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This Week in Cell: May 4, 2016

A Swedish team introduces a transcriptional map representing various stages of human embryo development that provides clues to lineage specification and X chromosome dosage compensation. The researchers used single-cell RNA sequencing to profile the transcriptional landscape in more than 1,500 individual cells from 88 pre-implantation human embryos that spanned various stages of development, from the eight-cell stage to immediately pre-implantation. By profiling cells from up to two-dozen embryos per embryonic day, they were able to identify gene expression shifts that accompany the advent of the embryo's main tissue lineages at the single-cell level, for example, along with differences found in cells from male and female embryos.

Researchers from the US, Spain, Germany and Sweden present findings from a study implicating circadian clock genes in acute myeloid leukemia. Using pooled, small hairpin RNAs, the team did in vivo, RNA interference screens aimed at uncovering essential transcription factors in a mouse model of AML carrying leukemia stem cells. The search led to two circadian clock-related transcription factors, called Clock and Bmal1, which appeared to be necessary to producing leukemic effects. In their absence, the investigators found that leukemia stem cells were depleted, cell proliferation declined, and myeloid cells maintained higher levels of differentiation.

Finally, a Scripps Translational Science Institute-led team presents initial findings from the Wellderly study, an effort to uncover genetic factors associated with disease-free aging. Through whole-genome sequencing on 600 chronic disease- and prescription-free participants between the ages of 80 years and 105 years old at Complete Genomics, the researchers determined that the healthy aging cohort was just as likely to carry rare, potentially pathogenic variants as were control individuals sequenced with the same platform. But the healthy agers seemed to have a somewhat lower genetic risk of heart disease and Alzheimer's, along with an over-representation of potentially protective variants involved in cognition. GenomeWeb has more on the study, here.