In:
PLOS ONE, Public Library of Science (PLoS), Vol. 16, No. 12 ( 2021-12-31), p. e0262180-
Abstract:
Trichoderma atroviride (Ascomycota, Sordariomycetes) is a well-known mycoparasite applied for protecting plants against fungal pathogens. Its mycoparasitic activity involves processes shared with plant and human pathogenic fungi such as the production of cell wall degrading enzymes and secondary metabolites and is tightly regulated by environmental cues. In eukaryotes, the conserved Target of Rapamycin (TOR) kinase serves as a central regulator of cellular growth in response to nutrient availability. Here we describe how alteration of the activity of TOR1, the single and essential TOR kinase of T . atroviride , by treatment with chemical TOR inhibitors or by genetic manipulation of selected TOR pathway components affected various cellular functions. Loss of TSC1 and TSC2, that are negative regulators of TOR complex 1 (TORC1) in mammalian cells, resulted in altered nitrogen source-dependent growth of T . atroviride , reduced mycoparasitic overgrowth and, in the case of Δ tsc1 , a diminished production of numerous secondary metabolites. Deletion of the gene encoding the GTPase RHE2, whose mammalian orthologue activates mTORC1, led to rapamycin hypersensitivity and altered secondary metabolism, but had an only minor effect on vegetative growth and mycoparasitic overgrowth. The latter also applied to mutants missing the npr1-1 gene that encodes a fungus-specific kinase known as TOR target in yeast. Genome-wide transcriptome analysis confirmed TOR1 as a regulatory hub that governs T . atroviride metabolism and processes associated to ribosome biogenesis, gene expression and translation. In addition, mycoparasitism-relevant genes encoding terpenoid and polyketide synthases, peptidases, glycoside hydrolases, small secreted cysteine-rich proteins, and G protein coupled receptors emerged as TOR1 targets. Our results provide the first in-depth insights into TOR signaling in a fungal mycoparasite and emphasize its importance in the regulation of processes that critically contribute to the antagonistic activity of T . atroviride .
Type of Medium:
Online Resource
ISSN:
1932-6203
DOI:
10.1371/journal.pone.0262180
DOI:
10.1371/journal.pone.0262180.g001
DOI:
10.1371/journal.pone.0262180.g002
DOI:
10.1371/journal.pone.0262180.g003
DOI:
10.1371/journal.pone.0262180.g004
DOI:
10.1371/journal.pone.0262180.g005
DOI:
10.1371/journal.pone.0262180.g006
DOI:
10.1371/journal.pone.0262180.g007
DOI:
10.1371/journal.pone.0262180.g008
DOI:
10.1371/journal.pone.0262180.s001
DOI:
10.1371/journal.pone.0262180.s002
DOI:
10.1371/journal.pone.0262180.s003
DOI:
10.1371/journal.pone.0262180.s004
DOI:
10.1371/journal.pone.0262180.s005
DOI:
10.1371/journal.pone.0262180.s006
DOI:
10.1371/journal.pone.0262180.s007
DOI:
10.1371/journal.pone.0262180.s008
DOI:
10.1371/journal.pone.0262180.s009
DOI:
10.1371/journal.pone.0262180.s010
DOI:
10.1371/journal.pone.0262180.s011
DOI:
10.1371/journal.pone.0262180.s012
DOI:
10.1371/journal.pone.0262180.s013
Language:
English
Publisher:
Public Library of Science (PLoS)
Publication Date:
2021
detail.hit.zdb_id:
2267670-3
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