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08.04.20 Miska lab probe mechanism of a heritable adaptation to infection in C. elegans

last modified Apr 08, 2020 10:12 AM
In this Nat Comms study using nematode worms, the Miska lab and collaborators show that parental exposure to a pathogen can increase the future offspring's resistance to infection, in a process mediated by two cysteine synthase enzymes.
08.04.20 Miska lab probe mechanism of a heritable adaptation to infection in C. elegans

Fig. 4c (excerpt): Embryos from worm parents fed pathogenic bacteria upregulate cysl-2 (green)

Cysteine synthases CYSL-1 and CYSL-2 mediate C. elegans heritable adaptation to P. vranovensis infection

Burton N O et al. (2020) Nature Communications

11, Article number: 1741.

DOI: 10.1038/s41467-020-15555-8.

 

Abstract from the paper

Parental exposure to pathogens can prime offspring immunity in diverse organisms. The mechanisms by which this heritable priming occurs are largely unknown.

Here we report that the soil bacterium Pseudomonas vranovensis is a natural pathogen of the nematode Caenorhabditis elegans and that parental exposure of animals to P. vranovensis promotes offspring resistance to infection. Furthermore, we demonstrate a multigenerational enhancement of progeny survival when three consecutive generations of animals are exposed to P. vranovensis.

By investigating the mechanisms by which animals heritably adapt to P. vranovensis infection, we found that parental infection by P. vranovensis results in increased expression of the cysteine synthases cysl-1 and cysl-2 and the regulator of hypoxia inducible factor rhy-1 in progeny and that these three genes are required for adaptation to P. vranovensis.

These observations establish a CYSL-1, CYSL-2, and RHY-1 dependent mechanism by which animals heritably adapt to infection.

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