The animal germline lineage needs to be maintained along generations. However, some Caenorhabditis elegans wild isolates display a mortal germline phenotype, leading to sterility after several generations at 25°C. Using a genome-wide association approach, we detect a significant peak on chromosome III around 5 Mb, confirmed by introgressions. Thus, a seemingly deleterious genotype is maintained at intermediate frequency in the species. Environmental rescue is a likely explanation, and indeed associated bacteria and microsporidia suppress the phenotype of wild isolates as well as mutants in small RNA inheritance (nrde-2) and histone modifications (set-2). Escherichia coli strains of the K-12 lineage suppress the phenotype compared to B strains. By shifting a wild strain from E. coli K-12 to E. coli B, we find that memory of the suppressing condition is maintained over several generations. Thus, the mortal germline phenotype of wild C. elegans is in part revealed by laboratory conditions and may represent variation in epigenetic inheritance and environmental interactions. This study also points to the importance of non-genetic memory in the face of environmental variation.

A conditioning lesion of the peripheral sensory axon triggers robust central axon regeneration in mammals. We trigger conditioned regeneration in the Caenorhabditis elegans ASJ neuron by laser surgery or genetic disruption of sensory pathways. Conditioning upregulates thioredoxin-1 (trx-1) expression, as indicated by trx-1 promoter-driven expression of green fluorescent protein and fluorescence in situ hybridization (FISH), suggesting trx-1 levels and associated fluorescence indicate regenerative capacity. The redox activity of trx-1 functionally enhances conditioned regeneration, but both redox-dependent and -independent activity inhibit non-conditioned regeneration. Six strains isolated in a forward genetic screen for reduced fluorescence, which suggests diminished regenerative potential, also show reduced axon outgrowth. We demonstrate an association between trx-1 expression and the conditioned state that we leverage to rapidly assess regenerative capacity.

Adaptive developmental plasticity is a common phenomenon across diverse organisms and allows a single genotype to express multiple phenotypes in response to environmental signals. Developmental plasticity is thus thought to reflect a key adaptation to cope with heterogenous habitats. Adaptive plasticity often relies on highly regulated processes in which organisms sense environmental cues predictive of unfavourable environments. The integration of such cues may involve sophisticated neuro-endocrine signaling pathways to generate subtle or complete developmental shifts. A striking example of adaptive plasticity is found in the nematode C. elegans, which can undergo two different developmental trajectories depending on the environment. In favourable conditions, C. elegans develops through reproductive growth to become an adult in three days at 20 °C. In contrast, in unfavourable conditions (high population density, food scarcity, elevated temperature) larvae can adopt an alternative developmental stage, called dauer. dauer larvae are highly stress-resistant and exhibit specific anatomical, metabolic and behavioural features that allow them to survive and disperse. In C. elegans, the sensation of environmental cues is mediated by amphid ciliated sensory neurons by means of G-coupled protein receptors. In favourable environments, the perception of pro-reproductive cues, such as food and the absence of pro-dauer cues, upregulates insulin and TGF-β signaling in the nervous system. In unfavourable conditions, pro-dauer cues lead to the downregulation of insulin and TGF-β signaling. In favourable conditions, TGF-β and insulin act in parallel to promote synthesis of dafachronic acid (DA) in steroidogenic tissues. Synthetized DA binds to the DAF-12 nuclear receptor throughout the whole body. DA-bound DAF-12 positively regulates genes of reproductive development in all C. elegans tissues. In poor conditions, the inhibition of insulin and TGF-β signaling prevents DA synthesis, thus the unliganded DAF-12 and co-repressor DIN-1 repress genes of reproductive development and promote dauer formation. Wild C. elegans have often been isolated as dauer larvae suggesting that dauer formation is very common in nature. Natural populations of C. elegans have colonized a great variety of habitats across the planet, which may differ substantially in environmental conditions. Consistent with divergent adaptation to distinct ecological niches, wild isolates of C. elegans and other nematode species isolated from different locations show extensive variation in dauer induction. Quantitative genetic and population-genomic approaches have identified many quantitative trait loci (QTL) associated with differences in dauer induction as well as a few underlying causative molecular variants. In this review, we summarize how C. elegans dauer formation is genetically regulated and how this trait evolves- both within and between species.
UNASSIGNED: Génétique et évolution de la plasticité développementale chez le nématode C. elegans : induction environnementale du stade dauer.
UNASSIGNED: La plasticité phénotypique est un phénomène très courant au cours duquel des phénotypes différents sont exprimés en fonction de facteurs environnementaux. La plasticité, lorsque qu’elle est dite « adaptative », permet aux organismes de faire face à des habitats hétérogènes. Bien que les mécanismes moléculaires régulant la plasticité développementale soient de mieux en mieux compris, nous n’avons encore que peu d’informations sur les bases moléculaires de la variation naturelle et de l’évolution de la plasticité. Le nématode C. elegans présente un exemple emblématique de plasticité adaptative car cette espèce a la capacité d’entrer dans un stade larvaire alternatif appelé « dauer » lorsque les conditions environnementales sont défavorables. Durant ce stade de diapause, les larves peuvent survivre pendant environ trois mois en milieu extrême et reprendre leur développement lorsque les conditions s’améliorent. Nous passons ici en revue les mécanismes moléculaires régulant l’entrée en dauer ainsi que les récents progrès réalisés dans la caractérisation de la variation naturelle et l’évolution de l’induction de ce stade de résistance chez C. elegans comme chez d’autres espèces de nématodes.