Transcription and replication complexes can coincide in space and time. Such coincidences may result in collisions that trigger genomic instability. The phosphorylation of Mrc1 by different signaling kinases is part of a general mechanism that serves to delay replication in response to different stresses that trigger a massive transcriptional response in S phase. This mechanism prevents Transcription-Replication Conflicts and maintains genomic integrity in response to unscheduled massive transcription during S phase.
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http://dx.doi.org/10.1080/23723556.2018.1451233 | DOI Listing |
PLoS Pathog
January 2025
Department of Microbiology, Immunology and Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, Colorado, USA.
The mosquito midgut functions as a key interface between pathogen and vector. However, studies of midgut physiology and virus infection dynamics are scarce, and in Culex tarsalis-an extremely efficient vector of West Nile virus (WNV)-nonexistent. We performed single-cell RNA sequencing on Cx.
View Article and Find Full Text PDFPLoS Pathog
January 2025
Department of Cancer and Genomic Sciences, College of Medicine and Health, University of Birmingham, Birmingham, United Kingdom.
Upon infection, human papillomavirus (HPV) manipulates host cell gene expression to create an environment that is supportive of a productive and persistent infection. The virus-induced changes to the host cell's transcriptome are thought to contribute to carcinogenesis. Here, we show by RNA-sequencing that oncogenic HPV18 episome replication in primary human foreskin keratinocytes (HFKs) drives host transcriptional changes that are consistent between multiple HFK donors.
View Article and Find Full Text PDFJ Virol
January 2025
Department of Translational Physiology, Infectiology and Public Health, Faculty of Veterinary Medicine, Ghent University, Merelbeke, Belgium.
Herpesviruses, a family of large enveloped DNA viruses, establish persistent infections in a wide range of hosts. This characteristic requires an intricate network of interactions with their hosts and host cells. In recent years, the interplay between herpesviruses and the epitranscriptome-chemical modifications in transcripts that may affect mRNA biology and fate-has emerged as a novel aspect of herpesvirus-host interactions.
View Article and Find Full Text PDFJ Virol
January 2025
Department of Laboratory Medicine, Clinical Center, National Institutes of Health, Bethesda, Maryland, USA.
Unlabelled: APOBEC3 proteins (A3s) play an important role in host innate immunity against viruses and DNA mutations in cancer. A3s-induced mutations in both viral and human DNA genomes vary significantly from non-lethal mutations in viruses to localized hypermutations, such as kataegis in cancer. How A3s are regulated remains largely unknown.
View Article and Find Full Text PDFJ Viral Hepat
February 2025
Medical School, Kunming University of Science and Technology, Kunming, People's Republic of China.
Hepatocellular carcinoma (HCC) is the most common primary liver cancer. Hepatitis B virus (HBV) is the main pathogen for HCC development. HBV covalently closed circular DNA (cccDNA) forms extra-host chromatin-like minichromosomes in the nucleus of hepatocytes with host histones, non-histones, HBV X protein (HBx) and HBV core protein (HBc).
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