ORIGINAL RESEARCH article

Front. Cell. Infect. Microbiol.

Sec. Veterinary and Zoonotic Infection

Volume 15 - 2025 | doi: 10.3389/fcimb.2025.1591206

This article is part of the Research TopicUnveiling Host-Pathogen Interactions: Insights into Animal Cellular Immunity and Novel Diagnostics - Volume IIView all 3 articles

FimC binds the promoter region of agn43 to modulate autoaggregation

Provisionally accepted
Zhihao  WangZhihao Wang1Xiangpeng  NiuXiangpeng Niu2Ningyuan  ZhongNingyuan Zhong1Lanfang  KongLanfang Kong1Saqib  NawazSaqib Nawaz1Haiyang  ZhangHaiyang Zhang1Wei  JiangWei Jiang1Yuanyuan  LiuYuanyuan Liu3Jian  TuJian Tu2Xiangan  HanXiangan Han1*
  • 1Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Shanghai, Shanghai Municipality, China
  • 2Anhui Province Key Laboratory of Veterinary Pathobiology and Disease Control, College of Animal Science and Technology, Anhui Agricultural University, Hefei, China
  • 3Qingdao Orisess Biotechnology Co.,Ltd, Qingdao, China

The final, formatted version of the article will be published soon.

Background: Avian pathogenic Escherichia coli (APEC) infection causes high mortality in chicks and leads to significant economic losses in the poultry industry. During the initial infection, APEC colonizes host cells using type 1 fimbriae and subsequently forms biofilms, resulting in persistent and chronic infections. FimC is a chaperone protein associated with type 1 fimbriae and plays a crucial role in the assembly of fimbriae. However, its regulatory role in agn43-mediated autoaggregation remains unclear.Methods: By constructing fimC gene mutant strains, autoaggregation, motility, biofilm formation, and the adhesion and invasion ability to HD-11 cell were examined. The transcriptome and electrophoretic mobility shift assay (EMSA) were used to screen and verify the regulation of FimC on downstream genes.Results: It demonstrated that lacking fimC but not fimbriae significantly increasing the autoaggregation (P < 0.001), meanwhile promoted the transcription of agn43 (P < 0.01).Transcriptomic analysis showed that deleting fimC caused significant changes in gene transcription levels in a variety of pathways, such as flagellar synthesis, biofilm formation, quorum sensing and c-di-GMP metabolism. Further investigation revealed that FimC directly interacts with the promoter region of agn43 and inhibits the transcription of the agn43. In adiition, both fimC and agn43 have regulatory effects on biofilm, motility, adhesion and invasion.This study demonstrated that FimC acts as an atypical DNA-binding protein to regulate the transcription of agn43. It also highlights the importance of fimC in biofilm formation and adhesion ability of APEC, which provides new insights into the functions of fimbriae chaperone proteins fimC.

Keywords: Avian pathogenic E. coli (APEC), type 1 fimbriae chaperone protein FimC, autoaggregation, DNA-binding, Biofim, c-di-GMP

Received: 10 Mar 2025; Accepted: 23 Apr 2025.

Copyright: © 2025 Wang, Niu, Zhong, Kong, Nawaz, Zhang, Jiang, Liu, Tu and Han. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Xiangan Han, Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Shanghai, 200241, Shanghai Municipality, China

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