Proteome Analysis Implicates Adaptive Changes in Metabolism and Body Wall Musculature of Caenorhabditis elegans Dauer Larva

Examination of the ultrastructure of the dauer larva of Caenorhabditis elegans showed that cells in the lateral cord and body wall muscle had irregular profiles, few Golgi bodies, and cisternae of endoplasmic reticulum, but they contained abundant lipid and glycogen. These cells and the esophageal cells had mitochondria in the condensed conformation. The intestinal lumen was small and the brush border was so compact that individual microvilli were difficult to discern. Intestinal cells had cytosomes with irregular profiles and unhomogeneous matrices. The striated layer was absent from the cuticle covering the lips and papillae. These ultrastructural features are correlated with the dauer larva's low metabolic rate, its resistance to toxic chemicals and to adverse environmental conditions, and its ability to detect food and to feed soon after exposure to a hospitable environment.

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Faculty Opinions recommendation of Alpha spectrin is essential for morphogenesis and body wall muscle formation in Caenorhabditis elegans.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1006072.75205 ◽

2002 ◽

Author(s):

Michel Labouesse

Keyword(s):

Caenorhabditis Elegans ◽

Body Wall ◽

Body Wall Muscle ◽

Muscle Formation ◽

Alpha Spectrin

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

Genetics ◽

10.1093/genetics/137.2.483 ◽

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.

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Mutations Affecting Nerve Attachment of Caenorhabditis elegans

Genetics ◽

10.1093/genetics/157.4.1611 ◽

2001 ◽

Vol 157 (4) ◽

pp. 1611-1622 ◽

Cited By ~ 1

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.

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Two Pleiotropic Classes of daf-2 Mutation Affect Larval Arrest, Adult Behavior, Reproduction and Longevity in Caenorhabditis elegans

Genetics ◽

10.1093/genetics/150.1.129 ◽

1998 ◽

Vol 150 (1) ◽

pp. 129-155 ◽

Cited By ~ 23

Author(s):

David Gems ◽

Amy J Sutton ◽

Mark L Sundermeyer ◽

Patrice S Albert ◽

Kevin V King ◽

...

Keyword(s):

Caenorhabditis Elegans ◽

Adult Longevity ◽

Temperature Sensitive ◽

Adult Behavior ◽

Dauer Larva ◽

Class 1 ◽

Low Levels ◽

Dauer Larvae ◽

Overlapping Classes ◽

Receptor Family

Abstract The nematode Caenorhabditis elegans responds to overcrowding and scarcity of food by arresting development as a dauer larva, a nonfeeding, long-lived, stress-resistant, alternative third-larval stage. Previous work has shown that mutations in the genes daf-2 (encoding a member of the insulin receptor family) and age-1 (encoding a PI 3-kinase) result in constitutive formation of dauer larvae (Daf-c), increased adult longevity (Age), and increased intrinsic thermotolerance (Itt). Some daf-2 mutants have additional developmental, behavioral, and reproductive defects. We have characterized in detail 15 temperature-sensitive and 1 nonconditional daf-2 allele to investigate the extent of daf-2 mutant defects and to examine whether specific mutant traits correlate with each other. The greatest longevity seen in daf-2 mutant adults was approximately three times that of wild type. The temperature-sensitive daf-2 mutants fell into two overlapping classes, including eight class 1 mutants, which are Daf-c, Age, and Itt, and exhibit low levels of L1 arrest at 25.5°. Seven class 2 mutants also exhibit the class 1 defects as well as some or all of the following: reduced adult motility, abnormal adult body and gonad morphology, high levels of embryonic and L1 arrest, production of progeny late in life, and reduced brood size. The strengths of the Daf-c, Age, and Itt phenotypes largely correlated with each other but not with the strength of class 2-specific defects. This suggests that the DAF-2 receptor is bifunctional. Examination of the null phenotype revealed a maternally rescued egg, L1 lethal component, and a nonconditional Daf-c component. With respect to the Daf-c phenotype, the dauer-defective (Daf-d) mutation daf-12(m20) was epistatic to daf-2 class 1 alleles but not the severe class 2 alleles tested. All daf-2 mutant defects were suppressed by the daf-d mutation daf-16(m26). Our findings suggest a new model for daf-2, age-1, daf-12, and daf-16 interactions.

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Duels without obvious sense: counteracting inductions involved in body wall muscle development in the Caenorhabditis elegans embryo

Development ◽

10.1242/dev.121.7.2219 ◽

1995 ◽

Vol 121 (7) ◽

pp. 2219-2232 ◽

Cited By ~ 4

Author(s):

R. Schnabel

Keyword(s):

