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 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 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.

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 ◽  
Colleen S. Deane ◽  
Siva A. Vanapalli ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Neuronal Morphology

The glycomes of Caenorhabditis elegans and other model organisms

2002 ◽  
Vol 69 ◽  
pp. 117-134 ◽  
Author(s):  
Stuart M. Haslam ◽  
David Gems ◽  
Howard R. Morris ◽  
Anne Dell
Keyword(s):  
Caenorhabditis Elegans ◽  
Current Knowledge ◽  
Structural Data ◽  
Model Organisms ◽  
Entire Genome ◽  
C Elegans ◽  
The Face ◽  
Area Of Concern ◽  
Nematode Worm

There is no doubt that the immense amount of information that is being generated by the initial sequencing and secondary interrogation of various genomes will change the face of glycobiological research. However, a major area of concern is that detailed structural knowledge of the ultimate products of genes that are identified as being involved in glycoconjugate biosynthesis is still limited. This is illustrated clearly by the nematode worm Caenorhabditis elegans, which was the first multicellular organism to have its entire genome sequenced. To date, only limited structural data on the glycosylated molecules of this organism have been reported. Our laboratory is addressing this problem by performing detailed MS structural characterization of the N-linked glycans of C. elegans; high-mannose structures dominate, with only minor amounts of complex-type structures. Novel, highly fucosylated truncated structures are also present which are difucosylated on the proximal N-acetylglucosamine of the chitobiose core as well as containing unusual Fucα1–2Gal1–2Man as peripheral structures. The implications of these results in terms of the identification of ligands for genomically predicted lectins and potential glycosyltransferases are discussed in this chapter. Current knowledge on the glycomes of other model organisms such as Dictyostelium discoideum, Saccharomyces cerevisiae and Drosophila melanogaster is also discussed briefly.

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