Molecular basis for oxidative stress induced by simulated microgravity in nematode Caenorhabditis elegans

2017 ◽  
Vol 607-608 ◽  
pp. 1381-1390 ◽  
Author(s):  
Li Zhao ◽  
Qi Rui ◽  
Dayong Wang
Keyword(s):  
Oxidative Stress ◽  
Caenorhabditis Elegans ◽  
Molecular Basis ◽  
Simulated Microgravity ◽  
Nematode Caenorhabditis Elegans

scholarly journals microRNAs involved in the control of toxicity on locomotion behavior induced by simulated microgravity stress in Caenorhabditis elegans

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Lingmei Sun ◽  
Wenjie Li ◽  
Dan Li ◽  
Dayong Wang
Keyword(s):  
Oxidative Stress ◽  
Functional Analysis ◽  
Caenorhabditis Elegans ◽  
Molecular Basis ◽  
Simulated Microgravity ◽  
Signaling Cascade ◽  
Protective Response ◽  
Epigenetic Control ◽  
Candidate Mirnas ◽  
Locomotion Behavior

Abstract microRNAs (miRNAs) post-transcriptionally regulate the expression of targeted genes. We here systematically identify miRNAs in response to simulated microgravity based on both expressions and functional analysis in Caenorhabditis elegans. After simulated microgravity treatment, we observed that 19 miRNAs (16 down-regulated and 3 up-regulated) were dysregulated. Among these dysregulated miRNAs, let-7, mir-54, mir-67, mir-85, mir-252, mir-354, mir-789, mir-2208, and mir-5592 were required for the toxicity induction of simulated microgravity in suppressing locomotion behavior. In nematodes, alteration in expressions of let-7, mir-67, mir-85, mir-252, mir-354, mir-789, mir-2208, and mir-5592 mediated a protective response to simulated microgravity, whereas alteration in mir-54 expression mediated the toxicity induction of simulated microgravity. Moreover, among these candidate miRNAs, let-7 regulated the toxicity of simulated microgravity by targeting and suppressing SKN-1/Nrf protein. In the intestine, a signaling cascade of SKN-1/Nrf-GST-4/GST-5/GST-7 required for the control of oxidative stress was identified to act downstream of let-7 to regulate the toxicity of simulated microgravity. Our data demonstrated the crucial function of miRNAs in regulating the toxicity of simulated microgravity stress in organisms. Moreover, our results further provided an important molecular basis for epigenetic control of toxicity of simulated microgravity.

scholarly journals Mutation of a putative sperm membrane protein in Caenorhabditis elegans prevents sperm differentiation but not its associated meiotic divisions.

1992 ◽  
Vol 119 (1) ◽  
pp. 55-68 ◽  
Author(s):  
S W L'Hernault ◽  
P M Arduengo
Keyword(s):  
Caenorhabditis Elegans ◽  
Membrane Protein ◽  
Molecular Basis ◽  
Close Association ◽  
Integral Membrane Protein ◽  
Nematode Caenorhabditis Elegans ◽  
C Elegans ◽  
Fibrous Body ◽  
Sperm Membrane ◽  
Internal Membrane Structure

Spermatogenesis in the nematode Caenorhabditis elegans uses unusual organelles, called the fibrous body-membranous organelle (FB-MO) complexes, to prepackage and deliver macromolecules to spermatids during cytokinesis that accompanies the second meiotic division. Mutations in the spe-4 (spermatogenesis-defective) gene disrupt these organelles and prevent cytokinesis during spermatogenesis, but do not prevent completion of the meiotic nuclear divisions that normally accompany spermatid formation. We report an ultrastructural analysis of spe-4 mutant sperm where the normally close association of the FB's with the MO's and the double layered membrane surrounding the FB's are both defective. The internal membrane structure of the MO's is also disrupted in spe-4 mutant sperm. Although sperm morphogenesis in spe-4 mutants arrests prior to the formation of spermatids, meiosis can apparently be completed so that haploid nuclei reside in an arrested spermatocyte. We have cloned the spe-4 gene in order to understand its role during spermatogenesis and the molecular basis of how mutation of this gene disrupts this process. The spe-4 gene encodes an approximately 1.5-kb mRNA that is expressed during spermatogenesis, and the sequence of this gene suggests that it encodes an integral membrane protein. These data suggest that mutation of an integral membrane protein within FB-MO complexes disrupts morphogenesis and prevents formation of spermatids but does not affect completion of the meiotic nuclear divisions in C. elegans sperm.

scholarly journals Protective effects of novel organic selenium compounds against oxidative stress in the nematode Caenorhabditis elegans

2015 ◽  
Vol 2 ◽  
pp. 961-967 ◽  
Author(s):  
Sílvio Terra Stefanello ◽  
Priscila Gubert ◽  
Bruna Puntel ◽  
Caren Rigon Mizdal ◽  
Marli Matiko Anraku de Campos ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Caenorhabditis Elegans ◽  
Protective Effects ◽  
Nematode Caenorhabditis Elegans ◽  
Selenium Compounds ◽  
Organic Selenium

scholarly journals Molecular basis of loss-of-function mutations in the glp-1 gene of Caenorhabditis elegans.

