scholarly journals Axonal guidance defects in a Caenorhabditis elegans mutant reveal cell- extrinsic determinants of neuronal morphology

1993 ◽  
Vol 13 (10) ◽  
pp. 4254-4271 ◽  
Author(s):  
S Hekimi ◽  
D Kershaw
Keyword(s):  
Caenorhabditis Elegans ◽  
Neuronal Morphology ◽  
Axonal Guidance

scholarly journals Dominant unc-37 mutations suppress the movement defect of a homeodomain mutation in unc-4, a neural specificity gene in Caenorhabditis elegans.

Genetics ◽  
1993 ◽  
Vol 135 (3) ◽  
pp. 741-753 ◽  
Author(s):  
D M Miller ◽  
C J Niemeyer ◽  
P Chitkara
Keyword(s):  
Caenorhabditis Elegans ◽  
Motor Neurons ◽  
Synaptic Input ◽  
Neuronal Morphology ◽  
Axonal Guidance ◽  
Temperature Sensitive ◽  
Homeodomain Protein ◽  
Loss Of Function ◽  
Selection Scheme ◽  
Synaptic Specificity

Abstract The unc-4 gene of Caenorhabditis elegans encodes a homeodomain protein that defines synaptic input to ventral cord motor neurons. unc-4 mutants are unable to crawl backward because VA motor neurons are miswired with synaptic connections normally reserved for their sister cells, the VB motor neurons. These changes in connectivity are not accompanied by any visible effects upon neuronal morphology, which suggests that unc-4 regulates synaptic specificity but not axonal guidance or outgrowth. In an effort to identify other genes in the unc-4 pathway, we have devised a selection scheme for rare mutations that suppress the Unc-4 phenotype. We have isolated four, dominant, extragenic, allele-specific suppressors of unc-4(e2322ts), a temperature sensitive allele with a point mutation in the unc-4 homeodomain. Our data indicate that these suppressors are gain-of-function mutations in the previously identified unc-37 gene. We show that the loss-of-function mutation unc-37(e262) phenocopies the Unc-4 movement defect but does not prevent unc-4 expression or alter VA motor neuron morphology. These findings suggest that unc-37 functions with unc-4 to specify synaptic input to the VA motor neurons. We propose that unc-37 may be regulated by unc-4. Alternatively, unc-37 may encode a gene product that interacts with the unc-4 homeodomain.

scholarly journals Spaceflight affects neuronal morphology and alters transcellular degradation of neuronal debris in adult Caenorhabditis elegans

iScience ◽  
2021 ◽  
Vol 24 (2) ◽  
pp. 102105
Author(s):  
Ricardo Laranjeiro ◽  
Girish Harinath ◽  
Amelia K. Pollard ◽  
Christopher J. Gaffney ◽  
Colleen S. Deane ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Neuronal Morphology

scholarly journals Analysis of the Caenorhabditis elegans axonal guidance and outgrowth gene unc-33.

Genetics ◽  
1992 ◽  
Vol 132 (3) ◽  
pp. 675-689 ◽  
Author(s):  
W Li ◽  
R K Herman ◽  
J E Shaw
Keyword(s):  
Caenorhabditis Elegans ◽  
Gamma Ray ◽  
Protein A ◽  
Genomic Region ◽  
Axonal Guidance ◽  
Significant Similarity ◽  
Spliced Leader ◽  
Neuronal Processes ◽  
Type Size ◽  
Intermediate Size

Abstract Mutations in the unc-33 gene of the nematode Caenorhabditis elegans lead to severely uncoordinated movement, abnormalities in the guidance and outgrowth of the axons of many neurons, and a superabundance of microtubules in neuronal processes. We have cloned unc-33 by tagging the gene with the transposable element Tc4. Three unc-33 messages, which are transcribed from a genomic region of at least 10 kb, were identified and characterized. The three messages have common 3' ends and identical reading frames. The largest (3.8-kb) message consists of the 22-nucleotide trans-spliced leader SL1 and 10 exons (I-X); the intermediate-size (3.3-kb) message begins with SL1 spliced to the 5' end of exon V and includes exons V-X; and the smallest (2.8-kb) message begins within exon VII and also includes exons VIII-X. A gamma-ray-induced deletion mutation situated within exon VIII reduces the sizes of all three messages by 0.5 kb. The three putative polypeptides encoded by the three messages overlap in C-terminal sequence but differ by the positions at which their N termini begin; none has significant similarity to any other known protein. A Tc4 insertion in exon VII leads to alterations in splicing that result in three approximately wild-type-size messages: the Tc4 sequence and 28 additional nucleotides are spliced out of the two larger messages; the Tc4 sequence is trans-spliced off the smallest message such that SL1 is added 13 nucleotides upstream of the normal 5' end of the smallest message.

scholarly journals An ankyrin-related gene (unc-44) is necessary for proper axonal guidance in Caenorhabditis elegans.

