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This Week in Nature: Apr 16, 2015

In Nature Genetics this week, a Stanford University-led research team reports on the creation of human and mouse tissue-specific maps of genomic imprinting, offering new insights into the evolution of this epigenetic process. The investigators generated an atlas of imprinting across 33 mouse and 45 human developmental stages and tissues, and found that almost all imprinted genes were imprinted in early development. Further, they discovered that the genes either retained their parent-of-origin expression in adults or lost it completely. Imprinted genes were also enriched for coexpressed pairs of maternally and paternally expressed genes, and also showed "accelerated expression divergence between human and mouse," while being more highly expressed than non-imprinted orthologs, the researchers say.

Meanwhile, in Nature Biotechnology, two independent research teams described the development of new computational methods for identifying the spatial origin of cells assayed by single-cell RNA-sequencing. In one study, researchers from the Broad Institute spatially mapped 851 single cells from dissociated zebrafish embryos and generated a transcriptome-wide map of spatial patterning. In the other paper, investigators from the European Molecular Biology Laboratory used an in situ hybridization-based expression atlas on the developing brain of a marine worm to identify the origins of more than 150 RNA-sequenced individual brain cells from that organism. GenomeWeb has more on these studies here.

Finally, in Nature, researchers from the Weizmann Institute of Science present data explaining why the CRISPR/Cas9 genome-editing system, which is an adaptive defense system in bacteria and archaea, shows a preference for exogenous DNA. As part of the CRISPR mode of action, short pieces of DNA called spacers are acquired from foreign elements and integrated into the CRISPR array. In their paper, the scientists showed that spacer acquisition is replication-dependent, and that DNA breaks formed at stalled replication forks promote spacer acquisition. Avoidance of the self-chromosome, meanwhile, is mediated by the RecBCD double-stranded DNA break repair complex.