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Antagonistic fungal enterotoxins intersect at multiple levels with host innate immune defences
Author(s) -
Xing Zhang,
Benjamin W. Harding,
Dina Aggad,
Damien Courtine,
JiaXuan Chen,
Nathalie Pujol,
Jonathan J. Ewbank
Publication year - 2021
Publication title -
plos genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.587
H-Index - 233
eISSN - 1553-7404
pISSN - 1553-7390
DOI - 10.1371/journal.pgen.1009600
Subject(s) - biology , innate immune system , virulence , caenorhabditis elegans , host–pathogen interaction , pathogen , genetics , immune system , host (biology) , gene , transcription factor , acquired immune system , immunity , microbiology and biotechnology
Animals and plants need to defend themselves from pathogen attack. Their defences drive innovation in virulence mechanisms, leading to never-ending cycles of co-evolution in both hosts and pathogens. A full understanding of host immunity therefore requires examination of pathogen virulence strategies. Here, we take advantage of the well-studied innate immune system of Caenorhabditis elegans to dissect the action of two virulence factors from its natural fungal pathogen Drechmeria coniospora . We show that these two enterotoxins have strikingly different effects when expressed individually in the nematode epidermis. One is able to interfere with diverse aspects of host cell biology, altering vesicle trafficking and preventing the key STAT-like transcription factor STA-2 from activating defensive antimicrobial peptide gene expression. The second increases STA-2 levels in the nucleus, modifies the nucleolus, and, potentially as a consequence of a host surveillance mechanism, causes increased defence gene expression. Our results highlight the remarkably complex and potentially antagonistic mechanisms that come into play in the interaction between co-evolved hosts and pathogens.

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