scholarly journals Repulsive Guidance Molecule Acts in Axon Branching in Caenorhabditis elegans

2021 ◽  
Author(s):  
Kaname Tsutsui ◽  
Hon-Song Kim ◽  
Chizu Yoshikata ◽  
Kenji Kimura ◽  
Yukihiko Kubota ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Axon Guidance ◽  
Small Body ◽  
Ectopic Expression ◽  
Axon Branching ◽  
Glycosylphosphatidylinositol Anchor ◽  
Evolutionarily Conserved ◽  
Vulval Precursor Cells ◽  
Repulsive Guidance Molecule ◽  
Guidance Molecule

Abstract Repulsive guidance molecules (RGMs) are evolutionarily conserved proteins implicated in repulsive axon guidance. Here we report the function of the Caenorhabditis elegans ortholog DRAG-1 in axon branching. The axons of hermaphrodite-specific neurons (HSNs) extend dorsal branches at the region abutting the vulval muscles. The drag-1 mutants exhibited defects in HSN axon branching in addition to a small body size phenotype. DRAG-1 expression in the hypodermal cells was required for the branching of the axons. Although DRAG-1 is normally expressed in the ventral hypodermis excepting the vulval region, its ectopic expression in vulval precursor cells was sufficient to induce the branching. The C-terminal glycosylphosphatidylinositol anchor of DRAG-1 was important for its function, suggesting that DRAG-1 should be anchored to the cell surface. Genetic analyses suggested that the membrane receptor UNC-40 acts in the same pathway with DRAG-1 in HSN branching. We propose that DRAG-1 expressed in the ventral hypodermis signals via the UNC-40 receptor expressed in HSNs to elicit branching activity of HSN axons.

scholarly journals Repulsive guidance molecule acts in axon branching in Caenorhabditis elegans

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Kaname Tsutsui ◽  
Hon-Song Kim ◽  
Chizu Yoshikata ◽  
Kenji Kimura ◽  
Yukihiko Kubota ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Axon Guidance ◽  
Small Body ◽  
Ectopic Expression ◽  
Axon Branching ◽  
Glycosylphosphatidylinositol Anchor ◽  
Evolutionarily Conserved ◽  
Vulval Precursor Cells ◽  
Repulsive Guidance Molecule ◽  
Guidance Molecule

AbstractRepulsive guidance molecules (RGMs) are evolutionarily conserved proteins implicated in repulsive axon guidance. Here we report the function of the Caenorhabditis elegans ortholog DRAG-1 in axon branching. The axons of hermaphrodite-specific neurons (HSNs) extend dorsal branches at the region abutting the vulval muscles. The drag-1 mutants exhibited defects in HSN axon branching in addition to a small body size phenotype. DRAG-1 expression in the hypodermal cells was required for the branching of the axons. Although DRAG-1 is normally expressed in the ventral hypodermis excepting the vulval region, its ectopic expression in vulval precursor cells was sufficient to induce the branching. The C-terminal glycosylphosphatidylinositol anchor of DRAG-1 was important for its function, suggesting that DRAG-1 should be anchored to the cell surface. Genetic analyses suggested that the membrane receptor UNC-40 acts in the same pathway with DRAG-1 in HSN branching. We propose that DRAG-1 expressed in the ventral hypodermis signals via the UNC-40 receptor expressed in HSNs to elicit branching activity of HSN axons.

scholarly journals Repulsive Guidance Molecule Acts in Axon Branching in Caenorhabditis elegans

2018 ◽  
Author(s):  
Kaname Tsutsui ◽  
Hon-Song Kim ◽  
Yukihiko Kubota ◽  
Yukimasa Shibata ◽  
Chenxi Tian ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Axon Guidance ◽  
Small Body ◽  
Egg Laying ◽  
Small Body Size ◽  
Axon Branching ◽  
Glycosylphosphatidylinositol Anchor ◽  
Evolutionarily Conserved ◽  
Repulsive Guidance Molecule ◽  
Guidance Molecule

ABSTRACTRepulsive guidance molecules (RGMs) are evolutionarily conserved proteins implicated in repulsive axon guidance. Here we report the function of the Caenorhabditis elegans ortholog DRAG-1 in axon branching. The axons of hermaphrodite-specific neurons (HSNs) branch at the region abutting the vulval muscles and innervate these muscles to control egg laying. The drag-1 mutants exhibited defects in HSN axon branching in addition to a small body size and egg laying–defective phenotype. DRAG-1 expression in the hypodermal cells was required for the branching of these axons. The C-terminal glycosylphosphatidylinositol anchor of DRAG-1 was important for its function. Genetic analyses suggested that the membrane receptor UNC-40, but neither SMA-1/βH-spectrin nor SMA-5/MAP kinase 7, acts in the same pathway with DRAG-1 in HSN branching. We propose that DRAG-1 expressed in the hypodermis signals via the UNC-40 receptor expressed in HSNs to elicit branching activity of HSN axons.

