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Girych, M.

Publications and source records attributed to Girych, M..

3 recordsLinked to original sources

Protease suppression by native I9 inhibitor improves recombinant protein production in Trichoderma reesei

Microbes are powerful cell factories for making molecules that are difficult or impossible to produce by other means. Filamentous fungi such as Trichoderma reesei are superior hosts for recombinant protein production, yet secreted proteases often degrade target proteins, reducing yields and limiting process robustness. Preventing proteolysis without relying on expensive commercial inhibitors or compromising strain fitness has been a longstanding challenge in fungal biotechnology, particularly for scaling up production to industrially relevant levels. Here, we report the identification of a native inhibitory protein from T. reesei, TrI9, and show that directing its secretion into the culture medium markedly reduces extracellular protease activity and enables production of the highly protease-sensitive spider silk-like protein CBM-AQ12-CBM, which could be used in high-performance biomaterials. Computational and in vitro analyses provide mechanistic insight, showing that TrI9 functions as a multi-target inhibitor of subtilisin-like proteases (SLPs), including SLP2, a protease that cannot be eliminated by gene deletion due to its crucial role in normal growth and development. This TrI9-based strategy for protease mitigation presents a novel approach for strain improvement, protecting a wide range of protease-labile products beyond silk proteins during large-scale fermentation. Protecting sensitive proteins without added inhibitors offers a cost-effective alternative for scaling up protein production across multiple applications, from protein-based materials manufacturing to pharmaceuticals, as well as enzyme and food applications. SignificanceThe discovery and characterization of an independently encoded I9 inhibitor (TrI9) in the filamentous fungus Trichoderma reesei reveals a new layer of biological regulation of subtilisin-like protease activity in fungi. We show that overexpressing and secreting TrI9 into the culture supernatant can suppress extracellular proteolysis, including activity from the essential SLP2 protease thereby overcoming a major barrier to production of protease-sensitive recombinant proteins without compromising strain fitness. For industrial biomanufacturing, this translates into higher effective titers, more consistent product integrity and reduced reliance on costly commercial protease inhibitors, hence, improving process robustness and economics. As a broadly applicable strain-and-process strategy, TrI9-enabled protease control strengthens T. reesei as a scalable platform for precision fermentation of diverse, otherwise hard-to-produce proteins.

bioengineering↗

Metabolic control of enteroendocrine cell fate through a redox state sensor CtBP

Enteroendocrine (EE) cells monitor the intestinal nutrient composition and consequently control organismal physiology through hormonal signaling. In addition to the immediate effects on hormone secretion, nutrients influence EE cell abundance by affecting the determination and maintenance of cell fate. EE cells are known to import and respond to dietary sugars, but how the sugar-induced changes in the intracellular metabolic state are sensed to control the immediate and long-term responses of EE cells, remains poorly understood. We report that the NADH binding transcriptional cofactor C-terminal binding protein (CtBP) acts at the interface between nutrient sensing and fate regulation of Drosophila larval EE cells, thus controlling organismal energy metabolism and survival on a high sugar diet. CtBP dimerization in EE cells is regulated through the redox balance of nicotinamide cofactors controlled by glycolysis and pentose phosphate pathway, allowing EE cells sense their internal metabolic state in response to sugar catabolism. CtBP interacts with the EE cell fate determining transcription factor Prospero through a conserved binding motif and binds to genomic targets controlling EE cell fate and size, such as components of Notch and insulin/mTOR pathways. Collectively, our findings uncover a modality where changes in intracellular redox state serve as an instructive signal to control EE cell function to globally control organismal homeostasis. GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=109 SRC="FIGDIR/small/662346v1_ufig1.gif" ALT="Figure 1"> View larger version (32K): org.highwire.dtl.DTLVardef@3baaeorg.highwire.dtl.DTLVardef@d505edorg.highwire.dtl.DTLVardef@178361dorg.highwire.dtl.DTLVardef@128e210_HPS_FORMAT_FIGEXP M_FIG C_FIG

physiology↗

Antidepressants act by binding to the cholesterol-interaction site at TRKB neurotrophin receptor

It is unclear how binding of antidepressant drugs to their targets gives rise to the clinical antidepressant effect. We discovered that the transmembrane domain of TRKB, the brain-derived neurotrophic factor (BDNF) receptor that promotes neuronal plasticity and antidepressant responses, has a cholesterol-sensing function that mediates synaptic effects of cholesterol. We then found that both typical and fast-acting antidepressants directly bind to TRKB, thereby facilitating synaptic localization of TRKB and its activation by BDNF. Extensive computational approaches including atomistic molecular dynamics simulations revealed a binding site at the transmembrane region of TRKB dimers. Mutation of the TRKB antidepressant-binding motif impaired cellular, behavioral and plasticity-promoting responses to antidepressants in vitro and in vivo. We suggest that binding to TRKB and the allosteric facilitation of BDNF signaling is the common mechanism for antidepressant action, which proposes a framework for how molecular effects of antidepressants are translated into clinical mood recovery.

neuroscience↗