Bacteriophages are viruses that infect bacteria and archaea and are classified as virulent or temperate phages based on their life cycles. A temperate phage, also known as a lysogenic phage, integrates its genomes into host bacterial chromosomes as a prophage. Previous studies have indicated that temperate phages are beneficial to their susceptible bacterial hosts by introducing additional genes to bacterial chromosomes, creating a mutually beneficial relationship. This article reviewed three primary ways temperate phages contribute to the bacterial pathogenicity of foodborne pathogens, including phage-mediated virulence gene transfer, antibiotic resistance gene mobilization, and biofilm formation. This study provides insights into mechanisms of phage–bacterium interactions in the context of foodborne pathogens and provokes new considerations for further research to avoid the potential of phage-mediated harmful gene transfer in agricultural environments.

Genome evolution can happen gradually or via bursts of rearrangements. Chromoplexy is an example of a process driving rapid genome evolution. This mutational signature is detected in ~18% of human cancers (PCAWG Consortium, 2020) and is frequently observed in prostate adenocarcinoma, lymphoid malignancies, and thyroid adenocarcinoma. Chromoplexy is inferred to happen as one catastrophic event that generates copy-neutral chains of translocations involving multiple chromosomes (Baca et al., 2013). Existing studies of chromoplexy monitor the outcome of massive cancer genome reorganization, thus early molecular events leading to catastrophic chromosome rearrangements remain elusive. In this work, we aimed to recapitulate molecular mechanisms underlying chromoplexy. For this, we set out to establish a cell line model and use fluorescence-based reporter systems to enrich for and allow isolation of cells containing signatures of chromoplexy. We additionally address whether colocalization of multiple double-strand breaks, for example in transcription hubs or abnormal nuclear structures, might stimulate chained inter- and intra- chromosomal translocations typical for chromoplexy. If successful, this work will provide a mechanistic understanding of an important mutational process driving rapid genome evolution in cancer, congenital disease, and potentially organismal evolution. Citation Format: Nataliia Serbyn, Myrthe M. Smit, Vimathi S. Gummalla, Gregory J. Brunette, David S. Pellman. Unravelling the mechanistic basis of chromoplexy, a mutational process driving early cancer genome evolution. [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 6105.