[
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.
[
Zhongguo Ji Sheng Chong Xue Yu Ji Sheng Chong Bing Za Zhi,
1999]
AIM: To determine whether immunization with recombinant filarial chitinase or a fragment containing the epitope recognized by McAbMF1 and SXP-1 could protect jirds against microfilaremia resulting from infection with B. malayi. METHODS: Test jirds were immunized with the following recombinant parasite antigens: filarial chitinase, the c-terminal fragments F7R2 or F8R2 of r-chitinase, filarial SXP-1, myosin or maltose binding protein (MBP). Employing immunochemical techniqe (SDS-PAGE, Western Blotting) and serology (ELISA) measured antifilarial antibodies level. RESULTS: Immunization of jirds with recombinant chitinase induced partial protection against microfilaremia resulting from subsequent infection with B. malayi, but did not reduce adult worm burdens. Vaccination was much less effective when administered during the prepatent stage of infection and was ineffective when given to microfilaremic jirds. Immunization of jirds with SXP-1, an antigen present in multiple worm stages also reduced microfilaremia and, in some experiments, adult worm burdens. CONCLUSION: The recombinant chitinase, fragments F7R2 and F8R2 and SXP-1 could provide partial protection against microfilaremia in jirds.
[
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).