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Replication mechanisms of circular ssDNA plant viruses and their potential implication in viral gene expression regulation

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MBIO
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AMER SOC MICROBIOLOGY
DOI: 10.1128/mbio.01692-23

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viruses; single-stranded DNA viruses; rolling-circle replication; recombination-dependent replication; replication; copy number variation; gene copy number; Geminiviridae; Nanoviridae; genome formula

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The replication of plant-infecting single-stranded DNA viruses, Geminiviridae and Nanoviridae, involves rolling-circle replication (RCR) and recombination-dependent replication (RDR) mechanisms. RCR relies on a virus-encoded Replication-associated protein (Rep) and specific sequences called iterons, while RDR is also observed in some double-stranded DNA viruses. This article provides a synthesis of the current understanding of these replication modes and discusses the potential role of gene copy number regulation in viral gene expression.
The replication of members of the two circular single-stranded DNA (ssDNA) virus families Geminiviridae and Nanoviridae, the only ssDNA viruses infecting plants, is believed to be processed by rolling-circle replication (RCR) and recombination-dependent replication (RDR) mechanisms. RCR is a ubiquitous replication mode for circular ssDNA viruses and involves a virus-encoded Replication-associated protein (Rep) which fulfills multiple functions in the replication mechanism. Two key genomic elements have been identifiedidentified for RCR in Geminiviridae and Nanoviridae: (i) short iterative sequences called iterons which determine the specific recognition of the viral DNA by the Rep and (ii) a sequence enabling the formation of a stem-loop structure which contains a conserved motif and constitutes the origin of replication. In addition, studies in Geminiviridae provided evidence for a second replication mode, RDR, which has also been documented in some double-stranded DNA viruses. Here, we provide a synthesis of the current understanding of the two presumed replication modes of Geminiviridae and Nanoviridae, and we identify knowledge gaps and discuss the possibility that these replication mechanisms could regulate viral gene expression through modulation of gene copy number.

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