@article{679,
  abstract     = {Protective responses against pathogens require a rapid mobilization of resting neutrophils and the timely removal of activated ones. Neutrophils are exceptionally short-lived leukocytes, yet it remains unclear whether the lifespan of pathogen-engaged neutrophils is regulated differently from that in the circulating steady-state pool. Here, we have found that under homeostatic conditions, the mRNA-destabilizing protein tristetraprolin (TTP) regulates apoptosis and the numbers of activated infiltrating murine neutrophils but not neutrophil cellularity. Activated TTP-deficient neutrophils exhibited decreased apoptosis and enhanced accumulation at the infection site. In the context of myeloid-specific deletion of Ttp, the potentiation of neutrophil deployment protected mice against lethal soft tissue infection with Streptococcus pyogenes and prevented bacterial dissemination. Neutrophil transcriptome analysis revealed that decreased apoptosis of TTP-deficient neutrophils was specifically associated with elevated expression of myeloid cell leukemia 1 (Mcl1) but not other antiapoptotic B cell leukemia/ lymphoma 2 (Bcl2) family members. Higher Mcl1 expression resulted from stabilization of Mcl1 mRNA in the absence of TTP. The low apoptosis rate of infiltrating TTP-deficient neutrophils was comparable to that of transgenic Mcl1-overexpressing neutrophils. Our study demonstrates that posttranscriptional gene regulation by TTP schedules the termination of the antimicrobial engagement of neutrophils. The balancing role of TTP comes at the cost of an increased risk of bacterial infections.},
  author       = {Ebner, Florian and Sedlyarov, Vitaly and Tasciyan, Saren and Ivin, Masa and Kratochvill, Franz and Gratz, Nina and Kenner, Lukas and Villunger, Andreas and Sixt, Michael K and Kovarik, Pavel},
  issn         = {00219738},
  journal      = {The Journal of Clinical Investigation},
  number       = {6},
  pages        = {2051 -- 2065},
  publisher    = {American Society for Clinical Investigation},
  title        = {{The RNA-binding protein tristetraprolin schedules apoptosis of pathogen-engaged neutrophils during bacterial infection}},
  doi          = {10.1172/JCI80631},
  volume       = {127},
  year         = {2017},
}

@article{960,
  abstract     = {The human cerebral cortex is the seat of our cognitive abilities and composed of an extraordinary number of neurons, organized in six distinct layers. The establishment of specific morphological and physiological features in individual neurons needs to be regulated with high precision. Impairments in the sequential developmental programs instructing corticogenesis lead to alterations in the cortical cytoarchitecture which is thought to represent the major underlying cause for several neurological disorders including neurodevelopmental and psychiatric diseases. In this review we discuss the role of cell polarity at sequential stages during cortex development. We first provide an overview of morphological cell polarity features in cortical neural stem cells and newly-born postmitotic neurons. We then synthesize a conceptual molecular and biochemical framework how cell polarity is established at the cellular level through a break in symmetry in nascent cortical projection neurons. Lastly we provide a perspective how the molecular mechanisms applying to single cells could be probed and integrated in an in vivo and tissue-wide context.},
  author       = {Hansen, Andi H and Düllberg, Christian F and Mieck, Christine and Loose, Martin and Hippenmeyer, Simon},
  issn         = {16625102},
  journal      = {Frontiers in Cellular Neuroscience},
  publisher    = {Frontiers Research Foundation},
  title        = {{Cell polarity in cerebral cortex development - cellular architecture shaped by biochemical networks}},
  doi          = {10.3389/fncel.2017.00176},
  volume       = {11},
  year         = {2017},
}