Bacteriophages, infecting bacterial hosts in every environment on our planet, are a driver of adaptive evolution in bacterial communities. At the same time, the host range of many bacteriophages—and thus one of the selective pressures acting on complex microbial systems in nature—remains poorly characterized. Here, we computationally inferred the putative host ranges of 40 cluster P mycobacteriophages, including members from six sub-clusters (P1-P6). A series of comparative genomic analyses revealed that mycobacteriophages of sub-cluster P1 are restricted to the Mycobacterium genus, whereas mycobacteriophages of sub-clusters P2 to P6 are likely also able to infect other genera, several of which are commonly associated with human disease. Further genomic analysis highlighted that the majority of cluster P mycobacteriophages harbor a conserved integration-dependent immunity system, hypothesized to be the ancestral state of a genetic switch that controls the shift between lytic and lysogenic life cycles—a temperate characteristic that impedes their usage in anti-bacterial applications.
We characterized the complete genome of the cluster P mycobacteriophage Phegasus. Its 47.5-kb genome contains 81 protein-coding genes, 36 of which could be assigned a putative function. Phegasus is most closely related to two subcluster P1 bacteriophages, Mangethe and Majeke, with an average nucleotide identity of 99.63% each.
The Ts-Biotag transgenic mouse reports the expression of receptor tyrosine kinase Tie2, a known marker of angiogenic states for both vascular endothelial cells and macrophages. We demonstrate Ts-Biotag labeling and Tie2 expression in a neural injury model to find the majority of labeling occurs in the myeloid derived and brain resident cell type, microglia. Additionally the ligand of Tie2, Ang1, is dynamically expressed, first in astrocytes then neural progenitor during wound signaling and healing. These results offer a Tie2 specific, in vivo view of a neuroimmune response to injury, suggesting a microglia/neural progenitor intercellular interaction guides recovery from a brain lesion.
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