Passive abortive infection mechanisms targeting phage long tail fiber proteins

Abstract

Bacteria employ diverse defense strategies against phage infection, yet mechanisms directly targeting viral proteins remain scarcely documented. In this study, we characterize two bacterial defense systems: TFAD1 featuring a serine protease and TFAD2 featuring a Ser/Thr kinase. We show that TFAD1 and TFAD2 act on phage long tail fiber proteins via protein degradation and phosphorylation, respectively. Intriguingly, both systems allow complete phage replication cycles but generate non-infective progeny—a mechanism distinct from classical abortive infection (Abi), which we term “passive Abi”. Our findings expand the paradigm of bacterial immunity by unveiling protease- and kinase-mediated incapacitation of phage structural proteins, offering insights into the molecular arms race between bacteria and phages.

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BibTeX RIS

BibTeX

@article{cheng2026passive,
  title = {{Passive abortive infection mechanisms targeting phage long tail fiber proteins}},
  author = {Jie Cheng and Hongfan Zhai and Rui Sun and Ting Liu and Qiang Chen and Yamei Yu},
  journal = {Nature Communications},
  year = {2026},
  month = oct,
  doi = {10.1038/s41467-026-78794-1},
  url = {https://www.nature.com/articles/s41467-026-78794-1},
  note = {CC BY 4.0},
}

RIS

TY  - JOUR
TI  - Passive abortive infection mechanisms targeting phage long tail fiber proteins
AU  - Jie Cheng
AU  - Hongfan Zhai
AU  - Rui Sun
AU  - Ting Liu
AU  - Qiang Chen
AU  - Yamei Yu
PY  - 2026
DA  - 2026/10/19
JO  - Nature Communications
DO  - 10.1038/s41467-026-78794-1
UR  - https://www.nature.com/articles/s41467-026-78794-1
AB  - Bacteria employ diverse defense strategies against phage infection, yet mechanisms directly targeting viral proteins remain scarcely documented. In this study, we characterize two bacterial defense systems: TFAD1 featuring a serine protease and TFAD2 featuring a Ser/Thr kinase. We show that TFAD1 and TFAD2 act on phage long tail fiber proteins via protein degradation and phosphorylation, respectively. Intriguingly, both systems allow complete phage replication cycles but generate non-infective progeny—a mechanism distinct from classical abortive infection (Abi), which we term “passive Abi”. Our findings expand the paradigm of bacterial immunity by unveiling protease- and kinase-mediated incapacitation of phage structural proteins, offering insights into the molecular arms race between bacteria and phages.
SN  - 2041-1723
ER  -

Abstract

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