Multi-omics analysis reveals Protein Kinase A-associated regulatory remodeling during adaptation of Trichoderma reesei to lignocellulosic substrate.

Authors

Hermano Zenaide-Neto, Wellington Ramos Pedersoli, David Batista Maués, Lucas Matheus Soares Pereira, Iasmin Cartaxo Taveira, Thiago de Andrade Simon, Andrei S Steindorff, Vitor Marcel Faça, Renato Graciano de Paula, Roberto N Silva

Published in

World journal of microbiology & biotechnology. Volume 42. Issue 9. Sep 08, 2026. Epub Sep 08, 2026.

Abstract

The filamentous fungus Trichoderma reesei is a major industrial source of holocellulolytic enzymes, and its response to complex carbon sources is regulated by nutrient-sensing mechanisms, including the cyclic adenosine monophosphate (cAMP)-protein kinase A (PKA) signaling pathway. Here, we integrated transcriptomics, quantitative proteomics, and phosphoproteomics to analyze PKAc1-associated responses in the parental strain QM9414 and a Δpkac1 strain cultivated under glucose or sugarcane bagasse conditions. Deletion of pkac1 was associated with altered growth-related phenotypes and reduced extracellular activities of selected biomass-depolymerizing enzymes. Multi-omics profiling revealed condition-dependent changes affecting subsets of carbohydrate-active enzymes (CAZymes) genes and proteins, nutrient transporters, stress-associated proteins, and regulatory factors. Phosphoproteomics identified phosphorylation-state changes associated with pkac1 deletion, including reduced phosphorylation at sites enriched for the PKA consensus motif. In silico peptide docking was used to prioritize candidate PKAc1-associated substrates for future validation, including a Sec 7-derived peptide with favorable docking behavior relative to the control peptide. Together, these data support a working model in which PKAc1 contributes to regulatory and phosphorylation-state remodeling during adaptation to sugarcane bagasse, with effects on the magnitude and/or timing of selected CAZyme-related outputs in T. reesei.

PMID:
42706388
Bibliographic data and abstract were imported from PubMed on 08 Sep 2026.

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