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This Week in Nature: Apr 21, 2016

In this week's Nature, a Harvard University-led team reports that a modified version of the gene-editing technology CRISPR can target and modify single nucleotides without introducing random insertions and deletions into the genome. The approach involves a version of the Cas9 protein that does not cut both strands of DNA, but can still bind to a target sequence. The researchers attached a base-modifying enzyme to Cas9 and were able to directly convert cytosine to uracil, essentially performing a thymine edit. A third protein was used to manipulate DNA repair processes so that the edited base pair became permanent in cells. The investigators also demonstrated their approach in cultured cells to reverse single-based mutations associated with diseases including late-onset Alzheimer's and breast cancer. GenomeWeb has more on this study here.

Also in Nature, an international research team publishes a new genome assembly for the Atlantic salmon, Salmo salar, and use it to show major patterns characterizing salmon evolution following a whole-genome duplication event that occurred 80 million years ago in the common ancestor of salmonids. The work also highlights genes that have taken on new functions since this duplication through neofunctionalization and subfunctionalization. The authors suggest that their assembly may serve as a reference sequence for the study of other salmonids. GenomeWeb also covers this paper here.

Over in Nature Microbiology, a group of Spanish scientists described the use of newly developed high-fidelity, ultra-deep sequencing technology to gain a better understanding of mutation in the hepatitis C viral genome. While RNA viruses are known to have extremely high mutation rates, these rates have been inferred from a small fraction of genome sites. By applying a technology known as duplex sequencing, which sequences both strands of DNA duplexes, to a modified HCV replicon system, the team was able to score more than 15,000 spontaneous mutations encompassing more than 90 percent of the HCV genome. This revealed greater than 1,000-fold differences in mutability across genome sites with "extreme variations" even between adjacent nucleotides. The researchers also identified base composition, the presence of high- and low-mutation clusters, and transition/transversion biases as the main factors driving this heterogeneity. Mutability was further correlated with the ability of the virus to diversify in patients.