Mechanistic interactions between Sulfolobus islandicus and its viruses

Rowland, Elizabeth F

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https://hdl.handle.net/2142/108601 Copy

Description

Title

Mechanistic interactions between Sulfolobus islandicus and its viruses

Author(s)

Rowland, Elizabeth F

Issue Date

2020-07-14

Director of Research (if dissertation) or Advisor (if thesis)

Whitaker, Rachel

Doctoral Committee Chair(s)

Whitaker, Rachel

Committee Member(s)

• Cann, Isaac
• Slauch, James
• Vanderpool, Carin

Department of Study

Microbiology

Discipline

Microbiology

Degree Granting Institution

University of Illinois at Urbana-Champaign

Degree Name

Ph.D.

Degree Level

Dissertation

Keyword(s)

• Sulfolobus
• Archaea
• Virus
• Pili

Abstract

Viruses infect all domains of life and play important ecological and evolutionary roles. In studying these virus-host interactions, fundamental mechanisms in cellular and molecular biology have been elucidated. The viruses of Sulfolobus are diverse in morphology, genomic content, and infection mechanisms. However, compared to bacterial and eukaryotic virus-host systems, little is known about these viruses or their interactions with their host. Utilizing Sulfolobus islandicus and isolated viruses I describe and characterize some of these mechanisms. In Chapter 2, I show that highly related and diversifying pilins are essential for viral infection for both Sulfolobus spindle-shaped viruses and Sulfolobus islandicus rod-shaped viruses. Double mutants of pilA1 and pilA2 are surface adhesion deficient but display no growth defect. The phenotype of this resistant cell is similar to an isolated host, Δcas6:SSV9.1, which is chronically infected leading to a superinfection exclusion hypothesis described in Chapter 3. This hypothesis proposes that downregulation of pilA1 and pilA2 provides resistance to potentially superinfecting viruses supported by the lack of surface structures observed in Δcas6:SSV9.1. In Chapter 4, I describe a novel pleomorphic virus with a 15,365 bp circular dsDNA genome containing sequence homology to 6 SSV-like ORFs. The viral genome also contains a CRISPR-Cas A2-like repeat sequence which is proposed to provide escape against host CRISPR-Cas immunity. In the last chapter, I share preliminary data on an evolved S-layer deficient host, ΔslaA_evol, which was created to test viral susceptibility and reveals that the S-layer is not the primary receptor for many viruses. In this thesis, I describe my work characterizing virus-host mechanisms to enhance our understanding of these fascinating and unique viruses and microbes.

Graduation Semester

2020-08

Type of Resource

Thesis

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Copyright and License Information

Copyright 2020 Elizabeth Rowland

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