DNA Damage, Repair and Mutagenesis

Dear Colleagues,

Damage to DNA occurs constantly due to the action of both metabolic and external agents. Incorrect repair can trigger genome instability and mutational events which, by compromising chromatin homeostasis, are the origin of some of the deadliest diseases, including cancer, neurodegenerative syndromes and other age-related disorders. This field is witnessing continuous development as the complexity of the factors, genetic, genomic and epigenomic, contributing to damage deposition and repair efficiency is unveiled. Yeast and lower metazoan models, such as S. cerevisiae, S. pombe or C. elegans, have set the basis for a detailed understanding of basic repair and damage tolerance pathways and the coordination of DNA metabolism processes such as replication, transcription and recombination. The utilization of rodent models and human cell lines, and also organoids or organ-on-a-chip systems, continues to reveal the relevance of the chromatin structure, ncRNA regulation, and gene expression changes in response to, and caused by, DNA damage; this is in addition to tissue specificities, and its relationship with metabolic network alterations and the microbiome. This Special Issue aims to offer a comprehensive and updated overview of the complexity of factors impacting the mechanisms determining the integrity of the genome, both in human and model systems.

Dr. Víctor González-Huici
Guest Editor

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• genomics
• epigenomics
• genome instability
• cancer
• neurodegeneration
• ageing
• chemotherapy
• replication
• transcription
• mutational signatures