Antagonistic fungal enterotoxins intersect at multiple levels with host innate immune defences

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 strategie...

Full description

Saved in:
Bibliographic Details
Published in:PLoS genetics 2021-06, Vol.17 (6), p.e1009600-e1009600
Main Authors: Zhang, Xing, Harding, Benjamin W, Aggad, Dina, Courtine, Damien, Chen, Jia-Xuan, Pujol, Nathalie, Ewbank, Jonathan J
Format: Article
Language:English
Subjects:
Antimicrobial peptides
Biochemistry, Molecular Biology
Biology and Life Sciences
Coevolution
Enterotoxins
Epidermis
Gene expression
Genomes
Genomics
Host-parasite relationships
Immune response
Immune system
Immunology
Infections
Innate immunity
Kinases
Life Sciences
Medicine and Health Sciences
Microbiological research
Microbiology and Parasitology
Microscopy
Mycology
Nucleoli
Pathogens
People and Places
Peptides
Physiological aspects
Plasmids
Proteins
Research and Analysis Methods
Toxins
Tropical diseases
Virulence
Virulence factors
Whooping cough
Worms
Young adults
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary: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.
ISSN:1553-7404
1553-7390
1553-7404
DOI:10.1371/journal.pgen.1009600