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. 2019 Oct 31;48(1):249–263. doi: 10.1093/nar/gkz1005

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© The Author(s) 2019. Published by Oxford University Press on behalf of Nucleic Acids Research.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 4. — RepA drives PLE replication in the presence of ICP1. (A) RepA complementation of PLE ΔrepA as assessed by qPCR. PLE fold copy increase 20 min post-infection is shown in different combinations with ICP1 and the inducer of the complementation construct. (B) A diagram of the midiPLE construct used to assess the minimal requirements for PLE replication (not to scale). Attachment sites, the PLE integrase, and the noncoding region (NCR) are present along with a kanamycin resistance gene (kanR). (C) Replication of a RepA complemented ΔrepA strain and midiPLE 20 min post ICP1 infection. The replication of these strains was compared to a wild-type PLE control, and the relative replication is displayed as a percentage above the bars.