Researchers from the Max Planck Institute for Evolutionary Anthropology and other international centers report on findings from an analysis of 17 ancient Yersinia pestis isolates going back 2,500 to 5,000 years from Late Neolithic and Early Bronze Age sites in Eurasia. The team turned to targeted DNA enrichment to analyze the isolates, found by screening more than 250 samples at 15 archeological sites, ultimately generating 17 Y. pestis genomes that were compared to Y. pestis sequences assessed in the past. Among other findings, the authors note that the results of their genomic and phylogenetic analyses point to the presence of "the long-term coexistence in western Eurasia of two forms of Y. pestis (a fully flea-adapted and a non-flea-adapted form), which likely lasted for at least 2,500 [years]."
A team from the UK, US, South Africa, and Zambia describes a maternally inherited form of brood parasitism in the cuckoo finch, Anomalospiza imberbis, which is capable of mimicking egg features of the host species it parasitizes. Using mitochondrial genome sequencing, double-digest restriction site-associated DNA sequencing, and other approaches, the researchers profiled mitochondrial lineages, sex chromosome sequence variants, and autosomal genotypes in almost 200 cuckoo finches from maternal lineages associated with distinct host bird species. "[O]ur results suggest that at least 2 million years ago, selection from host defenses drove cuckoo finches to transfer control of egg appearance to the maternally inherited part of the genome, allowing host-specific mimicry to remain distinct in the face of gene flow between males and females raised by different hosts," they report, noting that "this seemingly effective solution has likely limited future adaptive potential: while maternal inheritance allows cuckoo finches to exploit multiple hosts, it should slow counteradaptation to hosts that benefit from sexual recombination to evolve polymorphic egg signatures as a further defense."
Finally, investigators in Chile, the US, and Mexico delve into the mechanisms underlying myeloid-derived suppressor cell (MDSC) activity in a mouse model. The diverse immunosuppressive cells have been implicated in everything from infections or inflammation to immunosuppression in the tumor microenvironment, the team explains, including tumor microenvironment activity spurred on by NADPH oxidase 2 (NOX2) enzymes that prompt reactive oxygen species production. Through a series of protein interaction, flow cytometry, immunofluorescence microscopy, and biophysics experiments, the authors saw signs that "immunosuppression by MDSC is conditional to their ability to decrease the proton concentration elevated by the NOX2 activity, rendering [the NOX2-related voltage-gated proton channel] Hv1 a potential drug target for cancer treatment."