Submitted to: American Society for Microbiology
Publication Type: Abstract Only
Publication Acceptance Date: 2/15/2020
Publication Date: 7/15/2020
Citation: Wei, W., Burbank, L.P. 2020. Csp1, a cold-shock protein Homolog in Xylella fastidiosa is involved in biofilm formation. American Society for Microbiology.
Technical Abstract: Bacterial cold shock-domain proteins (CSPs) are conserved nucleic acid binding proteins that acts as chaperones to facilitate translation at low temperatures. Research on bacterial CSPs has highlighted the importance of these proteins in bacterial adaptation to environmental changes and stressors, including conditions unrelated to temperature. Csp1, a temperature-independent cold shock protein homolog, acts as a virulence factor in Xylella fastidiosa, a pathogen of grapevine and other plant species. In addition to virulence, Csp1 contributes to X. fastidiosa survival under high salt conditions and at low temperatures in vitro. However, little is known about the specific function of Csp1 in X. fastidiosa, aside from general single-stranded nucleic acid binding activity. To investigate the influence of Csp1 on X. fastidiosa gene expression under stress conditions RNA-Seq was used to compare transcriptomes of wild-type X. fastidiosa strain Stag’s Leap to a csp1 deletion mutant ('csp1) under standard growth conditions (28°C) and cold stress (15°C). The analysis revealed changes in expression of several genes important for motility and biofilm formation in 'csp1 compared to wild-type. One gene of intertest, pilA1, encodes a type IV pili subunit protein and was up-regulated in the 'csp1 mutant at 28°C. The type IV pili is required for twitching motility in X. fastidiosa and contributes to virulence by facilitating bacterial movement inside the host vascular tissue. As previous studies in other X. fastidiosa strains found that a deletion in pilA1 leads to overabundance of type IV pili and increased biofilm formation, biofilm formation in 'csp1 was quantified using crystal violet staining. A significant decrease in biofilm formation with the 'csp1 mutant was observed compared to the wild type strain in liquid media, which may be the result of increased expression of pilA1. As xylem vessel occlusion caused by biofilms is one major mechanism of X. fastidiosa pathogenicity, Csp1 may act as a virulence factor in X. fastidiosa by influencing the expression of genes involved in biofilm formation and motility.