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This Week in PNAS: Jun 16, 2015

In the early, online edition of the Proceedings of the National Academy of Sciences, researchers from China, Spain, and Switzerland explore the history of a Mycobacterium tuberculosis genotype known as the Beijing family. The team considered genome sequences for more than 350 global M. tuberculosis isolates — including dozens of Beijing and non-Beijing strains that were newly sequenced for the study — as well as genotyping patterns for around 1,400 more. From the relationships detected in these strains, the study's authors conclude that the Beijing strain likely originated in the southeastern region of East Asia within the past 30,000 years, reaching to other parts of the world with migration from the area.

Researchers from the Ludwig Institute for Cancer Research and the University of California, San Diego, introduce a new sequencing scheme for examining chromatin structure. To perform this methidiumpropyl-EDTA sequencing, or MPE-seq, method, the team did massively parallel sequencing on chromatin after a step to digest nuclei with a chemical called MPE-Fe(II), which breaks down linker sequences between nucleosomes. In their proof-of-principle application of this approach, the study's authors compared MPE-seq with micrococcal nuclease (MNase) sequencing for characterizing chromatin structure patterns in mouse embryonic stem cells. There, they found, "MPE-seq reveals non-canonical chromatin structures in active promoter regions that are not seen with standard MNase-seq conditions."

Finally, a team from China takes a look at mutations behind the cracked vertebra condition dysplastic spondylolysis. Through exome sequencing on members of a multi-generational family from China that was prone to dysplastic spondylolysis, the researchers uncovered two autosomal dominant missense mutations in the sulfate transporter gene SLC26A2 that were present in all five affected individuals, but absent in their unaffected relatives. They detected still more mutations in the gene through targeted sequencing on another 30 unrelated individuals with the disease. Follow-up functional experiments hint that mutations in the gene may contribute to dysplastic spondylolysis by interfering with sulfate uptake and spinal development.