Baumanns S et al. (2022) Biochim Biophys Acta Mol Cell Res "RNA-interference in the nematode Caenorhabditis elegans is effective using paraformaldehyde-inactivated E. coli HT115 bacteria as a food source."

Beis DM, Baumanns S, Wenzel U

[Biochim Biophys Acta Mol Cell Res, 2022]

The nematode Caenorhabditis elegans is a widely used research model for the investigation of metabolism, aging and age-associated diseases. However, when investigating the impact of natural compounds or drugs on those topics, a major confounder is the metabolism of these test substances by live E. coli bacteria, the standard food source of C. elegans. Using paraformaldehyde instead of heat to inactivate E. coli, which allows for high-throughput technologies and better food availability, it is shown here that RNA-interference works equally well, thus demonstrating the absence of considerable interfering modifications of paraformaldehyde with nucleic acids.

Edgar RS et al. (1977) Science "The nematode Caenorhabditis elegans: a new organism for intensive biological study."

Edgar RS, Wood WB

[Science, 1977]

At a recent conference in Woods Hole, Massachusetts, investigators met to discuss the nematode Caenorhabditis elegans. This free-living worm may, according to some workers, become the Escherichia coli or at least the bacteriophage T4 of the animal world. Small (about 1mm in length) and semitransparent, C. elegans provides for research the advantages of a short life cycle (3 days) and a simple anatomy-it contains about 810 nongonadal nuclei. It is both easy to cultivate, on E. coli as a food source, and convenient for genetic analysis. Its genes are carried on five autosomes and a sex chromosome (X), and it has a genome size about 20 times that of E. coli. It generally reproduces as a self-fertilizing hermaphrodite (XX), but occasional males (XO), which arise by nondisjunction, permit sexual reproduction as well....

Petcherski AG et al. (2000) Curr Biol "Mastermind is a putative activator for Notch."

Kimble J, Petcherski AG

[Curr Biol, 2000]

During signaling by the Notch receptor, Notch's intracellular domain is cleaved, moves to the nucleus and associates with a DNA-binding protein of the CSL class (CSL for CBF1, Suppressor of Hairless (Su(H)), LAG-1); as a result, target genes are transcriptionally activated (reviewed in [1,2]). In Caenorhabditis elegans, a glutamine-rich protein called LAG-3 forms a ternary complex with the Notch intracellular domain and LAG-1 and appears to serve as a transcriptional activator that is critical for signaling [3]. Although database searches failed to identify a LAG-3-related protein, we surmised that Notch signaling in other organisms might involve an analogous activity.

Noguez JH et al. (2012) ACS Chem Biol "A novel ascaroside controls the parasitic life cycle of the entomopathogenic nematode Heterorhabditis bacteriophora."

Ragains J, Ciche T, Butcher RA, Conner ES, Zhou Y, Noguez JH

[ACS Chem Biol, 2012]

Entomopathogenic nematodes survive in the soil as stress-resistant infective juveniles that seek out and infect insect hosts. Upon sensing internal host cues, the infective juveniles regurgitate bacterial pathogens from their gut that ultimately kill the host. Inside the host, the nematode develops into a reproductive adult and multiplies until unknown cues trigger the accumulation of infective juveniles. Here, we show that the entomopathogenic nematode Heterorhabditis bacteriophora uses a small-molecule pheromone to control infective juvenile development. The pheromone is structurally related to the dauer pheromone ascarosides that the free-living nematode Caenorhabditis elegans uses to control its development. However, none of the C. elegans ascarosides are effective in H. bacteriophora, suggesting that there is a high degree of species specificity. Our report is the first to show that ascarosides are important regulators of development in a parasitic nematode species. An understanding of chemical signaling in parasitic nematodes may enable the development of chemical tools to control these species.

Singh D et al. (2016) Genesis "Acute heat shock leads to cortical domain internalization and polarity loss in the C. elegans embryo."

Pohl C, Singh D, Odedra D, Lehmann C

[Genesis, 2016]

Many developmental processes are inherently robust due to network organization of the participating factors and functional redundancy. The heterogeneity of the factors involved and their connectivity puts these processes at risk of abrupt system collapse under stress. The polarization of the one-cell C. elegans embryo constitutes such an inherently robust process with functional redundancy. However, how polarization is affected by acute stress has not been thoroughly investigated. Here, we report that heat shock (34C, 1 h) triggers a highly reproducible loss of the anterior and collapse of the posterior polarity domains. Temperature-dependent loss of cortical non-muscle myosin II drastically reduces cortical tension and leads to internalization of large plasma membrane domains including the membrane-associated polarity factor PAR-2. After internalization, plasma membrane vesicles and associated factors cluster around centrosomes and are thereby withdrawn from the polarization process. Transient formation of the posterior polarity domain suggests that microtubule-induced self-organization of this domain is not compromised after heat shock. Hence, our data uncover that the polarization system undergoes a temperature-dependent collapse under acute stress. This article is protected by copyright. All rights reserved.