Transcriptomic insights into the effects of sublethal exposure to endolysin LNT113 on Escherichia coli
- 1Department of Molecular Science and Technology, Ajou University, Suwon 16499, Republic of Korea
- 2Division of Food Technology and Nutrition, Sun Moon University, Asan 31460, Republic of Korea
- 3College of Advanced Bio-Convergence Engineering, Ajou University, Suwon 16499, Republic of Korea
Abstract
The global rise of multidrug-resistant bacteria poses a critical threat to public health, and bacteriophage-derived endolysins have emerged as promising alternatives to conventional antibiotics. The engineered endolysin LNT113, derived from the Escherichia coli phage PBEC131 endolysin EC340, exhibits potent lytic activity against Gram-negative bacteria. This study investigated the transcriptomic responses of E. coli to sublethal LNT113 stress and identified genetic determinants required for bacterial adaptation to endolysin-induced stress. Transcriptomic analysis identified 552 differentially expressed genes (DEGs) following sublethal LNT113 exposure. Thirteen DEGs associated with stress response and envelope maintenance were individually deleted to generate thirteen mutant strains and to functionally evaluate their roles in bacterial stress tolerance. Among these, the ΔfabB and Δ(prmB–yfcL) mutants exhibited significantly reduced survival under sublethal LNT113 exposure, indicating increased susceptibility to the endolysin. Regarding the prmB–yfcL operon, individual genes were deleted to determine the gene critical for bacterial tolerance. Deletion of aroC and mepA rendered E. coli more susceptible to LNT113. Furthermore, 1-N-phenylnaphthylamine uptake assays demonstrated increased membrane permeability in the ΔfabB, ΔaroC, and ΔmepA mutants. Complementation with pWSK129::fabB, pWSK129::aroC, and pWSK129::mepA restored membrane integrity in the respective mutant strains. These findings suggest that fabB-mediated unsaturated fatty acid biosynthesis and mepA-dependent peptidoglycan remodeling are critical for maintaining envelope integrity under endolysin stress, whereas aroC may indirectly support bacterial tolerance to LNT113 via metabolic adaptation. This study provides insights into bacterial responses to LNT113 and offers a foundation for optimizing endolysin-based therapeutic strategies.
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BibTeX
@article{song2026transcriptomic,
title = {{Transcriptomic insights into the effects of sublethal exposure to endolysin LNT113 on Escherichia coli}},
author = {Heymin Song and Nanjoo Park and Eunsuk Kim and Seowon Jang and Sunghoon Kim and Jeongik Cho and Hyunjin Yoon},
journal = {The Journal of Microbiology},
year = {2026},
month = jul,
doi = {10.71150/jm.2605009},
url = {https://doi.org/10.71150/jm.2605009},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Transcriptomic insights into the effects of sublethal exposure to endolysin LNT113 on Escherichia coli
AU - Heymin Song
AU - Nanjoo Park
AU - Eunsuk Kim
AU - Seowon Jang
AU - Sunghoon Kim
AU - Jeongik Cho
AU - Hyunjin Yoon
PY - 2026
DA - 2026/07/31
JO - The Journal of Microbiology
DO - 10.71150/jm.2605009
UR - https://doi.org/10.71150/jm.2605009
AB - The global rise of multidrug-resistant bacteria poses a critical threat to public health, and bacteriophage-derived endolysins have emerged as promising alternatives to conventional antibiotics. The engineered endolysin LNT113, derived from the Escherichia coli phage PBEC131 endolysin EC340, exhibits potent lytic activity against Gram-negative bacteria. This study investigated the transcriptomic responses of E. coli to sublethal LNT113 stress and identified genetic determinants required for bacterial adaptation to endolysin-induced stress. Transcriptomic analysis identified 552 differentially expressed genes (DEGs) following sublethal LNT113 exposure. Thirteen DEGs associated with stress response and envelope maintenance were individually deleted to generate thirteen mutant strains and to functionally evaluate their roles in bacterial stress tolerance. Among these, the ΔfabB and Δ(prmB–yfcL) mutants exhibited significantly reduced survival under sublethal LNT113 exposure, indicating increased susceptibility to the endolysin. Regarding the prmB–yfcL operon, individual genes were deleted to determine the gene critical for bacterial tolerance. Deletion of aroC and mepA rendered E. coli more susceptible to LNT113. Furthermore, 1-N-phenylnaphthylamine uptake assays demonstrated increased membrane permeability in the ΔfabB, ΔaroC, and ΔmepA mutants. Complementation with pWSK129::fabB, pWSK129::aroC, and pWSK129::mepA restored membrane integrity in the respective mutant strains. These findings suggest that fabB-mediated unsaturated fatty acid biosynthesis and mepA-dependent peptidoglycan remodeling are critical for maintaining envelope integrity under endolysin stress, whereas aroC may indirectly support bacterial tolerance to LNT113 via metabolic adaptation. This study provides insights into bacterial responses to LNT113 and offers a foundation for optimizing endolysin-based therapeutic strategies.
SN - 1225-8873
SN - 1976-3794
ER -