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Science Papers Examine Eukaryotic Genome Folding, B Cells in Chronic Infectious Disease

An analysis of genome folding across the eukaryotic tree of life is reported in this week's Science, identifying condensin II — a protein complex involved in mitotic chromosome assembly — as a determinate of genome architecture. To better understand the mechanisms controlling nuclear architecture at the scale of whole chromosomes, a team led by scientists from the Netherlands Cancer Institute performed in situ Hi-C on 24 species covering all subphyla of chordates, all seven extant vertebrate classes, and seven of nine major animal phyla, plus plants and fungi. They discovered that the type of architecture exhibited by an organism correlates with the absence of condensin II subunits. They also found that condensin II depletion converts the human genome architecture to a state similar to that in organisms such as fungi or mosquitos, where centromeres cluster together at nucleoli and heterochromatin domains merge. Based on these observations, the researchers propose a model in which condensin II establishes interphase 3D genome architecture at the scale of whole chromosomes. This mechanism, they write, "likely has been conserved since the last common ancestor of all eukaryotes."

Chronic infectious diseases such as malaria and HIV affect the human B cell compartment, but the full extent of these effects is unknown. To increase their understanding, a group led by researchers from the US National Institutes of Health and Tel Aviv University used single-cell RNA sequencing and other approaches to perform in-depth transcriptional analyses of B cells from adults and children living in malaria-endemic Africa, HIV-infected individuals, and healthy US adults. They identify unique subpopulations of B cells, dubbed atypical B cells (ABCs), in malaria that show significant similarities to similar cells in HIV and in autoimmune diseases, which they call an unexpected observation that suggests ABCs represent a separate B cell lineage with a common initiator in different chronic diseases. Focusing on malaria, the researchers also identified ABC subsets based on isotype expression that differed in expansion in African children and in B cell receptor repertoire characteristics.