Positioning and maintenance of embryonic body wall muscle attachments in C. elegans requires the mup-1 gene

Development ◽  
1991 ◽  
Vol 111 (3) ◽  
pp. 667-681 ◽  
Author(s):  
P.Y. Goh ◽  
T. Bogaert
Keyword(s):  
Extracellular Matrix ◽  
Body Wall ◽  
Early Stage ◽  
Muscle Growth ◽  
The Body ◽  
Body Wall Muscle ◽  
C Elegans ◽  
Extracellular Matrix Molecule ◽  
Extracellular Matrix Components ◽  
Body Wall Muscles

As part of a general study of genes specifying a pattern of muscle attachments, we identified and genetically characterised mutants in the mup-1 gene. The body wall muscles of early stage mup-1 embryos have a wild-type myofilament pattern but may extend ectopic processes. Later in embryogenesis, some body wall muscles detach from the hypodermis. Genetic analysis suggests that mup-1 has both a maternal and a zygotic component and is not required for postembryonic muscle growth and attachment. mup-1 mutants are suppressed by mutations in several genes that encode extracellular matrix components. We propose that mup-1 may encode a cell surface/extracellular matrix molecule required both for the positioning of body wall muscle attachments in early embryogenesis and the subsequent maintenance of these attachments to the hypodermis until after cuticle synthesis.

Calsequestrin, a calcium sequestering protein localized at the sarcoplasmic reticulum, is not essential for body-wall muscle function in Caenorhabditis elegans

2000 ◽  
Vol 113 (22) ◽  
pp. 3947-3958 ◽  
Author(s):  
J.H. Cho ◽  
Y.S. Oh ◽  
K.W. Park ◽  
J. Yu ◽  
K.Y. Choi ◽  
...  
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Calcium Binding ◽  
Body Wall ◽  
Functional Characterization ◽  
The Body ◽  
Body Wall Muscle ◽  
C Elegans ◽  
Muscle Formation ◽  
Body Wall Muscles

Calsequestrin is the major calcium-binding protein of cardiac and skeletal muscles whose function is to sequester Ca(2+)in the lumen of the sarcoplasmic reticulum (SR). Here we describe the identification and functional characterization of a C. elegans calsequestrin gene (csq-1). CSQ-1 shows moderate similarity (50% similarity, 30% identity) to rabbit skeletal calsequestrin. Unlike mammals, which have two different genes encoding cardiac and fast-twitch skeletal muscle isoforms, csq-1 is the only calsequestrin gene in the C. elegans genome. We show that csq-1 is highly expressed in the body-wall muscles, beginning in mid-embryogenesis and maintained through the adult stage. In body-wall muscle cells, CSQ-1 is localized to sarcoplasmic membranes surrounding sarcomeric structures, in the regions where ryanodine receptors (UNC-68) are located. Mutation in UNC-68 affects CSQ-1 localization, suggesting that the two possibly interact in vivo. Genetic analyses of chromosomal deficiency mutants deleting csq-1 show that CSQ-1 is not essential for initiation of embryonic muscle formation and contraction. Furthermore, double-stranded RNA injection resulted in animals completely lacking CSQ-1 in body-wall muscles with no observable defects in locomotion. These findings suggest that although CSQ-1 is one of the major calcium-binding proteins in the body-wall muscles of C. elegans, it is not essential for body-wall muscle formation and contraction.

scholarly journals Cholinergic signalling at the body wall neuromuscular junction couples to distal inhibition of feeding in C. elegans

2021 ◽  
Author(s):  
Patricia G. Izquierdo ◽  
Thibana Thisainathan ◽  
James H. Atkins ◽  
Christian J. Lewis ◽  
John E.H. Tattersall ◽  
...  
Keyword(s):  
Body Wall ◽  
Neuromuscular Junctions ◽  
Model Organism ◽  
Inhibitory Effect ◽  
The Body ◽  
Body Wall Muscle ◽  
Cholinergic Transmission ◽  
Systematic Screening ◽  
C Elegans ◽  
Pharyngeal Pumping

AbstractComplex biological functions within organisms are frequently orchestrated by systemic communication between tissues. In the model organism C. elegans, the pharyngeal and body wall neuromuscular junctions are two discrete structures that control feeding and locomotion, respectively. These distinct tissues are controlled by separate, well-defined neural circuits. Nonetheless, the emergent behaviours, feeding and locomotion, are coordinated to guarantee the efficiency of food intake. We show that pharmacological hyperactivation of cholinergic transmission at the body wall muscle reduces the rate of pumping behaviour. This was evidenced by a systematic screening of the cholinesterase inhibitor aldicarb’s effect on the rate of pharyngeal pumping on food in mutant worms. The screening revealed that the key determinant of the inhibitory effect of aldicarb on pharyngeal pumping is the L-type nicotinic acetylcholine receptor expressed in body wall muscle. This idea was reinforced by the observation that selective hyperstimulation of the body wall muscle L-type receptor by the agonist levamisole inhibited pumping. Overall, our results reveal that body wall cholinergic transmission controls locomotion and simultaneously couples a distal inhibition of feeding.