scholarly journals Non-stringent tissue-source requirements for BMP ligand expression in regulation of body size in Caenorhabditis elegans

2011 ◽  
Vol 93 (6) ◽  
pp. 427-432 ◽  
Author(s):  
CATHY SAVAGE-DUNN ◽  
LING YU ◽  
KWESI GILL ◽  
MUHAMMAD AWAN ◽  
THILINI FERNANDO
Keyword(s):  
Body Size ◽  
Caenorhabditis Elegans ◽  
Small Body ◽  
Ectopic Expression ◽  
Target Tissue ◽  
Signal Transducers ◽  
Endogenous Expression ◽  
Adult Growth ◽  
Morphogenetic Protein ◽  
Ligand Expression

SummaryIn Caenorhabditis elegans, the Bone Morphogenetic Protein (BMP)-related ligand Dpp- and BMP-like-1 (DBL-1) regulates body size by promoting the larval and adult growth of the large epidermal syncytium hyp7 without affecting cell division. This system provides an excellent model for dissecting the growth-promoting activities of BMP ligands, since in this context the growth and differentiation functions of DBL-1 are naturally uncoupled. dbl-1 is expressed primarily in neurons and the DBL-1 ligand signals to its receptors and Smad signal transducers in the target tissue of the epidermis. The requirements constraining the source(s) of DBL-1, however, have not previously been investigated. We show here that dbl-1 expression requirements are strikingly relaxed. Expression in non-overlapping subsets of the endogenous expression pattern, as well as ectopic expression, can provide sufficient levels of activity for rescue of the small body size of dbl-1 mutants. By analysing dbl-1 expression levels in transgenic strains with different degrees of rescue, we corroborate the model that DBL-1 is a dose-dependent regulator of growth. We conclude that, for body size regulation, the site of expression of dbl-1 is less important than the level of expression.

scholarly journals The Nc1/Endostatin Domain of Caenorhabditis elegans Type Xviii Collagen Affects Cell Migration and Axon Guidance

2001 ◽  
Vol 152 (6) ◽  
pp. 1219-1232 ◽  
Author(s):  
Brian D. Ackley ◽  
Jennifer R. Crew ◽  
Harri Elamaa ◽  
Tania Pihlajaniemi ◽  
Calvin J. Kuo ◽  
...  
Keyword(s):  
Cell Migration ◽  
Caenorhabditis Elegans ◽  
Axon Guidance ◽  
Ectopic Expression ◽  
Basement Membranes ◽  
Protein Isoforms ◽  
Developmentally Regulated ◽  
C Elegans ◽  
Collagen Xviii ◽  
Nc1 Domain

Type XVIII collagen is a homotrimeric basement membrane molecule of unknown function, whose COOH-terminal NC1 domain contains endostatin (ES), a potent antiangiogenic agent. The Caenorhabditis elegans collagen XVIII homologue, cle-1, encodes three developmentally regulated protein isoforms expressed predominantly in neurons. The CLE-1 protein is found in low amounts in all basement membranes but accumulates at high levels in the nervous system. Deletion of the cle-1 NC1 domain results in viable fertile animals that display multiple cell migration and axon guidance defects. Particular defects can be rescued by ectopic expression of the NC1 domain, which is shown to be capable of forming trimers. In contrast, expression of monomeric ES does not rescue but dominantly causes cell and axon migration defects that phenocopy the NC1 deletion, suggesting that ES inhibits the promigratory activity of the NC1 domain. These results indicate that the cle-1 NC1/ES domain regulates cell and axon migrations in C. elegans.

scholarly journals Protruding Vulva Mutants Identify Novel Loci and Wnt Signaling Factors That Function During Caenorhabditis elegans Vulva Development

Genetics ◽  
2000 ◽  
Vol 156 (3) ◽  
pp. 1097-1116 ◽  
Author(s):  
David M Eisenmann ◽  
Stuart K Kim
Keyword(s):  
Caenorhabditis Elegans ◽  
Wnt Signaling ◽  
Genetic Characterization ◽  
Wnt Signaling Pathway ◽  
Vulval Development ◽  
Extracellular Signaling ◽  
Somatic Gonad ◽  
Evolutionarily Conserved ◽  
Vulval Precursor Cells

