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This Week in Science: Sep 15, 2017

In this week's Science, a California Institute of Technology team describes the construction of a DNA robot capable of carrying and delivering molecular cargo. The robot is formed from a single-stranded DNA with one leg and two foot domains for walking, and one arm and one hand domain for picking up and dropping off cargos. It moves along 2D tracks of DNA origami, and is capable of picking up multiple cargos of two types that are initially at unordered locations, and delivering them to specified destinations until all molecules are sorted into two distinct piles, according to the investigators. Notably, the robot is designed to perform a random walk without any energy supply, enabling a single robot to repeatedly sort multiple cargos.

Also in Science, an international research team publishes a genetic analysis of people from Papua New Guinea, revealing a sharp genetic divide between individuals from the highlands and lowlands, beginning 10,000 to 20,000 years ago. All highlanders were found to share ancestry within the last 10,000 years with major population growth in the same period, suggesting population structure was reshaped following a transition to a Neolithic lifestyle. "However, genetic differentiation between groups in Papua New Guinea is much stronger than in comparable regions in Eurasia, demonstrating that such a transition does not necessarily limit the genetic and linguistic diversity of human societies," the researchers write.

The Daily Scan's sister publication, GenomeWeb Daily News, has more on this study here.

Finally, a group of European researchers reports in Science on the use of CRISPR/Cas9 genome-editing technology to create a system for identifying the origins of cancer mutational signatures. They used CRISPR to delete key DNA repair genes in human colon organoids, followed by delayed subcloning and whole-genome sequencing. The investigators found that mutation accumulation in organoids lacking the mismatch repair gene MLH1 is "driven by replication errors and accurately models the mutation profiles observed in mismatch repair-deficient colorectal cancers." By applying their strategy to the cancer predisposition gene NTHL1 — which codes for a protein essential in genome maintenance — the researchers were able to pinpoint a mutational footprint previously found in a breast cancer patient who was confirmed to have harbored a germline-inactivating mutation in NTHL1. This approach, the study's authors state, may be used to "systematically dissect mutational signatures and potentially unveil their molecular origins."

GenomeWeb Daily News has more on this study here.