AI Article Synopsis
- - The study examines the mortal germline phenotype in some wild isolates of Caenorhabditis elegans, which leads to sterility after multiple generations at a specific temperature (25°C).
- - A genome-wide association study identified a significant genetic region on chromosome III linked to this phenotype, suggesting that a seemingly harmful genotype is maintained in the population due to environmental factors.
- - Environmental interactions, particularly with different strains of E. coli, influence the expression of the mortal germline phenotype, highlighting the role of epigenetic inheritance and non-genetic memory in response to changing conditions.
Article Abstract
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.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10702804 | PMC |
| http://dx.doi.org/10.15252/embr.202358116 | DOI Listing |
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- - A genome-wide association study identified a significant genetic region on chromosome III linked to this phenotype, suggesting that a seemingly harmful genotype is maintained in the population due to environmental factors.
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