@article{10614,
  abstract     = {The infiltration of immune cells into tissues underlies the establishment of tissue-resident macrophages and responses to infections and tumors. Yet the mechanisms immune cells utilize to negotiate tissue barriers in living organisms are not well understood, and a role for cortical actin has not been examined. Here, we find that the tissue invasion of Drosophila macrophages, also known as plasmatocytes or hemocytes, utilizes enhanced cortical F-actin levels stimulated by the Drosophila member of the fos proto oncogene transcription factor family (Dfos, Kayak). RNA sequencing analysis and live imaging show that Dfos enhances F-actin levels around the entire macrophage surface by increasing mRNA levels of the membrane spanning molecular scaffold tetraspanin TM4SF, and the actin cross-linking filamin Cheerio, which are themselves required for invasion. Both the filamin and the tetraspanin enhance the cortical activity of Rho1 and the formin Diaphanous and thus the assembly of cortical actin, which is a critical function since expressing a dominant active form of Diaphanous can rescue the Dfos macrophage invasion defect. In vivo imaging shows that Dfos enhances the efficiency of the initial phases of macrophage tissue entry. Genetic evidence argues that this Dfos-induced program in macrophages counteracts the constraint produced by the tension of surrounding tissues and buffers the properties of the macrophage nucleus from affecting tissue entry. We thus identify strengthening the cortical actin cytoskeleton through Dfos as a key process allowing efficient forward movement of an immune cell into surrounding tissues. },
  author       = {Belyaeva, Vera and Wachner, Stephanie and György, Attila and Emtenani, Shamsi and Gridchyn, Igor and Akhmanova, Maria and Linder, M and Roblek, Marko and Sibilia, M and Siekhaus, Daria E},
  issn         = {1545-7885},
  journal      = {PLoS Biology},
  number       = {1},
  pages        = {e3001494},
  publisher    = {Public Library of Science},
  title        = {{Fos regulates macrophage infiltration against surrounding tissue resistance by a cortical actin-based mechanism in Drosophila}},
  doi          = {10.1371/journal.pbio.3001494},
  volume       = {20},
  year         = {2022},
}

@unpublished{8557,
  abstract     = {The infiltration of immune cells into tissues underlies the establishment of tissue resident macrophages, and responses to infections and tumors. Yet the mechanisms immune cells utilize to negotiate tissue barriers in living organisms are not well understood, and a role for cortical actin has not been examined. Here we find that the tissue invasion of Drosophila macrophages, also known as plasmatocytes or hemocytes, utilizes enhanced cortical F-actin levels stimulated by the Drosophila member of the fos proto oncogene transcription factor family (Dfos, Kayak). RNA sequencing analysis and live imaging show that Dfos enhances F-actin levels around the entire macrophage surface by increasing mRNA levels of the membrane spanning molecular scaffold tetraspanin TM4SF, and the actin cross-linking filamin Cheerio which are themselves required for invasion. Cortical F-actin levels are critical as expressing a dominant active form of Diaphanous, a actin polymerizing Formin, can rescue the Dfos Dominant Negative macrophage invasion defect. In vivo imaging shows that Dfos is required to enhance the efficiency of the initial phases of macrophage tissue entry. Genetic evidence argues that this Dfos-induced program in macrophages counteracts the constraint produced by the tension of surrounding tissues and buffers the mechanical properties of the macrophage nucleus from affecting tissue entry. We thus identify tuning the cortical actin cytoskeleton through Dfos as a key process allowing efficient forward movement of an immune cell into surrounding tissues.},
  author       = {Belyaeva, Vera and Wachner, Stephanie and Gridchyn, Igor and Linder, Markus and Emtenani, Shamsi and György, Attila and Sibilia, Maria and Siekhaus, Daria E},
  booktitle    = {bioRxiv},
  title        = {{Cortical actin properties controlled by Drosophila Fos aid macrophage infiltration against surrounding tissue resistance}},
  doi          = {10.1101/2020.09.18.301481},
  year         = {2020},
}

@misc{8563,
  abstract     = {Supplementary data  provided for the provided for the publication:
Igor Gridchyn , Philipp Schoenenberger , Joseph O'Neill , Jozsef Csicsvari (2020) Optogenetic inhibition-mediated activity-dependent modification of CA1 pyramidal-interneuron connections during behavior. Elife.},
  author       = {Csicsvari, Jozsef L and Gridchyn, Igor and Schönenberger, Philipp},
  publisher    = {Institute of Science and Technology Austria},
  title        = {{Optogenetic alteration of hippocampal network activity}},
  doi          = {10.15479/AT:ISTA:8563},
  year         = {2020},
}

