PUBLICATION

Involvement of N-acetylneuraminate cytidylyltransferase in Edwardsiella piscicida pathogenicity

Authors
Tran, N.T., Vo, L.K., Komatsu, M., Shiozaki, K.
ID
ZDB-PUB-220428-9
Date
2022
Source
Fish & shellfish immunology   124: 534-542 (Journal)
Registered Authors
Shiozaki, Kazuhiro
Keywords
Edwardsiella piscicida, N-acetylneuraminate cytidylyltransferase, Pathogenicity, Sialic acid, Sialidase
MeSH Terms
  • Animals
  • Bacterial Proteins/genetics
  • Edwardsiella*/genetics
  • Enterobacteriaceae Infections*/microbiology
  • Enterobacteriaceae Infections*/veterinary
  • Fish Diseases*/microbiology
  • N-Acetylneuraminic Acid
  • Virulence
  • Zebrafish
PubMed
35477099 Full text @ Fish Shellfish Immunol.
Abstract
Edwardsiella piscicida is a gram-negative bacterium that causes Edwardsiellosis in cultured fish. Edwardsiellosis is accompanied by symptoms such as skin lesions, hemorrhage, and necrosis in fish organs, which leads to significant economic losses in the aquaculture industry. Recently, we found that bacterial sialoglycoconjugates may be involved in the infectivity of E. piscicida. The more infectious strains of E. piscicida contain more sialic acid in the bacterial body, and the mRNA level of putative CMP-Neu5Ac synthase (css) is upregulated compared to that in the non-pathogenic strain. However, this putative css gene is yet to be cloned, and the involvement of CSS in E. piscicida pathogenicity remains unclear. Here, we cloned and transferred the css gene from E. piscicida into the FPC498 strain. CSS promoted infection in cultured cells obtained from different fish species, and enhanced the mortality of E. piscicida-infected zebrafish larvae. CSS enhanced cell attachment and motility in E. piscicida, which differs from the decreased bacterial growth observed with the sialic acid-supplemented M9 medium. Both fractions (chloroform-methanol (CM))-soluble and -insoluble fraction) prepared from E. piscicida pellet exhibited the increment of sialo-conjugates induced by CSS. Further, lectin blotting revealed the increment of Sia α2-3- and α2-6-, but not α2-8-, -linked glycoprotein in CSS-overexpressing E. piscicida. Overall, these findings indicate the physiological significance of CSS and the role of sialylation in in E. piscicida pathogenicity.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping