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A key challenge in gene therapy is vector targeting to specific cells, while avoiding effects on other tissues. Several strategies have been developed recently to enable targeting of the main viral vectors, moving them a step closer to clinical use.
Spatial and temporal patterns of metazoan DNA replication are emerging as being dynamically regulated by tissue-specific and developmental cues, and by epigenetic modifications. These features might allow coordination with transcription and chromatin assembly, and enable changes in gene expression patterns.
Expression signatures have tremendous power to identify new cancer subtypes and to predict clinical outcomes. Using these signatures as surrogate phenotypes researchers can link diverse experimental systems to dissect the complexity of tumorigenesisin vivo.
Mutations can be deleterious, neutral or, in rare cases, advantageous. The relative frequencies of these types across a genome constitutes the distribution of fitness effects. The properties of this distribution have important consequences in both medical and evolutionary genetics.
Relatively little is known about what underlies mutation rate variation at an empirical level, particularly in multicellular eukaryotes. The authors review theoretical and empirical results to provide a framework for future studies of why and how mutation rate evolves in multicellular species.
Instead of taking a single-stakeholder perspective, the authors propose that a systematic approach that takes into account multiple stakeholders and their sometimes overlapping interests should be taken to facilitate decisions about genomic data sharing.
Copy number variation constitutes a major source of inter-individual genetic variation that could explain variable disease penetrance and variation in the phenotypic expression of aneuploidies, and could be an important factor in the aetiology of complex traits. Therefore, systematic exploration of both single nucleotide and copy number variation will be key to identifying the genomic contributors to polygenic traits and diseases.