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 EFF-1 promotes muscle fusion, paralysis and retargets infection by AFF-1-coated viruses in C. elegans

2020 ◽  
Author(s):  
Anna Meledin ◽  
Xiaohui Li ◽  
Elena Matveev ◽  
Boaz Gildor ◽  
Ofer Katzir ◽  
...  
Keyword(s):  
Cell Fusion ◽  
Body Wall ◽  
Muscle Development ◽  
Smooth Muscles ◽  
Muscle Cells ◽  
The Body ◽  
Host Interactions ◽  
C Elegans ◽  
Body Wall Muscles ◽  
Cell Cell

A hallmark of muscle development is that myoblasts fuse to form myofibers. However, smooth muscles and cardiomyocytes do not generally fuse. In C. elegans, the body wall muscles (BWMs), the physiological equivalents of skeletal muscles, are mononuclear. Here, to determine what would be the consequences of fusing BWMs, we express the cell-cell fusogen EFF-1 in these cells. We find that EFF-1 induces paralysis and dumpy phenotypes. To determine whether EFF-1-induced muscle fusion results in these pathologies we injected viruses pseudotyped with AFF-1, a paralog of EFF-1, into the pseudocoelom of C. elegans. When these engineered viruses encounter cells expressing EFF-1 or AFF-1 they are able to infect them as revealed by GFP expression from the viral genome. We find that AFF-1 viruses can fuse to EFF-1-expressing muscles revealing multinucleated fibers that cause paralysis and abnormal muscle morphogenesis. Thus, aberrant fusion of otherwise non-syncytial muscle cells may lead to pathological conditions.Graphical abstractSignificance statementMost cells are individual units that do not mix their cytoplasms. However, some cells fuse to become multinucleated in placenta, bones and muscles. In most animals, muscles are formed by myofibers that originate by cell-cell fusion. In contrast, in C. elegans the body wall muscles are mononucleated cells that mediate worm-like movement. EFF-1 and AFF-1 fusogens mediate physiological cell fusion in C. elegans. By ectopically expressing EFF-1 in body wall muscles we induce their fusion resulting in behavioral and morphological deleterious effects, revealing possible causes of congenital myopathies in humans. Using AFF-1-coated pseudoviruses we infect EFF-1-expressing muscle cells retargeting viral infection into these cells. We suggest that virus retargeting can be utilized to study myogenesis, neuronal regeneration, gamete fusion and screens for new fusogens in different organisms. In addition, our virus retargeting system can be used in gene-therapy, viral-based oncolysis and to study viral-host interactions.

CeMyoD accumulation defines the body wall muscle cell fate during C. elegans embryogenesis

Cell ◽  
1990 ◽  
Vol 63 (5) ◽  
pp. 907-919 ◽  
Author(s):  
Michael Krause ◽  
Andrew Fire ◽  
Susan White Harrison ◽  
James Priess ◽  
Harold Weintraub
Keyword(s):  
Cell Fate ◽  
Muscle Cell ◽  
Body Wall ◽  
The Body ◽  
Body Wall Muscle ◽  
C Elegans

scholarly journals LEA motifs promote desiccation tolerance in vivo

BMC Biology ◽  
2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Jonathan D. Hibshman ◽  
Bob Goldstein
Keyword(s):  
Osmotic Stress ◽  
Desiccation Tolerance ◽  
Body Wall ◽  
The Body ◽  
Body Wall Muscle ◽  
Lea Proteins ◽  
Lea Protein ◽  
C Elegans ◽  
Dauer Larvae

Abstract Background Cells and organisms typically cannot survive in the absence of water. However, some animals including nematodes, tardigrades, rotifers, and some arthropods are able to survive near-complete desiccation. One class of proteins known to play a role in desiccation tolerance is the late embryogenesis abundant (LEA) proteins. These largely disordered proteins protect plants and animals from desiccation. A multitude of studies have characterized stress-protective capabilities of LEA proteins in vitro and in heterologous systems. However, the extent to which LEA proteins exhibit such functions in vivo, in their native contexts in animals, is unclear. Furthermore, little is known about the distribution of LEA proteins in multicellular organisms or tissue-specific requirements in conferring stress protection. Here, we used the nematode C. elegans as a model to study the endogenous function of an LEA protein in an animal. Results We created a null mutant of C. elegans LEA-1, as well as endogenous fluorescent reporters of the protein. LEA-1 mutant animals formed defective dauer larvae at high temperature. We confirmed that C. elegans lacking LEA-1 are sensitive to desiccation. LEA-1 mutants were also sensitive to heat and osmotic stress and were prone to protein aggregation. During desiccation, LEA-1 expression increased and became more widespread throughout the body. LEA-1 was required at high levels in body wall muscle for animals to survive desiccation and osmotic stress, but expression in body wall muscle alone was not sufficient for stress resistance, indicating a likely requirement in multiple tissues. We identified minimal motifs within C. elegans LEA-1 that were sufficient to increase desiccation survival of E. coli. To test whether such motifs are central to LEA-1’s in vivo functions, we then replaced the sequence of lea-1 with these minimal motifs and found that C. elegans dauer larvae formed normally and survived osmotic stress and mild desiccation at the same levels as worms with the full-length protein. Conclusions Our results provide insights into the endogenous functions and expression dynamics of an LEA protein in a multicellular animal. The results show that LEA-1 buffers animals from a broad range of stresses. Our identification of LEA motifs that can function in both bacteria and in a multicellular organism in vivo suggests the possibility of engineering LEA-1-derived peptides for optimized desiccation protection.

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.

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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