temperature Sensitive ◽  
Filament Assembly ◽  
Thick Filaments ◽  
Body Wall Muscles

In the nematode Caenorhabditis elegans, animals mutant in the gene encoding the protein product of the unc-45 gene (UNC-45) have disorganized muscle thick filaments in body wall muscles. Although UNC-45 contains tetratricopeptide repeats (TPR) as well as limited similarity to fungal proteins, no biochemical role has yet been found. UNC-45 reporters are expressed exclusively in muscle cells, and a functional reporter fusion is localized in the body wall muscles in a pattern identical to thick filament A-bands. UNC-45 colocalizes with myosin heavy chain (MHC) B in wild-type worms as well as in temperature-sensitive (ts) unc-45 mutants, but not in a mutant in which MHC B is absent. Surprisingly, UNC-45 localization is also not seen in MHC B mutants, in which the level of MHC A is increased, resulting in near-normal muscle thick filament structure. Thus, filament assembly can be independent of UNC-45. UNC-45 shows a localization pattern identical to and dependent on MHC B and a function that appears to be MHC B–dependent. We propose that UNC-45 is a peripheral component of muscle thick filaments due to its localization with MHC B. The role of UNC-45 in thick filament assembly seems restricted to a cofactor for assembly or stabilization of MHC B.

scholarly journals Co-Contraction Analyses of the Body Wall Muscles in Caenorhabditis Elegans by Calcium Imaging Assay and Simulation

2021 ◽  
Author(s):  
Zu Soh ◽  
Hiroki Yamashita ◽  
Michiyo Suzuki ◽  
Kazuma Sakamoto ◽  
Toshio Tsuji
Keyword(s):  
Caenorhabditis Elegans ◽  
Calcium Imaging ◽  
Body Wall ◽  
The Body ◽  
Viscous Drag ◽  
Dynamics Model ◽  
Local Curvature ◽  
Significant Difference ◽  
Body Dynamics ◽  
Body Wall Muscles

Abstract Caenorhabditis elegans can generate locomotion under various environments with completely different drag levels. Therefore, animals should have strategies for adapting to the changes in the dynamics of locomotion imposed by various environments. We hypothesized that co-contraction between the ventral and dorsal body wall muscles plays such a role and validated the presence of a co-contraction strategy through both experimental and mathematical modeling approaches. To this end, the fluorescence of calcium ion (Ca2+) corresponding to a part of activities of the body wall muscles were measured. The results indicated a significant difference in the co-fluorescence rate between the animals moving in low- and high-drag environments. The contribution of co-contraction to the dynamics of locomotion was then analysed using a body dynamics model. The simulation results suggested that co-contraction allows the dominance of body stiffness over viscous drag so that the phase difference between the local curvature of the body and muscle activities can be maintained under different environmental drag levels. Therefore, co-contraction can be an effective strategy for adapting to environmental drag that changes the dynamics of locomotion.

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 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.

ISOLATION AND GENETIC CHARACTERIZATION OF CELL-LINEAGE MUTANTS OF THE NEMATODE CAENORHABDITIS ELEGANS

Genetics ◽  
1980 ◽  
Vol 96 (2) ◽  
pp. 435-454 ◽  
Author(s):  
H Robert Horvitz ◽  
John E Sulston
Keyword(s):  
Caenorhabditis Elegans ◽  
Cell Lineage ◽  
Embryonic Cell ◽  
Null Alleles ◽  
Recessive Mutation ◽  
Incomplete Penetrance ◽  
Nematode Caenorhabditis Elegans ◽  
Cell Lineages ◽  
Cell Divisions ◽  
Recessive Mutations

ABSTRACT Twenty-four mutants that alter the normally invariant post-embryonic cell lineages of the nematode Caenorhabditis elegans have been isolated and genetically characterized. In some of these mutants, cell divisions fail that occur in wild-type animals; in other mutants, cells divide that do not normally do so. The mutants differ in the specificities of their defects, so that it is possible to identify mutations that affect some cell lineages but not others. These mutants define 14 complementation groups, which have been mapped. The abnormal phenotype of most of the cell-lineage mutants results from a single recessive mutation; however, the excessive cell divisions characteristic of one strain, CB1322, require the presence of two unlinked recessive mutations. All 24 cell-lineage mutants display incomplete penetrance and/or variable expressivity. Three of the mutants are suppressed by pleiotropic suppressors believed to be specific for null alleles, suggesting that their phenotypes result from the complete absence of gene activity.

The Ligamentary System and the Segmental Musculature of Nephtys

1960 ◽  
Vol s3-101 (54) ◽  
pp. 149-176
Author(s):  
R. B. CLARK ◽  
M. E. CLARK
Keyword(s):  
Body Wall ◽  
The Body ◽  
Power Stroke ◽  
Coelomic Fluid ◽  
Unusual Structure ◽  
Shock Absorbers ◽  
Proximal Half ◽  
Unique System ◽  
Body Wall Muscles ◽  
The Impact

Nephtys lacks circular body-wall muscles. The chief antagonists of the longitudinal muscles are the dorso-ventral muscles of the intersegmental body-wall. The worm is restrained from widening when either set of muscles contracts by the combined influence of the ligaments, some of the extrinsic parapodial muscles, and possibly, to a limited extent, by the septal muscles. Although the septa are incomplete, they can and do form a barrier to the transmission of coelomic fluid from one segment to the next under certain conditions, particularly during eversion of the proboscis. Swimming is by undulatory movements of the body but the distal part of the parapodia execute a power-stroke produced chiefly by the contraction of the acicular muscles. It is suspected that the extrinsic parapodial muscles, all of which are inserted in the proximal half of the parapodium, serve to anchor the parapodial wall at the insertion of the acicular muscles and help to provide a rigid point of insertion for them. Burrowing is a cyclical process involving the violent eversion of the proboscis which makes a cavity in the sand. The worm is prevented from slipping backwards by the grip the widest segments have on the sides of the burrow. The proboscis is retracted and the worm crawls forward into the cavity it has made. The cycle is then repeated. Nephtys possesses a unique system of elastic ligaments of unusual structure. The anatomy of the system is described. The function of the ligaments appears to be to restrain the body-wall and parapodia from unnecessary and disadvantageous dilatations during changes of body-shape, and to serve as shock-absorbers against the high, transient, fluid pressures in the coelom, which are thought to accompany the impact of the proboscis against the sand when the worm is burrowing. From what is known of its habits, Nephtys is likely to undertake more burrowing than most other polychaetes.

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