Table of contents


From the editors

p565 | doi:10.1038/nrg2171

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Research Highlights

Genomics: Mysteries of heterochromatic sequences unravelled | PDF (214 KB)

p567 | doi:10.1038/nrg2161

Disease genetics: A pathway to complexity | PDF (190 KB)

p568 | doi:10.1038/nrg2163

Development: PGCs' epigenetic travelogue | PDF (285 KB)

p568 | doi:10.1038/nrg2169

RNA world: Introducing the mirtron | PDF (285 KB)

p568 | doi:10.1038/nrg2170

In brief

| PDF (87 KB)

p569 | doi:10.1038/nrg2175

Genetic screens: Cell-shape networks get a screening | PDF (286 KB)

p570 | doi:10.1038/nrg2168

Technology: Spotting variation from expression profiles | PDF (101 KB)

p570 | doi:10.1038/nrg2173

Chromatin: A blast of HOTAIR silences distant chromatin | PDF (119 KB)

p571 | doi:10.1038/nrg2174

Development: Alternative splicing switches on the brain | PDF (195 KB)

p572 | doi:10.1038/nrg2162

In brief

| PDF (87 KB)

p572 | doi:10.1038/nrg2176

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Reviews

Engineering targeted viral vectors for gene therapy

Reinhard Waehler, Stephen J. Russell & David T. Curiel

p573 | doi:10.1038/nrg2141

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.

Replication in context: dynamic regulation of DNA replication patterns in metazoans

Mirit I. Aladjem

p588 | doi:10.1038/nrg2143

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.

Mining gene expression profiles: expression signatures as cancer phenotypes

Joseph R. Nevins & Anil Potti

p601 | doi:10.1038/nrg2137

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 tumorigenesis in vivo.

The distribution of fitness effects of new mutations

Adam Eyre-Walker & Peter D. Keightley

p610 | doi:10.1038/nrg2146

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.

Mutation rate variation in multicellular eukaryotes: causes and consequences

Charles F. Baer, Michael M. Miyamoto & Dee R. Denver

p619 | doi:10.1038/nrg2158

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.

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Perspectives

Science and society

Share and share alike: deciding how to distribute the scientific and social benefits of genomic data

Morris W. Foster & Richard R. Sharp

p633 | doi:10.1038/nrg2124

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.

Opinion

Copy number variants and genetic traits: closer to the resolution of phenotypic to genotypic variability

Jacques S. Beckmann, Xavier Estivill & Stylianos E. Antonarakis

p639 | doi:10.1038/nrg2149

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.

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