@article{20859, abstract = {Effective immune responses rely on the efficient migration of leukocytes. Yet, how temperature regulates migration dynamics at the single-cell level has remained poorly understood. Using zebrafish embryos and mouse tissue explants, we found that temperature positively regulates leukocyte migration speed, exploration, and arrival frequencies to wounds and lymph vessels. Complementary 2D and 3D cultures revealed that this thermokinetic control of cell migration is conserved across immune cell types, independently of the 3D tissue environment. By applying precise (sub-)cellular temperature modulation, we identified a rapid and reversible thermo-response that depends on myosin II activity. Small physiological increases in temperature (1°C –2°C), as present during fever-like conditions, profoundly increased immune responses by accelerating arrival times at lymphatic vessels and tissue wounds. These findings identify myosin-II-dependent actomyosin contractility as a critical mechanical structure regulating single-cell thermo-adaptability, with physiological implications for tuning the speed of immune responses in vivo.}, author = {Company-Garrido, Iván and Zurita Carpio, Alberto and Colomer-Rosell, Mariona and Ciraulo, Bernard and Molkenbur, Ronja and Lanzerstorfer, Peter and Pezzano, Fabio and Agazzi, Costanza and Hauschild, Robert and Jain, Saumey and Jacques, Jeroen M. and Venturini, Valeria and Knapp, Christian and Xie, Yufei and Merrin, Jack and Weghuber, Julian and Schaaf, Marcel and Quidant, Romain and Kiermaier, Eva and Ortega Arroyo, Jaime and Ruprecht, Verena and Wieser, Stefan}, issn = {1878-1551}, journal = {Developmental Cell}, keywords = {thermobiology, cell migration, thermo-adaptability of immune cells}, number = {2}, pages = {356--371.e12}, publisher = {Elsevier}, title = {{Myosin II regulates cellular thermo-adaptability and the efficiency of immune responses}}, doi = {10.1016/j.devcel.2025.10.006}, volume = {61}, year = {2026}, } @phdthesis{14530, abstract = {Most motions of many-body systems at any scale in nature with sufficient degrees of freedom tend to be chaotic; reaching from the orbital motion of planets, the air currents in our atmosphere, down to the water flowing through our pipelines or the movement of a population of bacteria. To the observer it is therefore intriguing when a moving collective exhibits order. Collective motion of flocks of birds, schools of fish or swarms of self-propelled particles or robots have been studied extensively over the past decades but the mechanisms involved in the transition from chaos to order remain unclear. Here, the interactions, that in most systems give rise to chaos, sustain order. In this thesis we investigate mechanisms that preserve, destabilize or lead to the ordered state. We show that endothelial cells migrating in circular confinements transition to a collective rotating state and concomitantly synchronize the frequencies of nucleating actin waves within individual cells. Consequently, the frequency dependent cell migration speed uniformizes across the population. Complementary to the WAVE dependent nucleation of traveling actin waves, we show that in leukocytes the actin polymerization depending on WASp generates pushing forces locally at stationary patches. Next, in pipe flows, we study methods to disrupt the self--sustaining cycle of turbulence and therefore relaminarize the flow. While we find in pulsating flow conditions that turbulence emerges through a helical instability during the decelerating phase. Finally, we show quantitatively in brain slices of mice that wild-type control neurons can compensate the migratory deficits of a genetically modified neuronal sub--population in the developing cortex. }, author = {Riedl, Michael}, issn = {2663-337X}, keywords = {Synchronization, Collective Movement, Active Matter, Cell Migration, Active Colloids}, pages = {260}, publisher = {Institute of Science and Technology Austria}, title = {{Synchronization in collectively moving active matter}}, doi = {10.15479/14530}, year = {2023}, } @article{6354, abstract = {Blood platelets are critical for hemostasis and thrombosis, but also play diverse roles during immune responses. We have recently reported that platelets migrate at sites of infection in vitro and in vivo. Importantly, platelets use their ability to migrate to collect and bundle fibrin (ogen)-bound bacteria accomplishing efficient intravascular bacterial trapping. Here, we describe a method that allows analyzing platelet migration in vitro, focusing on their ability to collect bacteria and trap bacteria under flow.}, author = {Fan, Shuxia and Lorenz, Michael and Massberg, Steffen and Gärtner, Florian R}, issn = {2331-8325}, journal = {Bio-Protocol}, keywords = {Platelets, Cell migration, Bacteria, Shear flow, Fibrinogen, E. coli}, number = {18}, publisher = {Bio-Protocol}, title = {{Platelet migration and bacterial trapping assay under flow}}, doi = {10.21769/bioprotoc.3018}, volume = {8}, year = {2018}, } @misc{5570, abstract = {Matlab script to calculate the forward migration indexes (/) from TrackMate spot-statistics files.}, author = {Hauschild, Robert}, keywords = {Cell migration, tracking, forward migration index, FMI}, publisher = {Institute of Science and Technology Austria}, title = {{Forward migration indexes}}, doi = {10.15479/AT:ISTA:75}, year = {2017}, } @misc{5555, abstract = {This FIJI script calculates the population average of the migration speed as a function of time of all cells from wide field microscopy movies.}, author = {Hauschild, Robert}, keywords = {cell migration, wide field microscopy, FIJI}, publisher = {Institute of Science and Technology Austria}, title = {{Fiji script to determine average speed and direction of migration of cells}}, doi = {10.15479/AT:ISTA:44}, year = {2016}, }