Abstract
Characterizing the molecular interactions of viruses in natural microbial populations offers insights into virus–host dynamics in complex ecosystems. We identify the resistance of Sulfolobus islandicus to Sulfolobus spindle‐shaped virus (SSV9) conferred by chromosomal deletions of pilin genes, pilA1 and pilA2 that are individually able to complement resistance. Mutants with deletions of both pilA1 and pilA2 or the prepilin peptidase, PibD, show the reduction in the number of pilins observed in TEM and reduced surface adherence but still adsorb SSV9. The proteinaceous outer S‐layer proteins, SlaA and SlaB, are not required for adsorption nor infection demonstrating that the S‐layer is not the primary receptor for SSV9 surface binding. Strains lacking both pilins are resistant to a broad panel of SSVs as well as a panel of unrelated S. islandicus rod‐shaped viruses (SIRVs). Unlike SSV9, we show that pilA1 or pilA2 is required for SIRV8 adsorption. In sequenced Sulfolobus strains from around the globe, one copy of each pilA1 and pilA2 is maintained and show codon‐level diversification, demonstrating their importance in nature. By characterizing the molecular interactions at the initiation of infection between S. islandicus and two different types of viruses we hope to increase the understanding of virus–host interactions in the archaeal domain.
Highlights
A diverse array of novel viruses that infect the thermoacidophilic crenarchaea has been described (Peng, Garrett, & She, 2012; Prangishvili et al, 2017; Prangishvili & Garrett, 2005; Rice et al, 2001; Snyder, Bolduc, & Young, 2015)
After examining all available Sulfolobales genomes, we found that each genome contains two copies of sequence homologs to these pilin genes, some encoded on the same strand, while others on opposite strands, even those isolated from the same hot springs as lytic S. islandicus rod-shaped viruses (SIRVs)
We evolved CRISPR-Cas-independent resistance in S. islandicus strains derived from M.16.4 through the deletion of both copies of the type IV adhesive pilin genes pilA1 and pilA2
Summary
A diverse array of novel viruses that infect the thermoacidophilic crenarchaea has been described (Peng, Garrett, & She, 2012; Prangishvili et al, 2017; Prangishvili & Garrett, 2005; Rice et al, 2001; Snyder, Bolduc, & Young, 2015). To test whether PibD processing and surface localization of M164_2742 and M164_2746 are necessary for SSV9 infection we constructed a marker-insertion disruption strain, ΔpibD::argD (Figure S3a,b), in the pilus encoding S. islandicus strain, RJW004 (Zhang et al, 2013). This result shows that, while pilA1 and pilA2 are necessary for infection by SSV9, neither appears to be required for adsorption. Having shown that pilins encoded by pilA1 and pilA2 are necessary for infection, we tested the requirement for pili for susceptibility to SSVs and SIRVs isolated from multiple sources. This suggests that these positions in PilA1 and PilA2 may be under diversifying selection to evade lytic viruses
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