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1. Gypsy moth outbreaks cause severe defoliation in Holarctic forests, both in North America where it is invasive, and in its native range in Eurasia. Defoliation can hamper timber production and impact ecological communities and processes. Aerial insecticide applications are regularly performed in outbreak areas to mitigate economic losses. These operations can be financially costly and harmful to non-target species and may disrupt species interaction networks. However, replicated studies of the relative impacts of gypsy moth outbreaks and insecticide application on forest growth and animal communities are rare and have yet to be carried out in the species' indigenous range. 2. Here, we review the pathways in which gypsy moth outbreaks and the chemical control of these outbreaks affect forest ecosystems. We then present an experimental design established in South Central Germany in early 2019, aiming to study the ecological and economic consequences of gypsy moth eruptions and insecticide application in oak forests. The study's full factorial design comprises forest stands at high and low defoliation risk, either treated with tebufenozide or left unsprayed, within 12 experimental blocks. Measurements of forest growth and structure, tree mortality, gypsy moth density, and composition of lepidopteran, bird, bat, ground beetle, and canopy arthropod communities will be conducted for several years. 3. One-year intensive monitoring of gypsy moth populations and damage across the selected sites showed substantial differences in population density between plots at high and low defoliation risk and high efficacy of tebufenozide in suppressing gypsy moth populations in treated plots. In the first year of the experiment, gypsy moth density and defoliation in predicted outbreak plots differed strongly, confirming the This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
T cell activation and differentiation is associated with metabolic reprogramming to cope with the increased bioenergetic demand and to provide metabolic intermediates for the biosynthesis of building blocks. Antigen receptor stimulation not only promotes the metabolic switch of lymphocytes but also triggers the uptake of calcium (Ca2+) from the cytosol into the mitochondrial matrix. Whether mitochondrial Ca2+ influx through the mitochondrial Ca2+ uniporter (MCU) controls T cell metabolism and effector function remained, however, enigmatic. Using mice with T cell-specific deletion of MCU, we here show that genetic inactivation of mitochondrial Ca2+ uptake increased cytosolic Ca2+ levels following antigen receptor stimulation and store-operated Ca2+ entry (SOCE). However, ablation of MCU and the elevation of cytosolic Ca2+ did not affect mitochondrial respiration, differentiation and effector function of inflammatory and regulatory T cell subsets in vitro and in animal models of T cell-mediated autoimmunity and viral infection. These data suggest that MCU-mediated mitochondrial Ca2+ uptake is largely dispensable for murine T cell function. Our study has also important technical implications. Previous studies relied mostly on pharmacological inhibition or transient knockdown of mitochondrial Ca2+ uptake, but our results using mice with genetic deletion of MCU did not recapitulate these findings. The discrepancy of our study to previous reports hint at compensatory mechanisms in MCU-deficient mice and/or off-target effects of current MCU inhibitors.
Upon antigen-specific T Cell Receptor (TCR) engagement, human CD4+ T cells proliferate and differentiate, a process associated with rapid transcriptional changes and metabolic reprogramming. Here, we show that generation of extra-mitochondrial pyruvate is an essential step for acetyl-CoA production and subsequent H3K27ac-mediated epigenome remodeling. In contrast, neither acetate/ACSS2 nor citrate/ACLY metabolism are required for activation-induced transcriptional changes. Furthermore, T cell activation results in the nuclear translocation of PDC and its association with both the p300 acetyltransferase and histone H3K27ac. These data support tight integration of metabolic and histone-modifying enzymes, allowing metabolic reprogramming to fuel CD4+ T cell activation. Targeting this pathway may provide a novel therapeutic approach to specifically regulate antigen-driven T cell activation.
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