Bozkurt E.B., Baysal Ö., Marzec-Grządziel A., Silme R.S., Can A., Belen I.N., Capar U., Korkut A. (2025): Genomic Characterization of Serratia fonticola (EBS19) as a Biocontrol Agent against Botrytis cinerea. Current Microbiology, 82, 252, https://doi.org/10.1007/s00284-025-04224-y (40 pkt. MNiSW; IF 2.3)
DOI: https://doi.org/10.1007/s00284-025-04224-y
Abstract
Botrytis cinerea (Bc), a plant pathogenic fungus, is the causative agent of gray mold disease, which rapidly develops resistance to fungicides in cultivation areas. This study explores the biocontrol potential of various bacterial isolates collected from the rhizosphere of tomato plants (Solanum lycopersicum). Bacterial isolates were purified and neutralized through phenol vaporization for 2 days. Colonies that inhibited pathogen spore growth were confirmed via antibiosis effect using in vitro bioassays. Bacterial colonies demonstrated up to 84% inhibition of pathogen growth at 7-day post-inoculation (dpi) with a one-layer agar diffusion test and up to 70% inhibition with a double-layer agar diffusion test, compared to control plates. Both bacterial suspension and filtrate significantly suppressed pathogen mycelium growth at 11 and 14 dpi. The isolate used in further studies was identified as Serratia fonticola (EBS19) through whole-genome sequencing. Annotated genome data revealed the presence of genes encoding enzymes crucial for pathogen inhibition. Carbon preference analyses identified specific carbon sources unique to the bacterial strain. These findings are advantageous for developing effective biopreparations that ensure bacterial strain stability in practical applications. In addition, the primary focus was on the interaction between the pathogen’s major stress regulator protein (BAG1) and the bacterial glycoside hydrolase. Protein–protein docking analyses elucidated strong interaction between BAG1 and bacterial glycoside hydrolase. In conclusion, this study provides a knowledge for further research using recombinant DNA and gene cloning techniques on the bacterium’s mapped genome.