1995 ◽  
Vol 129 (4) ◽  
pp. 1081-1092 ◽  
Author(s):  
A J Otsuka ◽  
R Franco ◽  
B Yang ◽  
K H Shim ◽  
L Z Tang ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Nucleotide Sequence ◽  
Axon Guidance ◽  
Axonal Guidance ◽  
Related Gene ◽  
Sequence Analyses ◽  
Molecular Analyses ◽  
Molecular Studies ◽  
Alternatively Spliced ◽  
Related Proteins

Caenorhabditis elegans unc-44 mutations result in aberrant axon guidance and fasciculation with inappropriate partners. The unc-44 gene was cloned by transposon tagging, and verified by genetic and molecular analyses of six transposon-induced alleles and their revertants. Nucleotide sequence analyses demonstrated that unc-44 encodes a series of putative ankyrin-related proteins, including AO49 ankyrin (1815 aa, 198.8 kD), AO66 ankyrin (1867 aa, 204 kD), and AO13 ankyrin (< or = 4700 aa, < or = 517 kD). In addition to the major set of approximately 6 kb alternatively spliced transcripts, minor transcripts were observed at approximately 3, 5, 7, and 14 kb. Evidence is provided that mutations in the approximately 14-kb AO13 ankyrin transcript are responsible for the neuronal defects. These molecular studies provide the first evidence that ankyrin-related molecules are required for axonal guidance.

Cell interactions control the direction of outgrowth, branching and fasciculation of the HSN axons of Caenorhabditis elegans

Development ◽  
1993 ◽  
Vol 117 (3) ◽  
pp. 1071-1087 ◽  
Author(s):  
G. Garriga ◽  
C. Desai ◽  
H.R. Horvitz
Keyword(s):  
Caenorhabditis Elegans ◽  
Epithelial Cells ◽  
Motor Neurons ◽  
Growth Cone ◽  
Nerve Cord ◽  
Ventral Nerve Cord ◽  
Egg Laying ◽  
Axonal Guidance ◽  
Nematode Caenorhabditis Elegans ◽  
Vulval Precursor Cells

The two serotonergic HSN motor neurons of the nematode Caenorhabditis elegans innervate the vulval muscles and stimulate egg laying by hermaphrodites. By analyzing mutant and laser-operated animals, we find that both epithelial cells of the developing vulva and axons of the ventral nerve cord are required for HSN axonal guidance. Vulval precursor cells help guide the growth cone of the emerging HSN axon to the ventral nerve cord. Vulval cells also cause the two HSN axons to join the ventral nerve cord in two separate fascicles and to defasciculate from the ventral nerve cord and branch at the vulva. The axons of either the PVP or PVQ neurons are also necessary for the HSN axons to run in two separate fascicles within the ventral nerve cord. Our observations indicate that the outgrowth of the HSN axon is controlled in multiple ways by both neuronal and nonneuronal cells.

Axonal guidance mutants of Caenorhabditis elegans identified by filling sensory neurons with fluorescein dyes

1985 ◽  
Vol 111 (1) ◽  
pp. 158-170 ◽  
Author(s):  
Edward M. Hedgecock ◽  
Joseph G. Culotti ◽  
J.Nichol Thomson ◽  
Lizabeth A. Perkins
Keyword(s):  
Caenorhabditis Elegans ◽  
Sensory Neurons ◽  
Axonal Guidance ◽  
Fluorescein Dyes

scholarly journals cdc-25.4, a Caenorhabditis elegans Ortholog of cdc25, Is Required for Male Mating Behavior

2016 ◽  
Vol 6 (12) ◽  
pp. 4127-4138 ◽  
Author(s):  
Sangmi Oh ◽  
Ichiro Kawasaki ◽  
Jae-Hyung Park ◽  
Yhong-Hee Shim
Keyword(s):  
Caenorhabditis Elegans ◽  
Mating Behavior ◽  
Cell Cycle Progression ◽  
Neuronal Cells ◽  
Neuronal Morphology ◽  
Male Mating ◽  
Transgenic Expression ◽  
Neuronal Markers ◽  
Male Mating Behavior ◽  
Contact Response

Abstract Cell division cycle 25 (cdc25) is an evolutionarily conserved phosphatase that promotes cell cycle progression. Among the four cdc25 orthologs in Caenorhabditis elegans, we found that cdc-25.4 mutant males failed to produce outcrossed progeny. This was not caused by defects in sperm development, but by defects in male mating behavior. The cdc-25.4 mutant males showed various defects during male mating, including contact response, backing, turning, and vulva location. Aberrant turning behavior was the most prominent defect in the cdc-25.4 mutant males. We also found that cdc-25.4 is expressed in many neuronal cells throughout development. The turning defect in cdc-25.4 mutant males was recovered by cdc-25.4 transgenic expression in neuronal cells, suggesting that cdc-25.4 functions in neurons for male mating. However, the neuronal morphology of cdc-25.4 mutant males appeared to be normal, as examined with several neuronal markers. Also, RNAi depletion of wee-1.3, a C. elegans ortholog of Wee1/Myt1 kinase, failed to suppress the mating defects of cdc-25.4 mutant males. These findings suggest that, for successful male mating, cdc-25.4 does not target cell cycles that are required for neuronal differentiation and development. Rather, cdc-25.4 likely regulates noncanonical substrates in neuronal cells.

