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Phosphoproteomic Analysis Reveals Impairment of Rice Germination by Chloramphenicol
Rui Li1,2, Narumon Phaonakrop3, Sittiruk Roytrakul3
1Interdisciplinary Graduate Program in Bioscience, Faculty of Science, Kasetsart University, Bangkok 10900, Thailand.
Plants (Basel, Switzerland)
|September 27, 2025
Summary
Chloramphenicol (CAM) antibiotic hinders rice germination speed and seedling growth by altering phosphorylation networks. This study reveals CAM
Area of Science:
- Plant Biology
- Molecular Biology
- Biochemistry
Background:
- Seed germination is crucial for rice production, but sensitive to environmental and chemical stresses.
- Chloramphenicol (CAM) is a phytotoxic antibiotic known to inhibit rice seedling establishment.
- The molecular mechanisms of CAM's phytotoxicity in rice are not well understood.
Purpose of the Study:
- To investigate the effects of varying chloramphenicol (CAM) concentrations on rice germination and early seedling establishment.
- To uncover the molecular basis of CAM phytotoxicity using time-resolved phosphoproteomic profiling.
- To elucidate how CAM disrupts rice development at the molecular level.
Main Methods:
- Investigated CAM effects on rice germination and seedling growth at different concentrations.
- Conducted time-resolved phosphoproteomic profiling during germination and early seedling stages.
- Analyzed dynamic, stage-specific phosphorylation changes in response to CAM.
Main Results:
- CAM significantly retarded rice germination speed and seedling growth, but final germination rates were largely unaffected.
- Moderate phosphorylation changes occurred during germination, affecting metabolic and cytokinesis processes.
- Extensive disruptions in metabolic pathways, stress responses, DNA replication, and hormone signaling were observed during early seedling establishment.
Conclusions:
- CAM disrupts rice development by remodeling phosphorylation networks.
- CAM modulates key physiological and signaling pathways, leading to growth inhibition.
- This study provides novel insights into antibiotic-induced plant growth inhibition and stress responses in early development.

