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This Week in PNAS: May 2, 2017

In the early, online edition of the Proceedings of the National Academy of Sciences, an international team led by investigators in Israel explores genomic features associated with relapse in a form of B-cell acute lymphoblastic leukemia occurring in individuals with Down syndrome. The researchers did exome sequence data for samples taken at ALL diagnosis, remission, and relapse in 25 individuals with Down syndrome, identifying early rearrangements in CRLF2 — a gene previously implicated in the disease. In the diagnostic and relapse samples, they also uncovered activating mutations in the JAK-STAT pathway, prompting follow-up experiments to gauge the consequences of boosting or suppressing that signaling pathway.

Researchers from France, the US, Australia, and the Netherlands present evidence of strain structure in the malaria-causing Plasmodium falciparum parasites infecting children in a West African village called Bakoumba, in southeastern Gabon. Using deep, targeted sequencing, the researchers detected high levels of diversity across portions of var genes that code for important surface antigens on P. falciparum cells during the blood stage of malaria infection. The study's authors argue that the limited overlap between such genes "could facilitate persistence of the parasite in small host populations" and is expected to produce P. falciparum parasites that are particularly nimble at dodging human host immunity.

Finally, German investigators propose a role for the demethylase enzyme-coding gene Lsd1 in maintaining beige fat cells and staving off the transition to white fat cells in aging individuals. The team did a series of cell biology experiments in samples from young and old mice, including western blot analyses to track Lsd1 expression and fluorescence-tagged reporter proteins. Together, the results revealed Lsd1 expression dips in white adipose tissue from the elderly mice — a shift that appears to coincide with waning beige adipocyte numbers. "[A]dipocyte-specific increase of Lsd1 expression is sufficient to rescue the age-related transition of beige adipocytes in vivo," the authors write, "whereas loss of Lsd1 precipitates it."