# MTBLS13411

From MetaboLights, see:
[www.ebi.ac.uk/metabolights/editor/MTBLS13411](https://www.ebi.ac.uk/metabolights/editor/MTBLS13411/files)

Supports differential analysis, except ANCOVA as no covariates are available.

```python
factor = 'Factor Value[Strain type]'
group = 'group' # was generated based on sample names
```

Processed data files available:

| File type | Filename                      |
| --------- | ----------------------------- |
| omics     | MTBLS13411_processed_data.csv |
| metadata  | MTBLS13411_meta_data.csv      |

## Abstract

MTBLS13411: Comparative Transcriptome and Energy Metabolome Profiling Unravel the Key
Role of GlcN6P Metabolic Pathway in Resistance against Bacteriophage in
Enterotoxigenic Escherichia coli

The rapid emergence of phage-resistant bacterial mutants is a major challenge for phage
application in the food industry. The resistance mechanisms of Enterotoxigenic E. coli 
ETEC) against phage infection are largely unknown. In Escherichia coli, RapZ regulates
glucosamine-6-phosphate (GlcN6P) metabolism, the formation of which initiates synthesis
of the bacterial cell envelope, including lipopolysaccharides (LPS). Previously, RapZ
mediated phage-resistant mutants WRP and rapZE227Stop were identified in a phage aerosol
spray assay. In this study, comparative transcriptomic and energy metabolomic analyses
showed that the differentially expressed genes and differentially accumulated metabolites
from WRP and rapZE227Stop were mostly enriched in metabolic pathways, mainly in GlcN6P
biosynthesis. Additionally, GlcN6P biosynthesis-related gene expression was significantly
upregulated or downregulated in phage-resistant mutants compared to that in wild type (WT).
Some metabolites involved in GlcN6P metabolic pathways, such as GlcN6P, GlcNAc-6P,
GlcNAc-1P and UDP-GlcNAc were upregulated in phage-resistant mutants. Furthermore,
the reduction in LPS content and the resensitization to antibiotics reveal the
important role of the GlcN6P metabolic pathway in RapZ mediated phage resistance.
These results suggest that GlcN6P metabolic pathways play important roles in ETEC 
resistance to phage infection and provide useful insights for developing phage
based applications.
