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Alignment data for "Host translesion polymerases are required for viral genome integrity"

dataset
posted on 22.08.2022, 14:29 authored by Sebastian Zeltzer, Pierce Alyn LongmirePierce Alyn Longmire, Marek Svoboda, Giovanni Bosco, Felicia Goodrum

Human cells encode up to 14 DNA polymerases with specialized functions in chromosomal DNA synthesis and damage repair. By contrast, complex DNA viruses, such as those of the herpesviridae family, encode a single high-fidelity DNA polymerase. This disparity raises the possibility that DNA viruses may rely on host polymerases for synthesis through complex DNA geometries. We tested the importance of error-prone Y-family polymerases involved in translesion synthesis (TLS) to human cytomegalovirus (HCMV) infection. We find most Y-family polymerases involved in the nucleotide insertion and bypass of lesions restrict HCMV genome synthesis and replication. By contrast, other TLS polymerases, such as the polymerase z complex, which extends past lesions, was required for optimal genome synthesis and replication. Depletion of either the polz complex or the suite of insertion polymerases demonstrate that TLS polymerases suppress the frequency of viral genome rearrangements, particularly at GC-rich sites and repeat sequences. Moreover, while distinct from HCMV, replication of the related herpes simplex virus type 1 (HSV-1) is impacted by host TLS polymerases, suggesting a broader requirement for host polymerases for DNA virus replication. These findings reveal an unexpected role for host DNA polymerases in ensuring viral genome stability.

These data represent alignments used for Fig. 5 of the associated publication. Also included is a TB40E reference genome. Refer to the README.rtf file in Alignments.zip for further information. 


For inquiries regarding the contents of this dataset, please contact the Corresponding Author listed in the README.txt file. Administrative inquiries (e.g., removal requests, trouble downloading, etc.) can be directed to data-management@arizona.edu

Funding

Human Cytomegalovirus dysregulation of host hematopoietic progenitor cell signaling pathways to modulate latency and reactivation

National Institute of Allergy and Infectious Diseases

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Mechanisms of Human Cytomegalovirus Latency in Primary Human Hematopoietic Cells

National Institute of Allergy and Infectious Diseases

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