Abstract
Acinetobacter sp. Tol 5 exhibits an autoagglutinating nature and noteworthy adhesiveness to various abiotic surfaces from hydrophobic plastics to hydrophilic glass and stainless steel. Although previous studies have suggested that bacterionanofibers on Tol 5 cells are involved in the adhesive phenotype of Tol 5, the fiber that directly mediates Tol 5 adhesion has remained unknown. Here, we present a new member of trimeric autotransporter adhesins designated AtaA, which we discovered by analyzing a less adhesive mutant of Tol 5, T1, obtained by transposon mutagenesis. AtaA forms thinner and shorter nanofibers than fimbriae on Tol 5 cells. We performed target disruption of ataA by allelic marker exchange, and the resulting ΔataA strain was complemented with ataA on the Escherichia coli-Acinetobacter shuttle vector, which was newly constructed. These results proved that AtaA is essential for Tol 5’s autoagglutinating nature and high adhesiveness to surfaces of various materials. In addition, the adhesiveness to solid surfaces mediated by AtaA is notably higher than that mediated by YadA of Yersinia enterocolitica WA-314. Moreover, and importantly, these characteristics can be conferred to the non-adhesive, non-agglutinating bacterium Acinetobacter sp. ADP1 in trans by transformation with ataA, with expected applications to microbial immobilization.
Highlights
On bacterial cell surfaces, adhesive nanofibers, which are filamentous appendages of several nanometers in diameter, bind to host biomolecules and mediate infectious disease and tether cells to abiotic surfaces [1]
Most reports on Trimeric autotransporter adhesins (TAAs) have focused on their ability to adhere to biotic surfaces, several TAAs have been reported to be responsible for biofilm formation on various abiotic surfaces [8,13,29,35,36]
Biofilm formation ability is different from the initial attachment ability exhibited by AtaA [23]
Summary
Adhesive nanofibers, which are filamentous appendages of several nanometers in diameter, bind to host biomolecules and mediate infectious disease and tether cells to abiotic surfaces [1]. Many specific interactions between pathogenic bacteria and host cells and tissues are mediated by proteinaceous ‘‘bacterionanofibers’’, which can be divided into two major classes, fimbriae assembled from hundreds of subunits [2,3], and non-fimbrial fibers having a simple monomeric or oligomeric structure [4]. TAAs form homotrimeric structures with a Nterminus-head-neck-stalk-membrane anchor-C-terminus architecture [5,6]. The C-terminal anchor domain forms a 12-stranded bbarrel at the outer membrane (OM) and the head-neck-stalk domain, called a passenger domain, is secreted to the cell surface through the b-barrel pore. TAAs have been reported to mediate bacterial adhesion to host cells and/or extracellular matrix (ECM) proteins, such as collagen, fibronectin, and laminin, invasion of host cells, serum resistance, autoagglutination, and biofilm formation [4,6,8,9,10,11,12,13,14,15,16]
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