scholarly journals Dual roles of tropomyosin as an F-actin stabilizer and a regulator of muscle contraction inCaenorhabditis elegans body wall muscle

2006 ◽  
Vol 63 (11) ◽  
pp. 659-672 ◽  
Author(s):  
Robinson Yu ◽  
Shoichiro Ono
Keyword(s):  
Muscle Contraction ◽  
Body Wall ◽  
Body Wall Muscle ◽  
Dual Roles

scholarly journals unc-68 encodes a ryanodine receptor involved in regulating C. elegans body-wall muscle contraction.

1996 ◽  
Vol 134 (4) ◽  
pp. 885-893 ◽  
Author(s):  
E B Maryon ◽  
R Coronado ◽  
P Anderson
Keyword(s):  
Muscle Contraction ◽  
Ryanodine Receptor ◽  
Body Wall ◽  
Striated Muscle ◽  
Ryanodine Receptors ◽  
Binding Activity ◽  
Body Wall Muscle ◽  
Calcium Signal ◽  
C Elegans ◽  
Muscle Ultrastructure

Striated muscle contraction is elicited by the release of stored calcium ions through ryanodine receptor channels in the sarcoplasmic reticulum. ryr-1 is a C. elegans ryanodine receptor homologue that is expressed in body-wall muscle cells used for locomotion. Using genetic methods, we show that ryr-1 is the previously identified locus unc-68. First, transposon-induced deletions within ryr-1 are alleles of unc-68. Second, transformation of unc-68 mutants with ryr-1 genomic DNA results in rescue of the Unc phenotype. unc-68 mutants move poorly, exhibiting an incomplete flaccid paralysis, yet have normal muscle ultrastructure. The mutants are insensitive to the paralytic effects of ryanodine, and lack detectable ryanodine-binding activity. The Unc-68 phenotype suggests that ryanodine receptors are not essential for excitation-contraction coupling in nematodes, but act to amplify a (calcium) signal that is sufficient for contraction.

Ectopic Germ Cells Can Induce Niche-Like Enwrapment by Neighboring Body Wall Muscle

2018 ◽  
Author(s):  
Kacy L. Gordon ◽  
Sara G. Payne ◽  
Lara M. Linden-High ◽  
Ariel M. Pani ◽  
Bob Goldstein ◽  
...  
Keyword(s):  
Germ Cells ◽  
Body Wall ◽  
Body Wall Muscle

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.

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

Development ◽  
1995 ◽  
Vol 121 (7) ◽  
pp. 2219-2232 ◽  
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.

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

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

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.

The evolution of air-breathing respiratory faculties in craniotes

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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