The mechanism of component recognition of bipartite geminiviruses: Genetic studies of the replication of squash leaf curl virus, and, Genetic and functional studies of squash leaf curl virus coat protein AR1
Qin, Shenwei
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Permalink
https://hdl.handle.net/2142/22218
Description
Title
The mechanism of component recognition of bipartite geminiviruses: Genetic studies of the replication of squash leaf curl virus, and, Genetic and functional studies of squash leaf curl virus coat protein AR1
Author(s)
Qin, Shenwei
Issue Date
1996
Doctoral Committee Chair(s)
Lazarowitz, Sondra G.
Department of Study
Microbiology
Discipline
Microbiology
Degree Granting Institution
University of Illinois at Urbana-Champaign
Degree Name
Ph.D.
Degree Level
Dissertation
Keyword(s)
Biology, Molecular
Biology, Microbiology
Language
eng
Abstract
Both genomic components of bipartite geminiviruses encode functions essential for viral infection: the A component replicates the viral genome and the B component systemically spreads the virus throughout the host. Thus, correct recognition between the two components is required to ensure a constant co-presence of the two viral genomic components during viral infection. In this study, using two closely related yet sufficiently different strains of squash leaf curl virus (SqLCV) as a model system, I will show that: (1) viral replication is an important step in component recognition of SqLCV infection; (2) the sequence between the directly repeated motif and the stem-loop structure of SqLCV replication origin is involved in component recognition and contains specific sequence element for efficient viral replication; (3) replication protein AL1 interacts with the sequence between the directly repeated motif and the stem-loop structure to balance replication of the two viral components; (4) balanced replication of the two viral components constitutes the molecular basis of component recognition of SqLCV.
Separately, I will also study the mechanism by which the coat protein AR1 participates in the viral movement pathway using mutational analysis. I will show that (1) viral encapsidation is not linked to viral ssDNA accumulation; (2) the ability of AR1 to bind ssDNA, possibly cooperatively, is essential for its participation in viral movement. This work will suggest that AR1 switches the viral rolling circle replication to the production of ssDNA to provide a sufficient amount of viral genomes to ensure an efficient viral infection.
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