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Transcriptomics reveals the regulation of the immune system of the mushroom-forming fungus Schizophyllum commune during interaction with four competitors.

Authors :
Beijen EPW
van Maanen MH
Marian IM
Klusener JX
van Roosmalen E
Herman KC
Koster MC
Ohm RA
Source :
Microbiological research [Microbiol Res] 2024 Dec; Vol. 289, pp. 127929. Date of Electronic Publication: 2024 Oct 09.
Publication Year :
2024

Abstract

Mushroom-forming fungi frequently encounter competitors during their lifecycle, but their defense mechanisms remain largely unexplored. We studied the response of the mushroom-forming fungus Schizophyllum commune during interaction with the fungal competitors Trichoderma harzianum, Trichoderma aggressivum and Purpureocillium lilacinum and the bacterial competitor Serratia quinivorans. Transcriptomics revealed 632 up-regulated genes in the direct interaction zone, which were enriched in small secreted proteins and transporters. A set of 26 genes were up-regulated during all interactions, indicating a core transcriptomic defense response. In the non-interacting edge of the mycelium of S. commune, there were 154 up-regulated genes, suggesting that there is a systemic response due to a signal that reaches unaffected areas. The GATA zinc finger transcription factor gene gat1 was up-regulated during interaction and a Δgat1 strain displayed increased colonization by T. harzianum. Previously linked to mushroom development, this transcription factor apparently has a dual role. Moreover, 138 genes were up-regulated during both interaction and mushroom development, indicating priming of the defense response during development to prepare the fruiting body for future interactions. Overall, we unveiled a defensive response of S. commune during interaction with fungal and bacterial competitors and identified a regulator of this response.<br />Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.<br /> (Copyright © 2024 The Authors. Published by Elsevier GmbH.. All rights reserved.)

Details

Language :
English
ISSN :
1618-0623
Volume :
289
Database :
MEDLINE
Journal :
Microbiological research
Publication Type :
Academic Journal
Accession number :
39413670
Full Text :
https://doi.org/10.1016/j.micres.2024.127929