Quantitative Approaches for Studying Cellular Structures and Organelle Morphology in &lt;em&gt;Caenorhabditis elegans&lt;/em&gt;

Teoh, Jean-Sébastien; Soh, Ming S.; Byrne, Joseph J.; Neumann, Brent

doi:10.3791/59978

Cited by 2 publications

(2 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Although tig-2 ( ok3416 ) has normal expression and function of postsynaptic receptors and observed locomotion defect in tig-2 ( ok3416 ) could result from the functional defect in body wall muscle cells. We therefore crossed tig-2 ( ok3416 ) mutant with the strain expressing myo-3:GFP in muscle cells ( RW1596 [ myo-3 ( st386 ) V;stEx30 ( myo-3p:GFP:myo-3 + rol-6 ( su1006 ))]) ( Figure 5A ) to checked the morphology of muscles myosin following Jean et al’s protocol ( Teoh et al, 2019 ). The average length of muscle cell fiber branches in wild-type nematodes and tig-2 ( ok3416 ) mutants was found to be similar ( Figure 5B ), indicating that TIG-2 has no effect on the myosin morphology in body wall muscle cells.…”

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

The transforming growth factor beta ligand TIG-2 modulates the function of neuromuscular junction and muscle energy metabolism in Caenorhabditis elegans

Cheng

Yan

et al. 2022

Front. Mol. Neurosci.

View full text Add to dashboard Cite

Deciphering the physiological function of TGF-β (the transforming growth factor beta) family ligands is import for understanding the role of TGF-β in animals’ development and aging. Here, we investigate the function of TIG-2, one of the ligands in Caenorhabditis elegans TGF-β family, in animals’ behavioral modulation. Our results show that a loss-of-function mutation in tig-2 gene result in slower locomotion speed in the early adulthood and an increased density of cholinergic synapses, but a decreased neurotransmitter release at neuromuscular junctions (NMJs). Further tissue-specific rescue results reveal that neuronal and intestinal TIG-2 are essential for the formation of cholinergic synapses at NMJs. Interestingly, tig-2(ok3416) mutant is characterized with reduced muscle mitochondria content and adenosine triphosphate (ATP) production, although the function of muscle acetylcholine receptors and the morphology muscle fibers in the mutant are comparable to that in wild-type animals. Our result suggests that TIG-2 from different neuron and intestine regulates worm locomotion by modulating synaptogenesis and neurotransmission at NMJs, as well as energy metabolism in postsynaptic muscle cells.

show abstract

Section: Resultsmentioning

confidence: 99%

“…By dividing the cluster number with the length of nerve code, an average synapse number in every 100 μm nerve code was determined. For myosin fiber imaging, the analysis was performed following the previous publication ( Teoh et al, 2019 ).…”

Section: Methodsmentioning

confidence: 99%

The transforming growth factor beta ligand TIG-2 modulates the function of neuromuscular junction and muscle energy metabolism in Caenorhabditis elegans

Cheng

Yan

et al. 2022

Front. Mol. Neurosci.

View full text Add to dashboard Cite

show abstract

Disruption of genes associated with Charcot-Marie-Tooth type 2 lead to common behavioural, cellular and molecular defects in Caenorhabditis elegans

et al. 2020

Self Cite

View full text Add to dashboard Cite

Charcot-Marie-Tooth (CMT) disease is an inherited peripheral motor and sensory neuropathy. The disease is divided into demyelinating (CMT1) and axonal (CMT2) neuropathies, and although we have gained molecular information into the details of CMT1 pathology, much less is known about CMT2. Due to its clinical and genetic heterogeneity, coupled with a lack of animal models, common underlying mechanisms remain elusive. In order to gain an understanding of the normal function of genes associated with CMT2, and to draw direct comparisons between them, we have studied the behavioural, cellular and molecular consequences of mutating nine different genes in the nematode Caenorhabditis elegans (lin-41/ TRIM2, dyn-1/DNM2, unc-116/KIF5A, fzo-1/MFN2, osm-9/TRPV4, cua-1/ATP7A, hsp-25/ HSPB1, hint-1/HINT1, nep-2/MME). We show that C. elegans defective for these genes display debilitated movement in crawling and swimming assays. Severe morphological defects in cholinergic motors neurons are also evident in two of the mutants (dyn-1 and unc-116). Furthermore, we establish methods for quantifying muscle morphology and use these to demonstrate that loss of muscle structure occurs in the majority of mutants studied. Finally, using electrophysiological recordings of neuromuscular junction (NMJ) activity, we uncover reductions in spontaneous postsynaptic current frequency in lin-41, dyn-1, unc-116 and fzo-1 mutants. By comparing the consequences of mutating numerous CMT2-related genes, this study reveals common deficits in muscle structure and function, as well as NMJ signalling when these genes are disrupted.

show abstract

Quantitative Approaches for Studying Cellular Structures and Organelle Morphology in <em>Caenorhabditis elegans</em>

Cited by 2 publications

References 0 publications

The transforming growth factor beta ligand TIG-2 modulates the function of neuromuscular junction and muscle energy metabolism in Caenorhabditis elegans

The transforming growth factor beta ligand TIG-2 modulates the function of neuromuscular junction and muscle energy metabolism in Caenorhabditis elegans

Disruption of genes associated with Charcot-Marie-Tooth type 2 lead to common behavioural, cellular and molecular defects in Caenorhabditis elegans

Contact Info

Product

Resources

About