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[
Adv Exp Med Biol,
2019]
As the nervous system evolved from the diffused to centralised form, the neurones were joined by the appearance of the supportive cells, the neuroglia. Arguably, these non-neuronal cells evolve into a more diversified cell family than the neurones are. The first ancestral neuroglia appeared in flatworms being mesenchymal in origin. In the nematode C. elegans proto-astrocytes/supportive glia of ectodermal origin emerged, albeit the ensheathment of axons by glial cells occurred later in prawns. The multilayered myelin occurred by convergent evolution of oligodendrocytes and Schwann cells in vertebrates above the jawless fishes. Nutritive partitioning of the brain from the rest of the body appeared in insects when the hemolymph-brain barrier, a predecessor of the blood-brain barrier was formed. The defensive cellular mechanism required specialisation of bona fide immune cells, microglia, a process that occurred in the nervous system of leeches, bivalves, snails, insects and above. In ascending phylogeny, new type of glial cells, such as scaffolding radial glia, appeared and as the bran sizes enlarged, the glia to neurone ratio increased. Humans possess some unique glial cells not seen in other animals.
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[
Acta Physiol (Oxf),
2009]
Purines appear to be the most primitive and widespread chemical messengers in the animal and plant kingdoms. The evidence for purinergic signalling in plants, invertebrates and lower vertebrates is reviewed. Much is based on pharmacological studies, but important recent studies have utilized the techniques of molecular biology and receptors have been cloned and characterized in primitive invertebrates, including the social amoeba Dictyostelium and the platyhelminth Schistosoma, as well as the green algae Ostreococcus, which resemble P2X receptors identified in mammals. This suggests that contrary to earlier speculations, P2X ion channel receptors appeared early in evolution, while G protein-coupled P1 and P2Y receptors were introduced either at the same time or perhaps even later. The absence of gene coding for P2X receptors in some animal groups [e.g. in some insects, roundworms (Caenorhabditis elegans) and the plant Arabidopsis] in contrast to the potent pharmacological actions of nucleotides in the same species, suggests that novel receptors are still to be discovered.
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[
Front Cell Neurosci,
2014]
Glial cells of Caenorhabditis elegans can modulate neuronal activity and behavior, which is the focus of this review. Initially, we provide an overview of neuroglial evolution, making a comparison between C. elegans glia and their genealogical counterparts. What follows is a brief discussion on C. elegans glia characteristics in terms of their exact numbers, germ layers origin, their necessity for proper development of sensory organs, and lack of their need for neuronal survival. The more specific roles that various glial cells have on neuron-based activity/behavior are succinctly presented. The cephalic sheath glia are important for development, maintenance and activity of central synapses, whereas the amphid glia seem to set the tone of sensory synapses; these glial cell types are ectoderm-derived. Mesoderm-derived Glial-Like cells in the nerve Ring (GLRs) appear to be a part of the circuit for production of motor movement of the worm anterior. Finally, we discuss tools and approaches utilized in studying C. elegans glia, which are assets available for this animal, making it an appealing model, not only in neurosciences, but in biology in general.
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[
European Worm Meeting,
2008]
The endoplasmic reticulum (ER) is a membranous structure consisting of a. complex tubule and sheet network that may comprise more than half of all. membranes in a cell (Verkhratsky and Toescu, 2003 J Cell Mol Med, 7:351).. This multifunctional organelle participates in lipid and protein processing. as well as calcium regulation. In the early C. elegans embryo, the ER. undergoes dynamic re-organization during the cell cycle, exhibiting a. highly reticulate structure during metaphase and a more dispersed. organization in interphase (Poteryaev et al., 2005 MBC 16:2139). To examine. how the structure and function of the ER impact cytokinesis. We disrupted. ER function in the C. elegans embryo through the use of pharmacological. agents known to affect ER calcium regulation. We found that treatment with. caffeine, a compound that can activate the ER-resident calcium channel. ryanodine, resulting in a release of free calcium from the ER, severely. disrupts ER morphology, perturbs cell division and causes increased plasma. membrane activity. Furthermore, we found that the hyper-activation of the. plasma membrane motility that we observed is dependent on non-muscle myosin. function. We also observed that treatment with thapsigargin, which. inhibits calcium flow back into the ER through the SERCA pumps, increases. spindle movement during anaphase and the ER forms numerous dense. aggregates. These data indicate that perturbing the free calcium. regulation function of the ER can disrupt ER organization and has a. profound effect on cellular dynamics.
