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9SF2

Phage Phi106 repressor in complex with AimX

Summary for 9SF2
Entry DOI10.2210/pdb9sf2/pdb
Related9IAQ
DescriptorTranscriptional regulator, Bacillus phage phi106 antirepressor, ZINC ION, ... (7 entities in total)
Functional Keywordsphage repressor, antirepressor, viral protein
Biological sourceBacillus
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Total number of polymer chains2
Total formula weight18987.77
Authors
Marina, A.,Martinez Alonso, C.,Gallego del Sol, F. (deposition date: 2025-08-19, release date: 2026-01-14, Last modification date: 2026-02-25)
Primary citationKabel, S.,Omer Bendori, S.,Borenstein, T.,Guler, P.,Martinez-Alonso, C.,Mancheno-Bonillo, J.,Gallego-Del-Sol, F.,Marina, A.,Eldar, A.
A widespread extended arbitrium system controls lysis/lysogeny through antirepression.
Cell Host Microbe, 34:278-, 2026
Cited by
PubMed Abstract: Many temperate Bacillus phages use the arbitrium peptide-based signaling system to regulate lysis-lysogeny decisions. In this system, the secreted AimP peptide inhibits the AimR receptor to promote lysogeny. However, the downstream mechanism of AimR-mediated lysis control remains unclear for most systems. Here, we identify that ∼75% of arbitrium systems possess an extended five-gene module, including the aimX, aimC, and aimL genes. AimX encodes a small AimR-regulated antirepressor protein that binds the phage repressor AimC, preventing its oligomerization and DNA binding, thereby activating the pro-lytic aimL gene and additional lytic genes. This mechanism was validated across multiple phages and structurally characterized, revealing that AimX mimics the AimC oligomerization domain to prevent oligomerization and inhibit repressor function. These findings elucidate the predominant molecular strategy by which arbitrium systems control phage lysis-lysogeny transitions and highlight the central role of small proteins in phage decision-making.
PubMed: 41619737
DOI: 10.1016/j.chom.2026.01.007
PDB entries with the same primary citation
Experimental method
X-RAY DIFFRACTION (1.7 Å)
Structure validation

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PDB entries from 2026-03-11

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