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

Development ◽  
2000 ◽  
Vol 127 (6) ◽  
pp. 1197-1207 ◽  
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.

scholarly journals New Genes That Interact With lin-35 Rb to Negatively Regulate the let-60 ras Pathway in Caenorhabditis elegans

Genetics ◽  
2003 ◽  
Vol 164 (1) ◽  
pp. 135-151 ◽  
Author(s):  
Jeffrey H Thomas ◽  
Craig J Ceol ◽  
Hillel T Schwartz ◽  
H Robert Horvitz
Keyword(s):  
Caenorhabditis Elegans ◽  
Intercellular Signaling ◽  
Ras Pathway ◽  
Class A ◽  
New Genes ◽  
Isolation And Characterization ◽  
Vulval Precursor Cells ◽  
Class B ◽  
In The Wild

Abstract Previous studies have shown that a synthetic multivulva phenotype results from mutations in genes that antagonize the ras-mediated intercellular signaling system responsible for vulval induction in Caenorhabditis elegans. Synthetic multivulva mutations define two classes of genes, A and B, and a mutation in a gene of each class is required to produce the multivulva phenotype. The ectopic vulval tissue in multivulva animals is generated by vulval precursor cells that in the wild type do not generate vulval tissue. One of the class B synthetic multivulva genes, lin-35, encodes a protein similar to the retinoblastoma (Rb) protein. In this article, we describe the isolation and characterization of 50 synthetic multivulva mutations, the identification of new components of both the class A and class B lin-35 Rb pathways, and the cloning of lin-52, a class B gene that may have a conserved role in Rb-mediated signaling.

Isolation and Characterization of Collagen from the Body Wall of Sea CucumberStichopus monotuberculatus

2015 ◽  
Vol 80 (4) ◽  
pp. C671-C679 ◽  
Author(s):  
Ming Zhong ◽  
Ting Chen ◽  
Chaoqun Hu ◽  
Chunhua Ren
Keyword(s):  
Body Wall ◽  
The Body ◽  
Isolation And Characterization

scholarly journals Isolation and Characterization of High-Temperature-Induced Dauer Formation Mutants in Caenorhabditis elegans

Genetics ◽  
2003 ◽  
Vol 165 (1) ◽  
pp. 127-144 ◽  
Author(s):  
Michael Ailion ◽  
James H Thomas
Keyword(s):  
High Temperature ◽  
Caenorhabditis Elegans ◽  
Insulin Receptor ◽  
Transmembrane Protein ◽  
New Genes ◽  
Isolation And Characterization ◽  
Insulin Receptor Signaling ◽  
Dauer Formation ◽  
Receptor Signaling Pathway

Abstract Dauer formation in Caenorhabditis elegans is regulated by at least three signaling pathways, including an insulin receptor-signaling pathway. These pathways were defined by mutants that form dauers constitutively (Daf-c) at 25°. Screens for Daf-c mutants at 25° have probably been saturated, but failed to identify all the components involved in regulating dauer formation. Here we screen for Daf-c mutants at 27°, a more strongly dauer-inducing condition. Mutations identified include novel classes of alleles for three known genes and alleles defining at least seven new genes, hid-1–hid-7. Many of the genes appear to act in the insulin branch of the dauer pathway, including pdk-1, akt-1, aex-6, and hid-1. We also molecularly identify hid-1 and show that it encodes a novel highly conserved putative transmembrane protein expressed in neurons.

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.

Extraction and Characterization of Pepsin Soluble Collagen from the Body Wall of Sea Cucumber Acaudina leucoprocta

2017 ◽  
Vol 26 (5) ◽  
pp. 502-515 ◽  
Author(s):  
Saijun Lin ◽  
Ya-Ping Xue ◽  
Enli San ◽  
Tan Chee Keong ◽  
Lifang Chen ◽  
...  
Keyword(s):  
Sea Cucumber ◽  
Body Wall ◽  
The Body ◽  
Soluble Collagen ◽  
Pepsin Soluble Collagen

scholarly journals Preparation and Characterization of Anti-CeTNT-1 and Anti-CeTNT-4 Antibodies

1970 ◽  
Vol 44 (3) ◽  
pp. 371-376
Author(s):  
M Ziaul Amin ◽  
Hiroaki Kagawa ◽  
Mohammed A Satter
Keyword(s):  
Fusion Proteins ◽  
Tissue Specificity ◽  
Body Wall ◽  
Troponin T ◽  
Specific Interaction ◽  
The Body ◽  
Expression Vectors ◽  
Antibody Specificity ◽  
Sds Page

Among the four CeTNT isoforms, CeTNT-1, CeTNT-2 are body wall types, CeTNT-4 is pharynx type and CeTNT-3 is expressed in both the body wall and pharyngeal tissue. In our previous study, we used body wall and pharynx type anti-CeTNI, anti-CeTNC and anti-CeTM antibodies to observe the tissue specific interaction of the TNI isoforms with others TN subunits and tropomyosin isoforms. To extent the interaction study of CeTNT isoforms, in this study, we prepared and characterized the body wall type anti-CeTNT-1 and pharynx type anti- CeTNT-4 antibodies. For the preparation of the anti-CeTNT-1 and anti-CeTNT-4 antibodies, in this study we constructed the pCTNT-1 and pCTNT-4 expression vectors. The sub-cloned of the pCTNT-1 and pCTNT-4 expression vectors were verified by DNA sequencing. These expression vectors were used to generate fusion proteins of the body wall, TNT-1 and pharyngeal TNT-4 isoforms in Escherichia Ecoli. The expression of these fusion proteins were confirmed by SDS-PAGE analysis. The anti-CeTNT-1 and anti-CeTNT-4 antibodies were prepared in the rabbit by using the gel cut of the CeTNT-1 and CeTNT-4 fusion proteins. The antibody specificity of the CeTNT-1 and CeTNT-4 fusion proteins was also judged by Western-analysis using prepared anti-CeTNT-1 and anti-CeTNT-4 antibodies. The antibody specificity results indicated that anti-sera against each of both the body wall type TNT-1 and pharynx type TNT-4 isoforms had tissue specificity. Key words: Troponin T, Caenorhabditis elegans, Body wall, Pharynx DOI: 10.3329/bjsir.v44i3.4413 Bangladesh J. Sci. Ind. Res. 44(3), 371-376, 2009

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