ArticleG3 (Bethesda, Md.)2024
Characterization of mycobacteriophage Adephagia cytotoxic proteins.
Article in G3 (Bethesda, Md.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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
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Who cites it
4 citing papers in PubMed.
- Mycobacteriophage Adephagia gp48 inhibits essential host cell wall biosynthesis enzyme mannose-1-phosphate guanylyltransferase.bioRxiv : the preprint server for biology · 2026Article
- A systematic overexpression screen identifies cytotoxic genes encoded by the Cluster L1 mycobacteriophage LeBron.G3 (Bethesda, Md.) · 2026Article
- Genome-wide screen overexpressing mycobacteriophage Amelie genes identifies multiple inhibitors of mycobacterial growth.G3 (Bethesda, Md.) · 2025Article
- The HicAB System: Characteristics and Biological Roles of an Underappreciated Toxin-Antitoxin System.International journal of molecular sciences · 2024Review
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Mycobacterium phage Adephagia is a cluster K phage that infects Mycobacterium smegmatis and some strains of Mycobacterium pathogens. Adephagia has a siphoviral virion morphology and is temperate. Its genome is 59,646 bp long and codes for one tRNA gene and 94 predicted protein-coding genes; most genes not associated with virion structure and assembly are functionally ill-defined. Here, we determined the Adephagia gene expression patterns in lytic and lysogenic growth and used structural predictions to assign additional gene functions. We characterized 66 nonstructural genes for their toxic phenotypes when expressed in M. smegmatis, and we show that 25 of these (38%) are either toxic or strongly inhibit growth, resulting in either reduced viability or small colony sizes. Some of these genes are predicted to be involved in DNA metabolism or regulation, but others are of unknown function. We also characterize the HicAB-like toxin-antitoxin (TA) system encoded by Adephagia (gp91 and gp90, respectively) and show that the gp90 antitoxin is lysogenically expressed, abrogates gp91 toxicity, and is required for normal lytic and lysogenic growth.
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Registered trials
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