23or
Cryo-EM structure of the Retron-Eco8-SSB complex
Structural highlights
FunctionRT8_ECOLX Reverse transcriptase (RT) component of antiviral defense system retron Eco8, composed of this RT, the following endonuclease and a non-coding RNA (ncRNA) encoded between them. Expression of retron Eco8 confers protection against bacteriophages T4, T6, T7 and SECphi4, SECphi6 and SECphi18. At multiplicity of infection (MOI) of 0.02 cultures slow growth when infected with SECphi4 but do not collapse, at MOI 2 cultures collapse. Responsible for synthesis of msDNA (a branched molecule with RNA linked by a 2',5'-phosphodiester bond to ssDNA). The retron transcript serves as primer (from a conserved internal G residue) and template for the reaction, and codes for the RT.[1] Publication Abstract from PubMedThe Retron-Eco8 system, comprising a reverse transcriptase (RT), a non-coding RNA (ncRNA), and an OLD-family nuclease effector, protects bacteria from phage infection via abortive infection upon sensing a phage single-stranded DNA-binding protein (SSB). However, the molecular basis of this immunity remained unclear. Here, we report cryo-electron microscopy (cryo-EM) structures of Retron-Eco8 in inactive and activated states, revealing mechanisms of phage-triggered activation and effector function. Retron-Eco8 assembles into a tetrameric complex in which each protomer contains an RT, msrRNA-msdDNA duplex, and effector in an autoinhibited conformation. Upon phage infection, phage SSB binds msdDNA, relieving autoinhibition and activating the nuclease effector to degrade both phage and host DNA, triggering cell death to block phage propagation. Host SSB fails to activate the system, while DNA binding and oligomerization of phage SSB are essential for this activation, highlighting its specificity. These findings elucidate the molecular mechanism of Retron-Eco8-mediated immunity, facilitating retron-based biotechnological applications. Mechanistic insights into activation of bacterial Retron-Eco8 immunity by phage protein SSB.,Ji CG, Li Z, Wei XY, Li Y, Zhang JT, Liu X, Jia N Nat Commun. 2026 Jun 10. doi: 10.1038/s41467-026-74106-9. PMID:42270618[2] From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine. References
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