Caenorhabditis Elegans ◽

Body Wall ◽

Muscle Development ◽

Early Embryo ◽

Cell Interactions ◽

Body Wall Muscle ◽

Cellular Interactions ◽

Classical Criterion ◽

Founder Cells ◽

Cell Cell

During the first four cleavage rounds of the Caenorhabditis elegans embryo, five somatic founder cells AB, MS, E, C and D are born, which later form the tissues of the embryo. The classical criterion for a cell-autonomous specification of a tissue is the capability of primordial cells to produce this tissue in isolation from the remainder of the embryo. By this criterion, the somatic founder cells MS, C and D develop cell-autonomously. Laser ablation experiments, however, reveal that within the embryonic context these blastomeres form a network of duelling cellular interactions. During normal development, the blastomere D inhibits muscle specification in the MS and the C lineage inhibits muscle specification in the D lineage. These inhibitory interactions are counteracted by two activating inductions. As described before the inhibition of body wall muscle in MS is counteracted by an activating signal from the ABa lineage. Body wall muscle in the D lineage is induced by MS descendants, which suppress an inhibitory activity of the C lineage. The interaction between the D and the MS lineage occurs through the C lineage. An interesting feature of these cell-cell interactions is that they do not serve to discriminate between equivalent cells but are permissive or nonpermissive inductions. No evidence was found that the C-derived body wall muscle also depends on an induction, which suggests that possibly three different pathways coexist in the early embryo to specify body wall muscle, two of which are, in different ways, influenced by cell-cell interactions and a third that is autonomous. This work supplies evidence that cells may acquire transient states during embryogenesis that influence the specification of other cells in the embryo. These states, however, may not be reflected in the developmental potentials of the cells themselves. They can only be scored indirectly by their action on the specification of other cells in the embryo. Blastomeres that behave cell-autonomously in isolation are nevertheless subjected to cell-cell interactions in the embryonic context. Why this should be is an intriguing question. The classical notion has been that blastomeres are specified autonomously in nematodes. In recent years, it was established that at least five inductions are required to determine the AB descendants of C. elegans, whereas the P1 descendants have been typically viewed to develop more autonomously. It appears now that inductions also play a major role during the determination of P1-derived blastomeres.

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Ca^-binding to site IV and TnI-binding of body-wall muscle troponin C are essential for development in Caenorhabditis elegans

Seibutsu Butsuri ◽

10.2142/biophys.44.s65_3 ◽

2004 ◽

Vol 44 (supplement) ◽

pp. S65

Author(s):

T. Takaya ◽

H. Terami ◽

M. Sohda ◽

T. Iio ◽

H. Kagawa

Keyword(s):

Caenorhabditis Elegans ◽

Body Wall ◽

Troponin C ◽

Body Wall Muscle

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Comparative body wall musculature and muscle fibre ultrastructure in branchiobdellidans (Annelida: Clitellata), and their phylogenetic significance

Hydrobiologia ◽

10.1007/bf00142327 ◽

1994 ◽

Vol 278 (1-3) ◽

pp. 189-199 ◽

Cited By ~ 8

Author(s):

Roberto Valvassori ◽

Magda de Eguileor ◽

Giulio Lanzavecchia ◽

Stuart R. Gelde

Keyword(s):

Muscle Fibre ◽

Body Wall ◽

Phylogenetic Significance ◽

Body Wall Musculature

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Fragile skeletal muscle attachments in dystrophic mutants of Caenorhabditis elegans: isolation and characterization of the mua genes

Development ◽

10.1242/dev.127.6.1197 ◽

2000 ◽

Vol 127 (6) ◽

pp. 1197-1207 ◽

Cited By ~ 1

Author(s):

J.D. Plenefisch ◽

X. Zhu ◽

E.M. Hedgecock

Keyword(s):

Caenorhabditis Elegans ◽

Body Wall ◽

Local Strain ◽

Muscle Differentiation ◽

The Body ◽

Tissue Separation ◽

New Genes ◽

Isolation And Characterization ◽

Skin Fragility

Over 30 Caenorhabditis elegans mutants were identified with normal muscle differentiation and initial locomotion followed by catastrophic detachment of skeletal muscles from the body wall. Reducing the strength of muscle contraction in these mutants with a myosin gene mutation suppresses muscle detachment. These dystrophic mutants identify a novel class of genes required for growth and maintenance of functional muscle attachments, not exceptional alleles of genes required for muscle differentiation and contractility. Nine new genes, named mua, and two previously published loci, unc-23 and vab-10, cause fragile musscle attachments. The primary sites of muscle detachment, including the plane of tissue separation, are characteristic for each gene. We suggest these genes identify feedback mechanisms whereby local strain regulates the extent of myofibril contraction and the placement of new muscle attachments in functioning muscles. Finally, we draw some comparisons to vertebrate skin fragility diseases and muscular dystrophies.

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The evolution of air-breathing respiratory faculties in craniotes

Respiratory Biology of Animals ◽

10.1093/oso/9780199238460.003.0015 ◽

2019 ◽

pp. 177-191

Author(s):

Steven F. Perry ◽

Markus Lambertz ◽

Anke Schmitz

Keyword(s):

High Performance ◽

Body Wall ◽

Structure And Function ◽

Control Of Breathing ◽

Body Wall Muscle ◽

Positive Pressure ◽

Limiting Factor ◽

Swim Bladder ◽

Body Wall Musculature ◽

And Function

The origin of lungs from a swim bladder, swim bladder from lungs, or both from a relatively undifferentiated respiratory pharynx remains unresolved. Once present, the lungs can be ventilated by a positive-pressure buccal pump, which can be easily derived from the gill ventilation sequence in a lungfish, or by negative-pressure aspiration. Although aspiration breathing is characteristic of amniotes, it has also been observed in a lungfish and body wall muscle contraction in response to respiratory stimuli has even been reported in lamprey larvae. The hypaxial body wall musculature used for aspiration breathing is also necessary for locomotion in most amniotes, just when respiratory demand is greatest. This paradox, called Carrier’s constraint, is a major limiting factor in the evolution of high-performance faculties, and the evolution of anatomical and physiological specializations that circumvent it characterize most major amniote groups. Serendipitous combinations have resulted in evolutionary cascades and high-performance groups such as birds and mammals. Complementing evolution are the capacities for acclimatization and adaptation not only in the structure and function of the gas exchanger, but also in the control of breathing and the composition of the blood.

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