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Lookup NU author(s): Dr Katharina Trunk, Dr Julien Peltier, Professor Janet Quinn, Dr Henrik Strahl von SchultenORCiD, Professor Matthias TrostORCiD
This is the authors' accepted manuscript of an article that has been published in its final definitive form by Nature Publishing Group, 2018.
For re-use rights please refer to the publisher's terms and conditions.
© 2018, The Author(s). Interactions between bacterial and fungal cells shape many polymicrobial communities. Bacteria elaborate diverse strategies to interact and compete with other organisms, including the deployment of protein secretion systems. The type VI secretion system (T6SS) delivers toxic effector proteins into host eukaryotic cells and competitor bacterial cells, but, surprisingly, T6SS-delivered effectors targeting fungal cells have not been reported. Here we show that the ‘antibacterial’ T6SS of Serratia marcescens can act against fungal cells, including pathogenic Candida species, and identify the previously undescribed effector proteins responsible. These antifungal effectors, Tfe1 and Tfe2, have distinct impacts on the target cell, but both can ultimately cause fungal cell death. ‘In competition’ proteomics analysis revealed that T6SS-mediated delivery of Tfe2 disrupts nutrient uptake and amino acid metabolism in fungal cells, and leads to the induction of autophagy. Intoxication by Tfe1, in contrast, causes a loss of plasma membrane potential. Our findings extend the repertoire of the T6SS and suggest that antifungal T6SSs represent widespread and important determinants of the outcome of bacterial–fungal interactions.
Author(s): Trunk K, Peltier J, Liu Y-C, Dill BD, Walker L, Gow NAR, Stark MJR, Quinn J, Strahl H, Trost M, Coulthurst SJ
Publication type: Article
Publication status: Published
Journal: Nature Microbiology
Year: 2018
Volume: 3
Pages: 920-931
Online publication date: 23/07/2018
Acceptance date: 07/06/2018
Date deposited: 23/08/2018
ISSN (electronic): 2058-5276
Publisher: Nature Publishing Group
URL: https://doi.org/10.1038/s41564-018-0191-x
DOI: 10.1038/s41564-018-0191-x
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