Genome editing techniques based on bacterial-artificial-chromosome in herpesvirus research

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Genome editing techniques based on bacterial-artificial-chromosome in herpesvirus research
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Genome editing techniques based on bacterial-artificial-chromosome in herpesvirus research Chromosome Genome GenomeEditing Research Cas9 CRISPR herpesvirus reversegenetics Micro_MDPI

Review: Bacterial-Artificial-Chromosome-Based Genome Editing Methods and the Applications in Herpesvirus Research. Image Credit: Panuwach / Shutterstock

While the RecA-mediated homologous recombination approach for editing herpesvirus genomes present in eukaryotic cells is more effective than conventional methods, it has considerable limitations. Due to the existence of repetitive sequences in the genomes of the herpes virus, one key issue is that RecA expression can generate instability in the herpes virus's BAC clone, which can result in viral genome mutations.

Immunology eBook Compilation of the top interviews, articles, and news in the last year. Download a free copy Schematic diagram of base editing method: dCas9 mediates targeting without DSB formation; cytosine deaminase converts C to U; single-base precise editing is complete with the replication of DNA.

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Childhood adiposity and novel subtypes of adult-onset diabetes: a Mendelian randomisation and genome-wide genetic correlation study - DiabetologiaChildhood adiposity and novel subtypes of adult-onset diabetes: a Mendelian randomisation and genome-wide genetic correlation study - DiabetologiaAims/hypothesis We investigated whether the impacts of childhood adiposity on adult-onset diabetes differ across proposed diabetes subtypes using a Mendelian randomisation (MR) design. Methods We performed MR analysis using data from European genome-wide association studies of childhood adiposity, latent autoimmune diabetes in adults (LADA, proxy for severe autoimmune diabetes), severe insulin-deficient diabetes (SIDD), severe insulin-resistant diabetes (SIRD), mild obesity-related diabetes (MOD) and mild age-related diabetes (MARD). Results Higher levels of childhood adiposity had positive genetically predicted effects on LADA (OR 1.62, 95% CI 1.05, 2.52), SIDD (OR 2.11, 95% CI 1.18, 3.80), SIRD (OR 2.76, 95% CI 1.60, 4.75) and MOD (OR 7.30, 95% CI 4.17, 12.78), but not MARD (OR 1.06, 95% CI 0.70, 1.60). Conclusions/interpretation Childhood adiposity is a risk factor not only for adult-onset diabetes primarily characterised by obesity or insulin resistance, but also for subtypes primarily characterised by insulin deficiency or autoimmunity. These findings emphasise the importance of preventing childhood obesity. Graphical abstract
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