Editor's Note: Some of the articles described below are not yet available at the PNAS site, but they are scheduled to be posted some time this week.
For a paper scheduled to appear in PNAS this week, a team from the UK, Germany, the US, and elsewhere presents findings from a genomic analysis of the Hispaniolan solenodon, Solenodon paradoxus, a shrew-like, insect-eating mammal that produces venom. The researchers tapped into a new genome assembly generated with DNA from a captive male Hispaniolan solenodon from the Dominican Republic, together with proteomic, phylogenetic, and other data, to look at the roots of this venom production, demonstrating that the Hispaniolan solenodon shares venom features with other members of the eulipotyphlan mammalian order such as shrews that arose through convergent evolution. "We demonstrate that venom has evolved independently on at least [four] occasions in eulipotyphlans, and that molecular components of these venoms have also evolved convergently … in both solenodons and shrews following their divergence over 70 million years ago," they write.
University of Wisconsin at Madison and Beth Israel Deaconess Medical Center researchers track Epstein-Barr virus (EBV) amplification in replication compartments with quantitative PCR, single-cell assays such as fluorescence in situ hybridization or live-cell imaging, computational models, and other analytical strategies. Their results — using an EBV strain called P3HR1 and a shorter EBV-derived amplicon — suggest that individual EBV genomes can be dramatically amplified within 14 hours, for example, leading to increased replication compartment and nuclear volumes. The team also saw a shift from DNA template-limited DNA synthesis during the early stages of EBV amplification to later-stage processes marked by abundant template levels, but waning viral machinery levels. "These findings demonstrate that the amplification of EBV DNA in a population of cells is coordinated through the seeding and subsequent DNA synthesis supported in each replication compartment," the authors report.
Pennsylvania State University and University of California, Berkeley, investigators take a look at mitochondrial heteroplasmy in nearly 350 individuals from 96 multigenerational families. Using SNP profiling or sequencing on two tissues apiece, the team searched for situations in which individuals carried multiple mitochondrial DNA haplotypes, retracing the origins of the heteroplasmic events — from mtDNA mutation to the selection processes that take place in somatic tissue and the germline in relation to maternal age and other factors. "We show that mothers effectively transmit very few mitochondrial DNA to their offspring," the researchers report. "Because of this bottleneck, which intensifies with increasing maternal age at childbirth, mutation frequencies can change dramatically between a mother and her child."