Hot off the presses! Oct 01 Nat Rev Genet

The Oct 01 issue of the Nat Rev Genet is now up on Pubget (About Nat Rev Genet): if you're at a subscribing institution, just click the link in the latest link at the home page. (Note you'll only be able to get all the PDFs in the issue if your institution subscribes to Pubget.)

Latest Articles Include:

• From the editors
  - Nat Rev Genet 10(10):659 (2009)
  
• Synthetic biology: Avoiding the chop
  - Nat Rev Genet 10(10):660 (2009)
  
• Chromosome biology: Getting your Ys crossed
  - Nat Rev Genet 10(10):661 (2009)
  
• Technology: A step closer to personal genomics?
  - Nat Rev Genet 10(10):661 (2009)
  
• Human disease: iPSCs take the next step
  - Nat Rev Genet 10(10):662 (2009)
  
• Gene regulation: UTR cutbacks give free rein to oncogenes
  - Nat Rev Genet 10(10):662 (2009)
  
• In brief: Human disease, Evolution, Gene regulatory networks
  - Nat Rev Genet 10(10):662 (2009)
  
• Human epigenomics: Putting epigenetic variation on the map
  - Nat Rev Genet 10(10):663 (2009)
  
• Chromatin: A peak for exons
  - Nat Rev Genet 10(10):664 (2009)
  
• Epigenetics: Jump-starting transposons
  - Nat Rev Genet 10(10):664 (2009)
  
• In brief: Chromatin, Population genetics, Circadian rhythms
  - Nat Rev Genet 10(10):665 (2009)
  
• The expansion of newborn screening: is reproductive benefit an appropriate pursuit?
  - Nat Rev Genet 10(10):666 (2009)
  
• ChIP–seq: advantages and challenges of a maturing technology
  - Nat Rev Genet 10(10):669-680 (2009)
  Chromatin immunoprecipitation followed by sequencing (ChIP–seq) is a technique for genome-wide profiling of DNA-binding proteins, histone modifications or nucleosomes. Owing to the tremendous progress in next-generation sequencing technology, ChIP–seq offers higher resolution, less noise and greater coverage than its array-based predecessor ChIP–chip. With the decreasing cost of sequencing, ChIP–seq has become an indispensable tool for studying gene regulation and epigenetic mechanisms. In this Review, I describe the benefits and challenges in harnessing this technique with an emphasis on issues related to experimental design and data analysis. ChIP–seq experiments generate large quantities of data, and effective computational analysis will be crucial for uncovering biological mechanisms.
• Bayesian statistical methods for genetic association studies
  - Nat Rev Genet 10(10):681-690 (2009)
  Bayesian statistical methods have recently made great inroads into many areas of science, and this advance is now extending to the assessment of association between genetic variants and disease or other phenotypes. We review these methods, focusing on single-SNP tests in genome-wide association studies. We discuss the advantages of the Bayesian approach over classical (frequentist) approaches in this setting and provide a tutorial on basic analysis steps, including practical guidelines for appropriate prior specification. We demonstrate the use of Bayesian methods for fine mapping in candidate regions, discuss meta-analyses and provide guidance for refereeing manuscripts that contain Bayesian analyses.
• The impact of retrotransposons on human genome evolution
  - Nat Rev Genet 10(10):691-703 (2009)
  Their ability to move within genomes gives transposable elements an intrinsic propensity to affect genome evolution. Non-long terminal repeat (LTR) retrotransposons — including LINE-1, Alu and SVA elements — have proliferated over the past 80 million years of primate evolution and now account for approximately one-third of the human genome. In this Review, we focus on this major class of elements and discuss the many ways that they affect the human genome: from generating insertion mutations and genomic instability to altering gene expression and contributing to genetic innovation. Increasingly detailed analyses of human and other primate genomes are revealing the scale and complexity of the past and current contributions of non-LTR retrotransposons to genomic change in the human lineage.
• Causes and consequences of microRNA dysregulation in cancer
  - Nat Rev Genet 10(10):704-714 (2009)
  Over the past several years it has become clear that alterations in the expression of microRNA (miRNA) genes contribute to the pathogenesis of most — if not all — human malignancies. These alterations can be caused by various mechanisms, including deletions, amplifications or mutations involving miRNA loci, epigenetic silencing or the dysregulation of transcription factors that target specific miRNAs. Because malignant cells show dependence on the dysregulated expression of miRNA genes, which in turn control or are controlled by the dysregulation of multiple protein-coding oncogenes or tumour suppressor genes, these small RNAs provide important opportunities for the development of future miRNA-based therapies.
• The evolutionary consequences of erroneous protein synthesis
  - Nat Rev Genet 10(10):715-724 (2009)
  Error s in protein synthesis disrupt cellular fitness, cause disease phenotypes and shape gene and genome evolution. Experimental and theoretical results on this topic have accumulated rapidly in disparate fields, such as neurobiology, protein biosynthesis and degradation and molecular evolution, but with limited communication among disciplines. Here, we review studies of error frequencies, the cellular and organismal consequences of errors and the attendant long-range evolutionary responses to errors. We emphasize major areas in which little is known, such as the failure rates of protein folding, in addition to areas in which technological innovations may enable imminent gains, such as the elucidation of translational missense error frequencies. Evolutionary responses to errors fall into two broad categories: adaptations that minimize errors and their attendant costs and adaptations that exploit errors for the organism's benefit.
• The evolutionary significance of ancient genome duplications
  Van de Peer Y Maere S Meyer A - Nat Rev Genet 10(10):725-732 (2009)
  Many organisms are currently polyploid, or have a polyploid ancestry and now have secondarily 'diploidized' genomes. This finding is surprising because retained whole-genome duplications (WGDs) are exceedingly rare, suggesting that polyploidy is usually an evolutionary dead end. We argue that ancient genome doublings could probably have survived only under very specific conditions, but that, whenever established, they might have had a pronounced impact on species diversification, and led to an increase in biological complexity and the origin of evolutionary novelties.
• Correspondence: Non-invasive prenatal diagnosis: an ethical imperative
  - Nat Rev Genet 10(10):733 (2009)
  I want to purchase this article Register now Price: US$18 In order to purchase this article you must be a registered user. I want to subscribe to Nature Reviews Genetics Select this option to purchase a personal subscription to Nature Reviews Genetics.
• Correspondence: Reply: Non-invasive prenatal diagnosis: an ethical imperative
  - Nat Rev Genet 10(10):733 (2009)
  I want to purchase this article Register now Price: US$18 In order to purchase this article you must be a registered user. I want to subscribe to Nature Reviews Genetics Select this option to purchase a personal subscription to Nature Reviews Genetics.