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

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 [e-mail]

人类细胞编码多达14种具有特定功能的DNA聚合酶，这些聚合酶在染色体DNA的合成和损伤修复中发挥作用。相比之下，复杂的DNA病毒，如疱疹病毒科中的病毒，仅编码一种高保真DNA聚合酶。这种差异引发了一种可能性，即DNA病毒可能依赖宿主聚合酶在复杂DNA几何结构中进行合成。我们测试了参与转损伤合成（TLS）的错误倾向性Y家族聚合酶在人类巨细胞病毒（HCMV）感染中的重要性。我们发现，大多数参与核苷酸插入和损伤绕过的Y家族聚合酶限制了HCMV基因组的合成和复制。相比之下，其他TLS聚合酶，如超出损伤范围的聚合酶z复合物，对于最佳的基因组合成和复制是必需的。对polz复合物或插入聚合酶套件的耗竭表明，TLS聚合酶抑制了病毒基因组重排的频率，尤其是在GC富集区和重复序列中。此外，尽管与HCMV不同，相关单纯疱疹病毒1型（HSV-1）的复制也受宿主TLS聚合酶的影响，这表明宿主聚合酶对于DNA病毒复制有更广泛的需求。这些发现揭示了宿主DNA聚合酶在确保病毒基因组稳定性中出人意料的角色。这些数据代表了用于相关出版物图5的对齐数据。此外，还包括TB40E参考基因组。有关对齐数据的更多信息，请参阅Alignments.zip中的README.rtf文件。有关数据集内容的查询，请联系README.txt文件中列出的通讯作者。行政查询（例如，删除请求、下载问题等）可发送至[e-mail]。