Microbial communication can drive coordinated functions through sensing, analyzing and processing signal information, playing critical roles in biomanufacturing and life evolution. However, it is still a great challenge to develop effective methods to construct a microbial communication system with coordinated behaviors. Here, we report an electron transfer triggered redox communication network consisting of three building blocks including signal router, optical verifier and bio-actuator for microbial metabolism regulation and coordination. In the redox communication network, the Fe/Fe redox signal can be dynamically and reversibly transduced, channeling electrons directly and specifically into bio-actuator cells through iron oxidation pathway. The redox communication network drives gene expression of electron transfer proteins and simultaneously facilitates the critical reducing power regeneration in the bio-actuator, thus enabling regulation of microbial metabolism. In this way, the redox communication system efficiently promotes the biomanufacturing yield and CO fixation rate of bio-actuator. Furthermore, the results demonstrate that this redox communication strategy is applicable both in co-culture and microbial consortia. The proposed electron transfer triggered redox communication strategy in this work could provide an approach for reducing power regeneration and metabolic optimization and could offer insights into improving biomanufacturing efficiency.
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http://dx.doi.org/10.1038/s41467-023-42561-3 | DOI Listing |
Alzheimers Dement
December 2024
Neuroscience Graduate Program, Weill Cornell Medicine, New York, NY, USA.
Background: Mitochondrial reactive oxygen species (mROS), such as superoxide and hydrogen peroxide (HO), are implicated in aging-associated neurological disorders, including Alzheimer's Disease and frontotemporal dementia. Mitochondrial complex III of the respiratory chain has the highest capacity for mROS production and generates mROS toward the cytosol, poising it to regulate intracellular signaling and disease mechanisms. However, the exact triggers of complex III-derived ROS (CIII-ROS), its downstream molecular targets, and its functional roles in dementia-related pathogenesis remain unclear.
View Article and Find Full Text PDFBiosens Bioelectron
December 2024
Cnam, SATIE Laboratory, UMR, CNRS 8029, 292 rue Saint Martin, 75003, Paris, France. Electronic address:
This study aims to demonstrate that redox couples, regardless of their electrical charges, are unnecessary for detecting and quantifying electroactive proteins using an electrochemical sensor functionalized with a molecularly imprinted polymer. Our approach involved designing a polydopamine imprinted biosensor for detecting bovine serum albumin as the model protein. Electrochemical measurements were conducted in a phosphate-buffered solution (PBS) and solutions containing the negatively charged hexacyanoferrate, the neutral ferrocene, or the positively charged hexaammineruthenium (III) probes.
View Article and Find Full Text PDFFront Pharmacol
December 2024
Department of Medical Biochemistry, School of Medicine, Koc University, Istanbul, Türkiye.
Aging is influenced by cellular senescence mechanisms that are associated with oxidative stress. Oxidative stress is the imbalance between antioxidants and free radicals. This imbalance affects enzyme activities and causes mitochondrial dysfunction.
View Article and Find Full Text PDFBMJ Open
December 2024
Division of Endocrinology, Metabolism, and Lipids; Department of Medicine, Emory University School of Medicine, Atlanta, Georgia, USA
Introduction: People with cystic fibrosis (PwCF) are at high risk for developing cystic fibrosis (CF)-related diabetes (CFRD), which worsens morbidity and mortality. Although the pathological events leading to the development of CFRD are complex and not completely understood, dietary factors may play a role. For example, habitual intake of dietary added sugar (i.
View Article and Find Full Text PDFRedox Biol
December 2024
Baruch College and CUNY Graduate Center, 1 Baruch Way, New York, NY, 10010, USA. Electronic address:
The elevated emission of reactive oxygen species (ROS) from presynaptic mitochondria is well-documented in several inflammatory and neurodegenerative diseases. However, the potential role of mitochondrial ROS in presynaptic function and plasticity remains largely understudied beyond the context of disease. Here, we investigated this potential ROS role in presynaptic function and short-term plasticity by combining optogenetics, whole cell electrophysiological recordings, and live confocal imaging using a well-established protocol for induction and measurement of synaptic potentiation in Drosophila melanogaster neuromuscular junctions (NMJ).
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