@article{8740,
  abstract     = {In vitro work revealed that excitatory synaptic inputs to hippocampal inhibitory interneurons could undergo Hebbian, associative, or non-associative plasticity. Both behavioral and learning-dependent reorganization of these connections has also been demonstrated by measuring spike transmission probabilities in pyramidal cell-interneuron spike cross-correlations that indicate monosynaptic connections. Here we investigated the activity-dependent modification of these connections during exploratory behavior in rats by optogenetically inhibiting pyramidal cell and interneuron subpopulations. Light application and associated firing alteration of pyramidal and interneuron populations led to lasting changes in pyramidal-interneuron connection weights as indicated by spike transmission changes. Spike transmission alterations were predicted by the light-mediated changes in the number of pre- and postsynaptic spike pairing events and by firing rate changes of interneurons but not pyramidal cells. This work demonstrates the presence of activity-dependent associative and non-associative reorganization of pyramidal-interneuron connections triggered by the optogenetic modification of the firing rate and spike synchrony of cells.},
  author       = {Gridchyn, Igor and Schönenberger, Philipp and O'Neill, Joseph and Csicsvari, Jozsef L},
  issn         = {2050084X},
  journal      = {eLife},
  publisher    = {eLife Sciences Publications},
  title        = {{Optogenetic inhibition-mediated activity-dependent modification of CA1 pyramidal-interneuron connections during behavior}},
  doi          = {10.7554/eLife.61106},
  volume       = {9},
  year         = {2020},
}

@article{7684,
  author       = {Gridchyn, Igor and Schönenberger, Philipp and O'Neill, Joseph and Csicsvari, Jozsef L},
  issn         = {10974199},
  journal      = {Neuron},
  number       = {2},
  pages        = {291--300.e6},
  publisher    = {Elsevier},
  title        = {{Assembly-specific disruption of hippocampal replay leads to selective memory deficit}},
  doi          = {10.1016/j.neuron.2020.01.021},
  volume       = {106},
  year         = {2020},
}

@phdthesis{48,
  abstract     = {The hippocampus is a key brain region for spatial memory and navigation and is needed at all stages of memory, including encoding, consolidation, and recall. Hippocampal place cells selectively discharge at specific locations of the environment to form a cognitive map of the space. During the rest period and sleep following spatial navigation and/or learning, the waking activity of the place cells is reactivated within high synchrony events. This reactivation is thought to be important for memory consolidation and stabilization of the spatial representations. The aim of my thesis was to directly test whether the reactivation content encoded in firing patterns of place cells is important for consolidation of spatial memories. In particular, I aimed to test whether, in cases when multiple spatial memory traces are acquired during learning, the specific disruption of the reactivation of a subset of these memories leads to the selective disruption of the corresponding memory traces or through memory interference the other learned memories are disrupted as well. In this thesis, using a modified cheeseboard paradigm and a closed-loop recording setup with feedback optogenetic stimulation, I examined how the disruption of the reactivation of specific spiking patterns affects consolidation of the corresponding memory traces. To obtain multiple distinctive memories, animals had to perform a spatial task in two distinct cheeseboard environments and the reactivation of spiking patterns associated with one of the environments (target) was disrupted after learning during four hours rest period using a real-time decoding method. This real-time decoding method was capable of selectively affecting the firing rates and cofiring correlations of the target environment-encoding cells. The selective disruption led to behavioural impairment in the memory tests after the rest periods in the target environment but not in the other undisrupted control environment. In addition, the map of the target environment was less stable in the impaired memory tests compared to the learning session before than the map of the control environment. However, when the animal relearned the task, the same map recurred in the target environment that was present during learning before the disruption. Altogether my work demonstrated that the reactivation content is important: assembly-related disruption of reactivation can lead to a selective memory impairment and deficiency in map stability. These findings indeed suggest that reactivated assembly patterns reflect processes associated with the consolidation of memory traces. },
  author       = {Gridchyn, Igor},
  issn         = {2663-337X},
  pages        = {104},
  publisher    = {Institute of Science and Technology Austria},
  title        = {{Reactivation content is important for consolidation of spatial memory}},
  doi          = {10.15479/AT:ISTA:th_1042},
  year         = {2018},
}

@inproceedings{2276,
  abstract     = {The problem of minimizing the Potts energy function frequently occurs in computer vision applications. One way to tackle this NP-hard problem was proposed by Kovtun [19, 20]. It identifies a part of an optimal solution by running k maxflow computations, where k is the number of labels. The number of “labeled” pixels can be significant in some applications, e.g. 50-93% in our tests for stereo. We show how to reduce the runtime to O (log k) maxflow computations (or one parametric maxflow computation). Furthermore, the output of our algorithm allows to speed-up the subsequent alpha expansion for the unlabeled part, or can be used as it is for time-critical applications. To derive our technique, we generalize the algorithm of Felzenszwalb et al. [7] for Tree Metrics . We also show a connection to k-submodular functions from combinatorial optimization, and discuss k-submodular relaxations for general energy functions.},
  author       = {Gridchyn, Igor and Kolmogorov, Vladimir},
  location     = {Sydney, Australia},
  pages        = {2320 -- 2327},
  publisher    = {IEEE},
  title        = {{Potts model, parametric maxflow and k-submodular functions}},
  doi          = {10.1109/ICCV.2013.288},
  year         = {2013},
}