Abstract The Caenorhabditis elegans vulva develops from the progeny of three vulval precursor cells (VPCs) induced to divide and differentiate by a signal from the somatic gonad. Evolutionarily conserved Ras and Notch extracellular signaling pathways are known to function during this process. To identify novel loci acting in vulval development, we carried out a genetic screen for mutants having a protruding-vulva (Pvl) mutant phenotype. Here we report the initial genetic characterization of several novel loci: bar-1, pvl-4, pvl-5, and pvl-6. In addition, on the basis of their Pvl phenotypes, we show that the previously identified genes lin-26, mom-3/mig-14, egl-18, and sem-4 also function during vulval development. Our characterization indicates that (1) pvl-4 and pvl-5 are required for generation/survival of the VPCs; (2) bar-1, mom-3/mig-14, egl-18, and sem-4 play a role in VPC fate specification; (3) lin-26 is required for proper VPC fate execution; and (4) pvl-6 acts during vulval morphogenesis. In addition, two of these genes, bar-1 and mom-3/mig-14, are known to function in processes regulated by Wnt signaling, suggesting that a Wnt signaling pathway is acting during vulval development.

A Cuticle Collagen Encoded by the lon-3 Gene May Be a Target of TGF-β Signaling in Determining Caenorhabditis elegans Body Shape

Genetics ◽  
2002 ◽  
Vol 162 (4) ◽  
pp. 1631-1639
Author(s):  
Yo Suzuki ◽  
Gail A Morris ◽  
Min Han ◽  
William B Wood
Keyword(s):  
Caenorhabditis Elegans ◽  
Body Shape ◽  
Small Body ◽  
Dependent Manner ◽  
Loss Of Function ◽  
Cellular Mechanisms ◽  
C Elegans ◽  
Gene Expression Analyses ◽  
Dose Dependent

Abstract The signaling pathway initiated by the TGF-β family member DBL-1 in Caenorhabditis elegans controls body shape in a dose-dependent manner. Loss-of-function (lf) mutations in the dbl-1 gene cause a short, small body (Sma phenotype), whereas overexpression of dbl-1 causes a long body (Lon phenotype). To understand the cellular mechanisms underlying these phenotypes, we have isolated suppressors of the Sma phenotype resulting from a dbl-1(lf) mutation. Two of these suppressors are mutations in the lon-3 gene, of which four additional alleles are known. We show that lon-3 encodes a collagen that is a component of the C. elegans cuticle. Genetic and reporter-gene expression analyses suggest that lon-3 is involved in determination of body shape and is post-transcriptionally regulated by the dbl-1 pathway. These results support the possibility that TGF-β signaling controls C. elegans body shape by regulating cuticle composition.

scholarly journals The crest phenotype in domestic chicken is caused by a 197 bp duplication in the intron of HOXC10

2021 ◽  
Author(s):  
Jingyi Li ◽  
Mi-Ok Lee ◽  
Brian W Davis ◽  
Ping Wu ◽  
Shu-Man Hsieh-Li ◽  
...  
Keyword(s):  
Gene Expression ◽  
Whole Genome Sequencing ◽  
Diagnostic Test ◽  
Genome Sequencing ◽  
Ectopic Expression ◽  
Body Region ◽  
Whole Genome ◽  
Dorsal Skin ◽  
Conserved Sequence ◽  
Evolutionarily Conserved

Abstract The Crest mutation in chicken shows incomplete dominance and causes a spectacular phenotype in which the small feathers normally present on the head are replaced by much larger feathers normally present only in dorsal skin. Using whole genome sequencing, we show that the crest phenotype is caused by a 197 bp duplication of an evolutionarily conserved sequence located in the intron of HOXC10 on chromosome 33. A diagnostic test showed that the duplication was present in all 54 crested chickens representing eight breeds and absent from all 433 non-crested chickens representing 214 populations. The mutation causes ectopic expression of at least five closely linked HOXC genes, including HOXC10, in cranial skin of crested chickens. The result is consistent with the interpretation that the crest feathers are caused by an altered body region identity. The upregulated HOXC gene expression is expanded to skull tissue of Polish chickens showing a large crest often associated with cerebral hernia, but not in Silkie chickens characterized by a small crest, both homozygous for the duplication. Thus, the 197 bp duplication is required for the development of a large crest and susceptibility to cerebral hernia because only crested chicken show this malformation. However, this mutation is not sufficient to cause herniation because this malformation is not present in breeds with a small crest, like Silkie chickens.

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