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Metformin regulates cellulase production in Trichoderma reesei via calcium signaling and mitochondrial function

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Abstract Background Trichoderma reesei is renowned for its cellulase-producing ability and is used for the biofuel-production-sourced lignocellulose. In plants and fungi, cellulase production is induced by cellulose and suppressed by glucose; however, whether metformin can enhance cellulase production and mitochondrial function in T. reesei remains unclear. Metformin may reduce blood glucose levels by inhibiting hepatic gluconeogenesis; therefore, it is worth investigating whether metformin transmission modulates cellulase biosynthesis in T. reesei. Results Metformin increases cellulase activity and the transcription of cellulase-related genes. It also enhances the concentrations of Ca2+ in the cytosol and mitochondria and regulates the transcription levels of cellulase-related genes by modulating calcium homeostasis in T. reesei QM6a. In addition, metformin was identified as an antioxidant that can enhance cellulase activity by reducing reactive oxygen species (ROS). Our results demonstrated that metformin influences the state of the mitochondria by enhancing mitochondrial activity and membrane potential to promote cellulase production. Conclusion Collectively, these results indicate that metformin is a potential novel inducer that can scavenge ROS, protect mitochondrial activity, and enhance cellulase production in T. reesei.
Springer Science and Business Media LLC
Title: Metformin regulates cellulase production in Trichoderma reesei via calcium signaling and mitochondrial function
Description:
Abstract Background Trichoderma reesei is renowned for its cellulase-producing ability and is used for the biofuel-production-sourced lignocellulose.
In plants and fungi, cellulase production is induced by cellulose and suppressed by glucose; however, whether metformin can enhance cellulase production and mitochondrial function in T.
reesei remains unclear.
Metformin may reduce blood glucose levels by inhibiting hepatic gluconeogenesis; therefore, it is worth investigating whether metformin transmission modulates cellulase biosynthesis in T.
reesei.
Results Metformin increases cellulase activity and the transcription of cellulase-related genes.
It also enhances the concentrations of Ca2+ in the cytosol and mitochondria and regulates the transcription levels of cellulase-related genes by modulating calcium homeostasis in T.
reesei QM6a.
In addition, metformin was identified as an antioxidant that can enhance cellulase activity by reducing reactive oxygen species (ROS).
Our results demonstrated that metformin influences the state of the mitochondria by enhancing mitochondrial activity and membrane potential to promote cellulase production.
Conclusion Collectively, these results indicate that metformin is a potential novel inducer that can scavenge ROS, protect mitochondrial activity, and enhance cellulase production in T.
reesei.

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