Csp1, a cold-shock protein homolog in Xylella fastidiosa is involved in stress response and biofilm formation

Authors: Wei, Wei; Burbank, Lindsey

Submitted to: World Microbe Forum
Publication Type: Abstract Only
Publication Acceptance Date: 4/15/2021
Publication Date: 6/20/2021
Citation: Wei, W., Burbank, L.P. 2021. Csp1, a cold-shock protein homolog in Xylella fastidiosa is involved in stress response and biofilm formation. World Microbe Forum.

Interpretive Summary:

Technical Abstract: Bacterial cold shock-domain proteins (CSPs) are conserved nucleic acid binding proteins that acts as chaperones to facilitate translation during cellular stress, including conditions unrelated to temperature. Csp1, a temperature-independent cold shock protein homolog, acts as a virulence factor in Xylella fastidiosa, a bacterial pathogen of grapevine and other economically important crops. In addition to virulence, Csp1 contributes to X. fastidiosa survival at low temperatures and under high salt and oxidative stress, in vitro. However, little is known about the specific function(s) 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 an Oxford Nanopore MinION was used to sequence transcriptomes of wild-type X. fastidiosa strain Stag’s Leap and a csp1 deletion mutant ('csp1). 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. 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. Previous studies in other strains of X. fastidiosa showed deleting pilA1 leads to overabundance of type IV pili and increased biofilm formation. Xylem vessel occlusion caused by biofilms is one major mechanism of X. fastidiosa pathogenicity, so Csp1 may act as a virulence factor in X. fastidiosa by influencing expression of genes involved in biofilm formation and motility. Significant decrease in biofilm formation was observed in the 'csp1 mutant compared to the wild type strain in liquid medium, which may be the result of increased expression of pilA1. The csp1 mutant was also less viable during long term growth compared to the wild type strain, in vitro, further suggesting Csp1 plays a role in stress response. Studies in other bacteria have identified links between stress response and biofilm formation, suggesting that Csp1 may play a role in both virulence and stress adaptation by influencing genes important for biofilm formation.