TY - JOUR TI - Modulation of occluding junctions alters the hematopoietic niche to trigger immune activation AU - Khadilkar, Rohan J AU - Vogl, Wayne AU - Goodwin, Katharine AU - Tanentzapf, Guy A2 - Yamashita, Yukiko M VL - 6 PY - 2017 DA - 2017/08/25 SP - e28081 C1 - eLife 2017;6:e28081 DO - 10.7554/eLife.28081 UR - https://doi.org/10.7554/eLife.28081 AB - Stem cells are regulated by signals from their microenvironment, or niche. During Drosophila hematopoiesis, a niche regulates prohemocytes to control hemocyte production. Immune challenges activate cell-signalling to initiate the cellular and innate immune response. Specifically, certain immune challenges stimulate the niche to produce signals that induce prohemocyte differentiation. However, the mechanisms that promote prohemocyte differentiation subsequent to immune challenges are poorly understood. Here we show that bacterial infection induces the cellular immune response by modulating occluding-junctions at the hematopoietic niche. Occluding-junctions form a permeability barrier that regulates the accessibility of prohemocytes to niche derived signals. The immune response triggered by infection causes barrier breakdown, altering the prohemocyte microenvironment to induce immune cell production. Moreover, genetically induced barrier ablation provides protection against infection by activating the immune response. Our results reveal a novel role for occluding-junctions in regulating niche-hematopoietic progenitor signalling and link this mechanism to immune cell production following infection. KW - occluding junctions KW - hematopoiesis KW - immunity KW - infection KW - permeability barrier KW - prohemocytes JF - eLife SN - 2050-084X PB - eLife Sciences Publications, Ltd ER -