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PNAS Papers on Phytoplankton Microbes, Common Fragile Site Replication, Mesothelioma Susceptibility

Editor's Note: Some of the articles described below are not yet available at the PNAS site but are scheduled to be posted this week.

Researchers at the University of Rhode Island and Duke University explore ties between marine phytoplankton genotype and the microbial communities associated with them. Using 16S ribosomal RNA gene sequencing and host genotyping, the team initially characterized microbiome features found in environmental ocean samples collected at nine sites in three oceans at 12 time points, focusing on samples that contained single-celled Thalassiosira rotula phytoplankton. The results revealed eight T. rotula populations that fell into distinct genetic clusters with non-overlapping microbial community members — findings the authors explored further in a phytoplankton garden experiments involving T. rotula representatives spanning three populations and eight genotypes. "Through examination of a single phytoplankton species' microbiome across the global ocean, we found that host genotype strongly influenced microbiome community composition," they report, "with associations that potentially persist across generations and ocean basins but assembly rapidly (within days)."

For another paper slated to appear in PNAS this week, a team from Albert Einstein College of Medicine, the University of Texas, and Rutgers University outline a role for a polymerase (Pol)-coding gene called POLH and the eta enzyme it encodes in DNA replication at genetically unstable "common fragile sites" (CFSs) in the human genome. "Repetitive sequences located at CFS loci are inefficiently copied by replicative DNA polymerase (Pol) delta," the authors say, noting that the "translesion synthesis Pol eta has been shown to efficiently polymerize CFS-associated repetitive sequences in vitro and facilitate CFS stability by a mechanism that is not fully understood." Based on results from their locus-specific "single-molecule analysis of replicated DNA" (SMARD) DNA replication assay experiments in fibroblast and lymphoblast cells, the researchers saw signs that Pol eta involved in CFS replication, including replication across genetically variable sites in human populations.

An international team led by University of Hawaii Cancer Center investigators dig into potential mechanisms for increased risk of mesothelioma after asbestos exposure in individuals carrying one mutated copy of the BAP1 gene. With protein interaction and other cell line and mouse experiments, the researchers detected interactions between BAP1, an inflammation-related high-mobility group box 1 protein (HMGB1), and the histone deacetylase enzyme HDAC1, prompting them to suggest a model for the gene-by-environment links between BAP1 mutations and asbestos carcinogenesis that involves excess HDAC1 ubiquitylation and degradation, along with enhanced HMGB1 acetylation and secretion. On the other hand, they note that HMGB1 inhibition can dial down mesothelioma risk and boost survival in mouse models of "BAP1 cancer syndrome" that carry one altered version of the BAP1 gene.