Abstract: In order to determine the effect of fimC gene, the wild type avian pathogenic Escherichia coli (APEC) isolate O₂ was selected as the prototype of the (APEC) Type Ⅰfimbriae. Based on the original sequences of TypeⅠ fimbriae operon gene clusters in the GenBank, fimC deletion mutant was constructed. fimC gene, which missed 169 bp, was amplified by PCR and cloned into a suicide vector pCVD442. The recombinant plasmid pCVD442 ∷△fimC was transformed into a host cell SM10λpir, then conjugated from SM10λpir (pCVD442∷△fimC) into E. coli O₂ (NalR). The strain of E. coli O₂ fimC deletion mutant was constructed by homologous recombination. The O₂(△fimC) mutant obtained was further confirmed by fimC PCR amplification,sequencing and transmission electron microscopy.There were some differences in the biochemical reaction between the wild type and the O₂(△fimC) mutant, but no difference in the drug allergy test. Compared with the wild type isolate, the O₂(△fimC) mutant grew slowly during all stages of growth in vitro. The animal experiments indicated that adherence of bacteria to avian tracheal epithelial cell and pathogenicity of the mutant strain was much slighter than those of the wild strain. This work provides the important basis for us to understand the role of fimC in the molecular pathogenesis mechanisms and the interaction between the Type Ⅰ Fimbriae and susceptible host cell and other biological characterizations of the O₂(△fimC) mutant.