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[
International Worm Meeting,
2019]
Degenerin channels are conserved proteins throughout urbilaterian phylogeny. These channels are mainly found in central and peripheral nervous systems and have in common functional domains involved in the control of channel activity and in the formation of the pore (Kellenberger and Schild, 2002). In C. elegans, MEC-4 is the pore-forming unit of the mechanosensory channel expressed in the Touch Receptor Neurons (TRNs) that transduces changes in membrane pressure through sodium currents. An amino acid switch (A713T) in the second transmembrane domain changes MEC-4 selectivity and gating (Driscoll and Chalfie, 1991; Kellenberger and Schild, 2002; Brown et al., 2007). This hyperactivated channel is called MEC-4d and permeates calcium in addition to sodium (Goodman et al., 2002; Bianchi et al., 2004; O'Hagan et al., 2005). The influx of calcium through MEC-4d is thought to promote calcium release from the endoplasmic reticulum and mitochondrion, followed by caspase and protease activation and results in the necrotic death of the TRNs (Verkhratsky and Shmigol, 1996; Xu et al., 2001; Syntichaki et al., 2002; Newmeyer and Ferguson-Miller, 2003; Bianchi et al., 2004; Brookes et al., 2004; Calixto et al., 2012). Notably, TRN neuroprotection in MEC-4d worms can also be seen in physiological conditions. Under diapause arrest, damaged TRNs in C. elegans exhibit an extraordinary capacity for regeneration, in which the axon can functionally regenerate from the soma alone (Caneo et al., 2019). The underlying regenerative mechanisms are unclear. Given the pivotal role of calcium in MEC-4d degeneration, we hypothesize that diapause, triggered by environmental stressors such as starvation, ameliorates calcium dysregulation in the TRNs of MEC-4d worms. To understand how diapause changes calcium homeostasis, we will monitor intracellular calcium in vivo with the use of a two-photon laser scanning microscope. The setup for two-photon calcium imaging involves the simultaneous expression of the fluorescent calcium indicator GCaMP and the calcium-insensitive cellular marker tag-RFP in TRNs. Here we present a protocol for reliable in vivo calcium imaging in TRNs of MEC-4d mutants and dauers to study environmentally induced axonal regeneration in a model of genetically encoded degeneration.
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Pennington PR, Quartey MO, Nyarko JNK, Parsons MP, Maley JM, Heistad RM, Leary SC, Barnes JR, Knudsen KJ, De Carvalho CE, Bolanos MAC, Buttigieg J, Mousseau DD
[
Sci Rep,
2021]
The pool of -Amyloid (A) length variants detected in preclinical and clinical Alzheimer disease (AD) samples suggests a diversity of roles for A peptides. We examined how a naturally occurring variant, e.g. A(1-38), interacts with the AD-related variant, A(1-42), and the predominant physiological variant, A(1-40). Atomic force microscopy, Thioflavin T fluorescence, circular dichroism, dynamic light scattering, and surface plasmon resonance reveal that A(1-38) interacts differently with A(1-40) and A(1-42) and, in general, A(1-38) interferes with the conversion of A(1-42) to a -sheet-rich aggregate. Functionally, A(1-38) reverses the negative impact of A(1-42) on long-term potentiation in acute hippocampal slices and on membrane conductance in primary neurons, and mitigates an A(1-42) phenotype in Caenorhabditis elegans. A(1-38) also reverses any loss of MTT conversion induced by A(1-40) and A(1-42) in HT-22 hippocampal neurons and APOE 4-positive human fibroblasts, although the combination of A(1-38) and A(1-42) inhibits MTT conversion in APOE 4-negative fibroblasts. A greater ratio of soluble A(1-42)/A(1-38) [and A(1-42)/A(1-40)] in autopsied brain extracts correlates with an earlier age-at-death in males (but not females) with a diagnosis of AD. These results suggest that A(1-38) is capable of physically counteracting, potentially in a sex-dependent manner, the neuropathological effects of the AD-relevant A(1-42).
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[
Worm Breeder's Gazette,
2003]
Wormgenes is a new resource for C.elegans offering a detailed summary about each gene and a powerful query system.
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[
International Journal of Developmental Biology,
1998]
Pleiotropy , a situation in which a single gene influences multiple phenotypic tra its, can arise in a variety of ways. This paper discusses possible underlying mechanisms and proposes a classification of the various phenomena involved.
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[
Front Pharmacol,
2020]
Oligomeric assembly of Amyloid- (A) is the main toxic species that contribute to early cognitive impairment in Alzheimer's patients. Therefore, drugs that reduce the formation of A oligomers could halt the disease progression. In this study, by using transgenic <i>Caenorhabditis elegans</i> model of Alzheimer's disease, we investigated the effects of frondoside A, a well-known sea cucumber <i>Cucumaria frondosa</i> saponin with anti-cancer activity, on A aggregation and proteotoxicity. The results showed that frondoside A at a low concentration of 1 M significantly delayed the worm paralysis caused by A aggregation as compared with control group. In addition, the number of A plaque deposits in transgenic worm tissues was significantly decreased. Frondoside A was more effective in these activities than ginsenoside-Rg3, a comparable ginseng saponin. Immunoblot analysis revealed that the level of small oligomers as well as various high molecular weights of A species in the transgenic <i>C. elegans</i> were significantly reduced upon treatment with frondoside A, whereas the level of A monomers was not altered. This suggested that frondoside A may primarily reduce the level of small oligomeric forms, the most toxic species of A. Frondoside A also protected the worms from oxidative stress and rescued chemotaxis dysfunction in a transgenic strain whose neurons express A. Taken together, these data suggested that low dose of frondoside A could protect against A-induced toxicity by primarily suppressing the formation of A oligomers. Thus, the molecular mechanism of how frondoside A exerts its anti-A aggregation should be studied and elucidated in the future.