期刊
NATURE COMMUNICATIONS
卷 11, 期 1, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41467-020-16249-x
关键词
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资金
- DTRA [HDTRA1-19-0021]
- NSF (DMREF) [1435957]
- NSF (ECCS) [1807604]
- NSF (CBET) [1805274]
- National Institutes of Health [R21EB024102]
- Agilent, Inc.
- Directorate For Engineering
- Div Of Chem, Bioeng, Env, & Transp Sys [1805274] Funding Source: National Science Foundation
- Directorate For Engineering
- Div Of Electrical, Commun & Cyber Sys [1807604] Funding Source: National Science Foundation
Electronic information can be transmitted to cells directly from microelectronics via electrode-activated redox mediators. These transmissions are decoded by redox-responsive promoters which enable user-specified control over biological function. Here, we build on this redox communication modality by establishing an electronic eCRISPR conduit of information exchange. This system acts as a biological signal processor, amplifying signal reception and filtering biological noise. We electronically amplify bacterial quorum sensing (QS) signaling by activating LasI, the autoinducer-1 synthase. Similarly, we filter out unintended noise by inhibiting the native SoxRS-mediated oxidative stress response regulon. We then construct an eCRISPR based redox conduit in both E. coli and Salmonella enterica. Finally, we display eCRISPR based information processing that allows transmission of spatiotemporal redox commands which are then decoded by gelatin-encapsulated E. coli. We anticipate that redox communication channels will enable biohybrid microelectronic devices that could transform our abilities to electronically interpret and control biological function. Redox-responsive transcriptional regulators can enable user-specified electronic control over biological functions. Here the authors demonstrate electronic control of CRISPRa and CRISPRi using redox signalling.
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