Stenotrophomonas rhizophila Chitinase Variation and Its Role in Suppressing Fusarium oxysporum Pathogenesis in Tomato
Abstract
The bacterium Stenotrophomonas maltophilia (S. maltophilia) and its family 18 glycoside hydrolase (GH18) was utilized to reduce soil pathogenic fungi growth before it was known to cause human infections. S. rhizophila, a closely related species, is not pathogenic to humans and has its own GH18 protein. However, S. rhizophila canonically does not possess a copy of the chitinase gene with a chitin binding domain (ChtBD3), reducing its affinity to chitin. Previous work by Lally 2021 found evidence of a potential copy or multiple copies of the chitinase gene in S. rhizophila with the ChtBD3, but it was necessary to provide greater clarity to the sequencing data collected. Sequencing of the chitinase gene from three isolates of S. maltophilia in full was attempted. Growth experiments of tomato plants using two S. rhizophila and two S. maltophilia isolates against the fungal tomato pathogen Fusarium oxysporum f. sp. lycopersici (F. oxysporum)were performed to compare the antifungal effects between the two species.Genetic analysis confirmed chitinase genes that differed between S. rhizophila isolates. The amino acid sequences between the chitinases also exhibited heterogeneity. Challenge assays showed both S. rhizophila and S. maltophilia isolates produced significant growth inhibition of F. oxysporum. S. rhizophila isolates produced statistically significant differences in plant growth metrics compared to controls in growth experiments. This study further confirms the utilization of S. rhizophila as a fungal pathogen deterrent and prompts the future study of how variation in the gene can provide different levels of protection from these pathogens to plants.
Subject Area
Cellular biology|Molecular biology
Recommended Citation
Imparato, Victor Michael, "Stenotrophomonas rhizophila Chitinase Variation and Its Role in Suppressing Fusarium oxysporum Pathogenesis in Tomato" (2022). ETD Collection for Fordham University. AAI29207881.
https://research.library.fordham.edu/dissertations/AAI29207881