Ancestral roles of glia suggested by the nervous system of Caenorhabditis elegans

2007 ◽  
Vol 3 (1) ◽  
pp. 55-61 ◽  
Author(s):  
Maxwell G. Heiman ◽  
Shai Shaham
Keyword(s):  
Nervous System ◽  
Caenorhabditis Elegans ◽  
Glial Cell ◽  
Glial Cells ◽  
Cell Types ◽  
Neuronal Morphology ◽  
Sensory Organs ◽  
Nematode Caenorhabditis Elegans ◽  
C Elegans

AbstractThe nematode Caenorhabditis elegans has a simple nervous system with glia restricted primarily to sensory organs. Some of the activities that would be provided by glia in the mammalian nervous system are either absent or provided by non-glial cell types in C. elegans, with only a select set of mammalian glial activities being similarly provided by specialized glial cells in this animal. These observations suggest that ancestral roles of glia may be to modulate neuronal morphology and neuronal sensitivity in sensory organs.

scholarly journals Dishevelled attenuates the repelling activity of Wnt signaling during neurite outgrowth in Caenorhabditis elegans

2015 ◽  
Vol 112 (43) ◽  
pp. 13243-13248 ◽  
Author(s):  
Chaogu Zheng ◽  
Margarete Diaz-Cuadros ◽  
Martin Chalfie
Keyword(s):  
Caenorhabditis Elegans ◽  
Wnt Signaling ◽  
Neurite Outgrowth ◽  
Planar Cell Polarity ◽  
Feedback Inhibition ◽  
Neuronal Morphology ◽  
Inhibitory Function ◽  
Wnt Proteins ◽  
Signaling Components ◽  
Fine Tune

Wnt proteins regulate axonal outgrowth along the anterior–posterior axis, but the intracellular mechanisms that modulate the strength of Wnt signaling in axon guidance are largely unknown. Using the Caenorhabditis elegans mechanosensory PLM neurons, we found that posteriorly enriched LIN-44/Wnt acts as a repellent to promote anteriorly directed neurite outgrowth through the LIN-17/Frizzled receptor, instead of controlling neuronal polarity as previously thought. Dishevelled (Dsh) proteins DSH-1 and MIG-5 redundantly mediate the repulsive activity of the Wnt signals to induce anterior outgrowth, whereas DSH-1 also provides feedback inhibition to attenuate the signaling to allow posterior outgrowth against the Wnt gradient. This inhibitory function of DSH-1, which requires its dishevelled, Egl-10, and pleckstrin (DEP) domain, acts by promoting LIN-17 phosphorylation and is antagonized by planar cell polarity signaling components Van Gogh (VANG-1) and Prickle (PRKL-1). Our results suggest that Dsh proteins both respond to Wnt signals to shape neuronal projections and moderate its activity to fine-tune neuronal morphology.

scholarly journals Spaceflight Affects Neuronal Morphology and Alters Transcellular Degradation of Neuronal Debris in Adult Caenorhabditis elegans

2020 ◽  
Author(s):  
Ricardo Laranjeiro ◽  
Girish Harinath ◽  
Amelia K. Pollard ◽  
Christopher J. Gaffney ◽  
Colleen S. Deane ◽  
...  
Keyword(s):  
Nervous System ◽  
Caenorhabditis Elegans ◽  
Human Health ◽  
Morphological Changes ◽  
Neuronal Response ◽  
Space Station ◽  
Adult Life ◽  
Neuronal Morphology ◽  
Extended Space

AbstractExtended space travel, such as crewed missions to Mars and beyond, is a goal for both government space agencies and private companies. Research over the past decades, however, has shown that spaceflight poses risks to human health, including negative effects on musculoskeletal, cardiovascular, and immune systems. Details regarding effects on the nervous system have been less well described. The use of animal models holds great potential to identify and dissect conserved mechanisms of neuronal response to spaceflight. Here, we exploited the unique experimental advantages of the nematode Caenorhabditis elegans to explore how spaceflight affects adult neurons in vivo, at the single-cell level. We found that animals that lived 5 days of their adult life on the International Space Station exhibited considerable dendritic remodeling of the highly branched PVD neuron and modest morphological changes in touch receptor neurons when compared to ground control animals. Our results indicate hyperbranching as a common response of adult neurons to spaceflight. We also found that, in the presence of a neuronal proteotoxic stress, spaceflight promotes a remarkable accumulation of neuronal-derived waste in the surrounding tissues (especially hypodermis), suggesting an impaired transcellular degradation of debris that is released from neurons. Overall, our data reveal that spaceflight can significantly affect adult neuronal morphology and clearance of neuronal trash, highlighting the need to carefully assess the risks of long-duration spaceflight on the nervous system and to develop countermeasures to protect human health during space exploration.

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