Comparative Genetic and Genomic Analysis of the Novel Fusellovirus Sulfolobus Spindle-shaped Virus 10
Viruses that infect thermophilic Archaea are unique in both their structure and genetic makeup. The lemon-shaped fuselloviruses - which infect members of the order Sulfolobales, growing optimally at 80º C and pH 3 - are some of the most ubiquitous and best studied viruses of the thermoacidophilic Ar...
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Format: | Others |
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PDXScholar
2018
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Online Access: | https://pdxscholar.library.pdx.edu/open_access_etds/4496 https://pdxscholar.library.pdx.edu/cgi/viewcontent.cgi?article=5567&context=open_access_etds |
Summary: | Viruses that infect thermophilic Archaea are unique in both their structure and genetic makeup. The lemon-shaped fuselloviruses - which infect members of the order Sulfolobales, growing optimally at 80º C and pH 3 - are some of the most ubiquitous and best studied viruses of the thermoacidophilic Archaea. They provide a malleable and useful genetic tool for probing into the functions of their host, as well as the host responses to infection. Nonetheless, much about these viruses remains to be learned to further understand their morphological, genetic, and life cycle characteristics.
In order to investigate these aspects of these Fuselloviridae, as well as their evolution, this work reports the isolation and characterization of a novel fusellovirus, Sulfolobus Spindle-shaped virus 10 (formerly SSV-L1). Genetic and genomic analyses highlight significant homology with both SSV8 and SSV9, as well as conservation of promoter elements within the Fuselloviridae. SSV10 encodes five ORFs with no homology within or outside of the Fuselloviridae, as well as a putatively functional Cas4-like ORF which may play a role in anti-CRISPR host evasion. Moreover, we demonstrate the ability of SSV10 to withstand mutation in a fashion consistent with mutagenesis in SSV1. Lastly, analysis of predicted protein structures from SSV10 provide new insights into virus-host interactions. These analyses help to expand our understanding of the viral life cycle while contextualizing the mutagenesis data presented in the following chapters. |
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