Ontology highlight
ABSTRACT:
PROVIDER: PRJNA690982 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR13396628_1.fastq.gz | Fastqsanger.gz | |||
| SRR13396628_2.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 3 of 3 |
Similar Datasets
Project description:Isolation of lytic bacteriophage vB_Fpr_FP01
| PRJEB102423 | ENA
Project description:Isolation of lytic bacteriophage vB_Fpr_FP01
| PRJEB102752 | ENA
Project description:The choice between cell death (lysis) and viral dormancy (lysogeny) following bacteriophage infection serves as a founding paradigm for the emergence of cellular heterogeneity in a genetically uniform population. The determination of host fate arises through the stochastic transcription from multiple viral genomes present within each cell, but this activity remains hidden from empirical interrogation, which typically stops at the whole-cell level. Here we use parallel sequential fluorescence in situ hybridization (par-seqFISH), followed by spatial clustering of phage-encoded transcripts within each cell, to profile the transcriptional activity of individual phages during synchronized infection of Escherichia coli (E. coli) by bacteriophage lambda. At the whole-cell level, transcription kinetics capture the developmental choice between lysis and lysogeny, and further demonstrate that viral replication is required for the emergence of diverging fate decisions. Zooming in to the single-phage level illuminates an individuality of viral activity during infection. We find that, while cells pursuing lysogeny display consensus activity of all in-habiting phages, lytic cells may contain phages that exhibit lysogenic activity. These findings support an earlier suggestion that consensus among coinfecting phages is required for cell dormancy. More broadly, our results highlight the need to identify how whole-cell behavior emerges from the activity of physically distinct copies of the same genetic circuit.
2026-04-30 | GSE308589 | GEO
Project description:LUZ19 is a lytic Pseudomonas aeruginosa bacteriophage of the family Autographivirinae, of phages with short tails. We determined the structure of the LUZ19 virion using cryo-electron microscopy and visualized its attachment to host cells by cryo-electron tomography.
2026-05-25 | PXD074244 | Pride
Project description:Mucin hypersecretion, a hallmark of chronic respiratory diseases (CRD), creates a complex microenvironment that reshapes host immunity and microbial behavior. However, its impact on bacteriophage therapy remains poorly understood. Here, we demonstrate that, despite reducing Pseudomonas aeruginosa internalization, mucin increases bacterial-induced cytotoxicity and inflammation in airway epithelial cells, while driving CRD-like transcriptional changes, including hypoxia and stress responses. Mucin selectively downregulates virulence factors without impairing bacterial growth. P. aeruginosa-infecting bacteriophage DMS3vir retained full lytic activity in mucin-rich conditions and, in synergy with mucin, enhanced epithelial cells protection against cytotoxicity. DMS3vir also reduced IL-8 gene expression without triggering antiviral responses. Furthermore, mucin shaped phage-resistant P. aeruginosa phenotypes, altering pigmentation, pigmentation, pyocyanin production, and motility. These changes influenced virulence trade-offs. These findings uncover the dual role of mucins as modulators of infection and sensitizers to phage protection, paving the way for optimized, mucosa-adapted phage therapies in chronic lung diseases.
2025-10-19 | GSE307737 | GEO