In a paper published online in advance in Nature this week, a team led by investigators at the University of Exeter reports on a new fungal clade, which they've named "cryptomycota in anticipation of formal classification." Using environmental DNA analyses and fluorescent detection via DNA probes, coupled to phylogenetic analyses, the team found that this new clade — which is "present in numerous ecosystems including soil, freshwater and aquatic sediments" — should be placed with Rozella, the putative primary branch of the fungal kingdom.
In another Nature advance online publication, an international team led by researchers at the Academy of Athens in Greece describes "a novel tumor-suppressor function for the Notch pathway in myeloid leukemia." More specifically, using transcriptome and other analyses, the Athens-led team found that "Notch signaling regulates an extensive myelomonocytic-specific gene signature, through the direct suppression of gene transcription by the Notch target Hes1," which, when combined with previous reports, suggests that the "Notch pathway can play both tumor-promoting and -suppressive roles within the same tissue," the authors write.
Researchers at Children's Hospital Boston and elsewhere this week present two approaches to profile the genomic localization of 5-hydroxymethylcytosine, or 5hmC. The first involves glucosylation, periodate oxidation, and biotinylation — or GLIB — to "isolate DNA fragments containing as few as a single 5hmC," the team writes. The second involved the conversion of 5hmC to cytosine 5-methylenesulphonate via sodium bisulphite, "followed by immunoprecipitation of CMS-containing DNA with a specific antiserum to CMS5." Using either approach coupled to high-throughput sequencing of 5hmC-containing DNA derived from mouse embryonic stem cells, the team found "strong enrichment within exons and near transcriptional start sites," suggesting that "5hmC has a probable role in transcriptional regulation," the authors write.
Over in Nature Genetics this week, investigators at the Sutton, UK-based Institute of Cancer Research and their colleagues report the use of exome sequencing and a variant prioritization strategy to identify the cause of mosaic variegated aneuploidy syndrome — biallelic, loss-of-function mutations in CEP57, a centrosomal protein involved in microtubule nucleating and stabilizing.