[
Zhonghua Yu Fang Yi Xue Za Zhi,
2009]
OBJECTIVE: To study the possibly transferable properties of multi-biological toxicities caused by aluminium exposure from exposed animals to their progeny. METHODS: Multi-biological toxicities in aluminium (2.5 micromol/L, 75 micromol/L, and 200 micromol/L) exposed animals and their progeny were analyzed by using model organism Caenorhabditis elegans. Endpoints of lifespan, development, reproduction, locomotion behavior and behavioral plasticity were selected for the assay of multiple toxicities and their transfer properties. Four groups of experiments were performed for each endpoint assay. Twenty animals were used for assay of lifespan, development, reproduction and locomotion behaviors, and 100 animals were used for assay of behavioral plasticity in each group experiment. The data were performed for statistical analysis using SPSS 13.0 software. RESULTS: Our data suggest that the aluminium exposure could result in multi-biological defects of phenotypes and behaviors. As compared to those average survival days, 24 d, body size, (1.30 +/- 0.05) mm; brood size, (278 +/- 20); generation time (64.0 +/- 1.2) h; body bend, (45.8 +/- 3.0) times, head thrash, (109.33 +/- 7.30) times, behavioral plasticity (3 +/- 4)% in 0 micromol/L aluminum exposed animals, the low-concentration (2.5 micromol/L) aluminium exposure caused severe defects of average survival days (20 d), body size [(1.12 +/- 0.02 ) mm, t = 14.55, P<0.01], brood size [(145 +/- 23), t = 30.62, P< 0.01], body bend [(29.8 +/- 3.0), t = 20.31, P<0.01], and head thrash, (95.8 +/- 6.2), t = 16.43, P < 0.01]. High-concentration aluminium exposure could further result in severe defects of generation time [75 micromol/L, (67.0 +/- 1.7 ) h, t = 8.92, P<0.01; 200 micromol/L, (70.7 +/- 1.5) h, t =15.13, P<0.01] and behavioral plasticity [75 micromol/L, (16.5 +/- 3.0)%, t = 27.11, P<0.05; 200 micromol/L, (23.5 +/- 4.0)%, t = 16.43, P<0.01]. Moreover, most of these toxicities caused by high-concentration aluminium exposure could be transferred from exposed animals to their progeny. In progeny animals, the phenotypic and behavioral defects might be only partially (such as body size, brood size, and locomotion behaviors) or very slightly (such as the lifespan defects induced by high concentrations of aluminium exposure) rescued. Especially, the generation time defects induced by aluminium exposure would become more severe in progeny animals than in their parents. CONCLUSION: The multi-biological defects caused by aluminium exposure might be largely transferred from exposed animals to their progeny in Caenorhabditis elegans.
[
Trends Genet,
2023]
Prenatal exposure to environmental agents can influence the fitness of not only the fetus, but also subsequent generations. In a recent study, Wang et al. demonstrated that feeding ursolic acid (UA), a plant-derived compound, to Caenorhabditis elegans mothers during their reproductive period prevented neurodegeneration in not only their offspring, but also the F2 progeny.
[
Neuron,
2016]
Transmembrane channel-like (TMC) proteins have been implicated in hair cell mechanotransduction, Drosophila proprioception, and sodium sensing in the nematode C.elegans. In this issue of Neuron, Wang etal. (2016) report that C.elegans TMC-1 mediates nociceptor responses to high pH, not sodium, allowing the nematode to avoid strongly alkaline environments in which most animals cannot survive.
[
STAR Protoc,
2022]
Live imaging is an important tool to track dynamic processes such as neuronal patterning events. Here, we describe a protocol for time-lapse microscopy analysis using neuronal migration and dendritic growth as examples. This protocol can provide detailed information for understanding cellular dynamics during postembryonic development in Caenorhabditis elegans (C. elegans). For complete details on the use and execution of this protocol, please refer to Feng etal. (2020), Li etal. (2021), and Wang etal. (2021).
[
MicroPubl Biol,
2019]
Several techniques are available for spatiotemporal control of genome recombination and gene expression in the nematode Caenorhabditis elegans. Here we report a novel tool to combine the powerful FLP-Frt and GAL4-UAS systems to increase their versality and to offer additional levels of control.FLP is an enzyme that catalyzes recombination between two short Frt DNA sequences and is frequently used to excise genomic fragments flanked by Frt sites, thereby either activating or knocking out gene expression, depending on the experimental design (Hubbard, 2014). Recently, we generated multiple strains that stably express FLP in different somatic tissues from single-copy transgenes and demonstrated that they in most cases induce recombination in ~100% of the cells of the expected tissue (Munoz-Jimenez et al., 2017). We subsequently constructed a strain for germline recombination to permanently knock out Frt-flanked genes or exons (Macas-Len and Askjaer, 2018).The GAL4-UAS system is based on the Saccharomyces cerevisiae Gal4p transcription factor and its cognate DNA target called upstream activating sequence (UAS). Typically, this bipartite system includes a series of driver strains expressing GAL4 in specific tissues and one or several strains with an effector gene downstream of UAS repeats. Wang and colleagues from the Sternberg laboratory recently optimized the GAL4-UAS system for C. elegans (cGAL) and reported several tissue-specific cGAL drivers (Wang et al., 2017). Moreover, they have developed a split cGAL toolkit where the DNA binding and activation domains are expressed as individual polypeptides, thereby enabling further fine-tuning of spatiotemporal control: only when and where the two components are co-expressed they will activate the UAS::effector transgene (Wang et al., 2018).