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ARS Home » Pacific West Area » Parlier, California » San Joaquin Valley Agricultural Sciences Center » Crop Diseases, Pests and Genetics Research » Research » Publications at this Location » Publication #373041

Research Project: Identification of Novel Management Strategies for Key Pests and Pathogens of Grapevine with Emphasis on the Xylella Fastidiosa Pathosystem

Location: Crop Diseases, Pests and Genetics Research

Title: Xylella fastidiosa cold shock protein homolog Csp1 is involved in biofilm formation

item Wei, Wei
item Burbank, Lindsey

Submitted to: American Phytopathological Society Abstracts
Publication Type: Abstract Only
Publication Acceptance Date: 5/13/2020
Publication Date: 8/4/2020
Citation: Wei, W., Burbank, L.P. 2020. Xylella fastidiosa cold shock protein homolog Csp1 is involved in biofilm formation. American Phytopathological Society Abstracts.

Interpretive Summary:

Technical Abstract: Xylella fastidiosa (Xf), the causal agent of Pierce’s disease of grapevine, does not have the temperature-inducible cold shock proteins (CSPs) that many bacteria use to adapt to low temperatures. CSPs are conserved nucleic acid binding proteins that help cells respond to environmental stresses. In addition to temperature-inducible CSPs, other CSP homologs are involved in response to cellular stress unrelated to temperature. In Xf, a temperature-independent CSP homolog acts as a virulence factor, and promotes survival under osmotic and low temperature stress. However, little is known about the specific function of Csp1 in Xf aside from general nucleic acid binding activity. RNA-Seq was used to compare gene expression of wild-type Xf strain Stag’s Leap to a csp1 deletion mutant ('csp1) at 28°C and 15°C. Changes were observed in expression of genes important for motility and biofilm formation in 'csp1 compared to wild-type, including pilA1 which encodes a type IV pili subunit protein. The type IV pili is required for twitching motility in Xf and contributes to virulence by facilitating bacterial movement inside the host vascular tissue. Previous work in other Xf strains found that a deletion in pilA1 leads to increased biofilm formation. Stag’s Leap 'csp1 had a significant decrease in biofilm formation compared to the wild type, which may be the result of increased expression of pilA1. As biofilm formation is a major mechanism of Xf pathogenicity, the role of Csp1 in virulence may be through expression of genes involved in biofilm formation and motility.