1992 ◽  
Vol 3 (11) ◽  
pp. 1199-1213 ◽  
Author(s):  
V Kodoyianni ◽  
E M Maine ◽  
J Kimble
Keyword(s):  
Caenorhabditis Elegans ◽  
Growth Factor ◽  
Molecular Basis ◽  
Missense Mutations ◽  
Loss Of Function ◽  
Nematode Caenorhabditis Elegans ◽  
Nonsense Mutations ◽  
Epidermal Growth ◽  
Repeated Motifs

The glp-1 gene encodes a membrane protein required for inductive cell interactions during development of the nematode Caenorhabditis elegans. Here we report the molecular characterization of 15 loss-of-function (lf) mutations of glp-1. Two nonsense mutations appear to eliminate glp-1 activity; both truncate the glp-1 protein in its extracellular domain and have a strong loss-of-function phenotype. Twelve missense mutations and one in-frame deletion map to sites within the repeated motifs of the glp-1 protein (10 epidermal growth factor [EGF]-like and 3 LNG repeats extracellularly and 6 cdc10/SWI6, or ankyrin, repeats intracellularly). We find that all three types of repeated motifs are critical to glp-1 function, and two individual EGF-like repeats may have distinct functions. Intriguingly, all four missense mutations in one phenotypic class map to the N-terminal EGF-like repeats and all six missense mutations in a second phenotypic class reside in the intracellular cdc10/SWI6 repeats. These two clusters of mutations may identify functional domains within the glp-1 protein.

Systematic screen for genes involved in the regulation of oxidative stress in the nematode Caenorhabditis elegans

2012 ◽  
Vol 420 (3) ◽  
pp. 552-557 ◽  
Author(s):  
Shunsuke Ueno ◽  
Kiichi Yasutake ◽  
Daisuke Tohyama ◽  
Tsutomu Fujimori ◽  
Dai Ayusawa ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Caenorhabditis Elegans ◽  
Nematode Caenorhabditis Elegans

scholarly journals Insulin signaling regulates the toxicity of traffic-related PM2.5 on intestinal development and function in nematode Caenorhabditis elegans

2015 ◽  
Vol 4 (2) ◽  
pp. 333-343 ◽  
Author(s):  
Ruilong Yang ◽  
Yunli Zhao ◽  
Xiaoming Yu ◽  
Zhiqing Lin ◽  
Zhuge Xi ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Signaling Pathway ◽  
Insulin Signaling ◽  
Molecular Basis ◽  
Insulin Signaling Pathway ◽  
Intestinal Development ◽  
Nematode Caenorhabditis Elegans ◽  
And Function

Insulin signaling pathway may act as an important molecular basis for the toxicity of traffic-related PM2.5 in Caenorhabditis elegans, a non-mammalian toxicological model.

scholarly journals Analysis of a mutator activity necessary for germline transposition and excision of Tc1 transposable elements in Caenorhabditis elegans.

Genetics ◽  
1988 ◽  
Vol 120 (2) ◽  
pp. 397-407
Author(s):  
I Mori ◽  
D G Moerman ◽  
R H Waterston
Keyword(s):  
Caenorhabditis Elegans ◽  
Transposable Elements ◽  
Transposable Element ◽  
Molecular Basis ◽  
Copy Number ◽  
Nematode Caenorhabditis Elegans ◽  
Transposable Element Family ◽  
Genetic Components ◽  
Mutator Activity ◽  
Low Copy Number

Abstract The Tc1 transposable element family of the nematode Caenorhabditis elegans consists primarily of 1.6-kb size elements. This uniformity of size is in contrast to P in Drosophila and Ac/Ds in maize. Germline transposition and excision of Tc1 are detectable in the Bergerac (BO) strain, but not in the commonly used Bristol (N2) strain. A previous study suggested that multiple genetic components are responsible for the germline Tc1 activity of the BO strain. To analyze further this mutator activity, we derived hybrid strains between the BO strain and the N2 strain. One of the hybrid strains exhibits a single locus of mutator activity, designated mut-4, which maps to LGI. Two additional mutators, mut-5 II and mut-6 IV, arose spontaneously in mut-4 harboring strains. This spontaneous appearance of mutator activity at new sites suggests that the mutator itself transposes. The single mutator-harboring strains with low Tc1 copy number generated in this study should be useful in investigations of the molecular basis of mutator activity. As a first step toward this goal, we examined the Tc1 elements in these low copy number strains for elements consistently co-segregating with mutator activity. Three possible candidates were identified: none was larger than 1.6 kb.

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