ArticleNature communications2026
Phage portal proteins counteract stringent-response-mediated restriction.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- When phage restriction is not immunity: Immune gates, replication-niche barriers, and assay-limited phenotypes.Engineering microbiology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Bacteria restrict viral replication not only through dedicated defense systems but also by entering physiological states that limit cellular resources, yet how phages overcome such host-imposed barriers remains unclear. The stringent response, driven by the alarmone nucleotides ppGpp and pppGpp, can impose a growth-restrictive state that hinders phage infection in specific phage-host contexts. Here, we show that alarmone signaling constrains bacteriophage T7 infection and that the portal protein Gp8 counteracts this barrier by engaging RelA and SpoT, inhibiting their synthetase activities and suppressing alarmone accumulation. Portal mutations that disrupt this interaction sustain alarmone elevation, delay lysis and impair replication in a manner relieved in alarmone-deficient hosts. Portal proteins from representative coliphages share related stringent-response-linked features, indicating that essential virion components can moonlight as antagonists of host stress physiology and that this mechanism is not unique to T7 and may extend to additional coliphages.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.