Manganese activates the CBASS immunity to protect bacteria from phage infection

Bacteriophages pose a persistent threat to bacterial survival, driving the evolution of diverse antiviral systems, including the cyclic-oligonucleotide-based antiphage signaling system (CBASS) immunity. Here, we reveal that manganese (Mn<sup>2+</sup>) acts as a pivotal cofactor for CBASS, directly enhancing the activity of the cGAS-like cyclase DncV to generate 3'3'-cGAMP, which, in turn, activates the phospholipase CapV. This Mn<sup>2+</sup>-driven DncV activation induces rapid bacterial cell death, thereby limiting phage replication. These findings underscore a striking parallel with mammalian cGAS-STING, where Mn<sup>2+</sup> likewise amplifies antiviral responses. By illuminating the importance of Mn<sup>2+</sup> homeostasis in bacterial phage resistance, our study broadens the understanding of bacterial innate immunity and highlights a deeply conserved mechanism across prokaryotes and eukaryotes.

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Publication Details

Journal
mBio
Published
2025-12-08
DOI
https://doi.org/10.1128/mbio.02758-25
Citations
1
Primary Topic
interferon and immune responses
Type
article
Field-Weighted Citation Impact
0.80
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article

Manganese activates the CBASS immunity to protect bacteria from phage infection

Hongxia Ni, Chonghua Hao, Miaoxing Liu, Xinwei Hao et al.
1 citations
mBio
interferon and immune responses
0.80
article

Manganese activates the CBASS immunity to protect bacteria from phage infection

Hongxia Ni, Chonghua Hao, Miaoxing Liu, Xinwei Hao, Conghui Wu, Song Li, Xihui Shen, Shukun Chen, Xiao Wang, Wenjing Zhang, Xiao Wang, Yongdong Li, Lei Xu, Yi Chen, Tianyuan Chang
article en
1 citations

Abstract

Bacteriophages pose a persistent threat to bacterial survival, driving the evolution of diverse antiviral systems, including the cyclic-oligonucleotide-based antiphage signaling system (CBASS) immunity. Here, we reveal that manganese (Mn<sup>2+</sup>) acts as a pivotal cofactor for CBASS, directly enhancing the activity of the cGAS-like cyclase DncV to generate 3'3'-cGAMP, which, in turn, activates the phospholipase CapV. This Mn<sup>2+</sup>-driven DncV activation induces rapid bacterial cell death, thereby limiting phage replication. These findings underscore a striking parallel with mammalian cGAS-STING, where Mn<sup>2+</sup> likewise amplifies antiviral responses. By illuminating the importance of Mn<sup>2+</sup> homeostasis in bacterial phage resistance, our study broadens the understanding of bacterial innate immunity and highlights a deeply conserved mechanism across prokaryotes and eukaryotes.

mBioVol. 17(1)
Shanxi Medical University (CN), Agriculture and Forestry University (NP), North West Agriculture and Forestry University (CN), Ningbo Center for Disease Control and Prevention (CN), Northwest A&F University (CN)
Openalex Percentile: Top 21%
interferon and immune responses
0.80
DOIOpen Access PDFOpenAlex
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