PUBLICATION
HU-induced polymorphous filamentation in fish pathogen Edwardsiella tarda leading to reduced invasion and virulence in zebrafish
- Authors
- Wang, L., Xiao, J., Cui, S., Wang, Q., Wu, H., Liu, Q., Zhang, Y.
- ID
- ZDB-PUB-140513-46
- Date
- 2014
- Source
- Veterinary Microbiology 171: 165-74 (Journal)
- Registered Authors
- Liu, Qin
- Keywords
- Edwardsiella tarda, Filamentation, Nucleoid-associated protein, Virulence
- MeSH Terms
-
- Animals
- Bacterial Outer Membrane Proteins/genetics*
- Bacterial Outer Membrane Proteins/metabolism
- Bacterial Proteins/genetics
- Bacterial Proteins/metabolism
- Carrier Proteins/genetics*
- Carrier Proteins/metabolism
- Edwardsiella tarda/genetics*
- Edwardsiella tarda/pathogenicity*
- Enterobacteriaceae Infections/microbiology
- Enterobacteriaceae Infections/mortality
- Enterobacteriaceae Infections/veterinary*
- Fish Diseases/microbiology*
- Fish Diseases/mortality
- Mutation
- Sequence Deletion
- Up-Regulation
- Virulence/genetics*
- Zebrafish/microbiology
- PubMed
- 24793099 Full text @ Vet. Microbiol.
Citation
Wang, L., Xiao, J., Cui, S., Wang, Q., Wu, H., Liu, Q., Zhang, Y. (2014) HU-induced polymorphous filamentation in fish pathogen Edwardsiella tarda leading to reduced invasion and virulence in zebrafish. Veterinary Microbiology. 171:165-74.
Abstract
Edwardsiella tarda is a rod-shaped Gram-negative pathogenic bacterium that causes hemorrhagic septicemia in fish. Nucleoid-associated protein HU is a basic DNA-binding protein with structural specificity in regulating genes expression. In wild-type E. tarda EIB202, HU is composed of two subunits HUα (hupA) and HUβ (hupB), and exists in homodimer or heterodimer forms. Different from the wild-type and ΔhupB mutant, ΔhupA mutant was found to be defective in cell growth, H2S production, acid adaptation, and exhibited abnormal cell division resulting in a filamentous phenotype in log phase bacteria. The qRT-PCR result showed that deletion of hupA significantly up-regulated the transcription levels of recA and sulA, which in turn stimulated RecA-dependent pathway to prevent cell division, resulting in filamentous morphology in E. tarda. Furthermore, the elongated ΔhupA cells showed a striking defect in EPC cell invasion, and the adhesion and internalization rates were reduced to 25% and 27% of the wild-type in log phase cultures. Confocal laser scanning microscopy revealed that filamentous bacteria failed to adhere to and could not be internalized into EPC. When some of the bacteria regained the rod-shape morphology in stationary cultures, the ΔhupA mutants showed increased adhesion and internalization rates into EPC. Moreover, ΔhupA mutant exhibited delayed mortalities (for two days) in zebrafish but the LD50 increased 17 folds. Immunohistochemical analysis showed that ΔhupA mutant reduced proliferation abilities in the muscle, liver and intestine of zebrafish. This study indicates that HU protein and strains morphology play essential roles in the virulence network of E. tarda.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping