Epithelia remove excess cells through extrusion, and prevent accumulation of unnecessary or pathological cells. The extrusion process can be triggered by apoptotic signaling1, oncogenic transformation2,3, and overcrowding of cells4–6. Despite the important links of cell extrusion to developmental7, homeostatic5 and pathological processes2,8,9 such as cancer metastasis, its underlying mechanism and connections to the intrinsic mechanics of the epithelium are largely unexplored. Here, we show that apoptotic cell extrusion is provoked by singularities in cell alignments9,10 in the form of comet-like topological defects. We find a universal correlation between the extrusion sites and positions of nematic defects in the cell orientation field in different epithelium types. We model the epithelium as an active nematic liquid crystal and compare numerical simulations to strain rate and stress measurements within cell monolayers. The results confirm the active nematic nature of epithelia for the first time, and demonstrate that defect-induced isotropic stresses are the primary precursor of mechanotransductive responses in cells such as YAP (Yes-associated protein) transcription factor activity11, caspase-3 mediated cell death, and extrusions. Importantly, the defect-driven extrusion mechanism depends on intercellular junctions, since the weakening of cell-cell interactions in α-catenin knockdown (α-catKD) monolayer reduces the defect size and increases both the number of defects and extrusion rates, as also predicted by our model. We further demonstrate the ability to control extrusion hotspots by geometrically inducing defects through microcontact-printing of patterned monolayers. Together we propose a novel mechanism for apoptotic cell extrusion: spontaneously formed topological defects in epithelia govern cell fate. This new finding has important implications in predicting extrusion hotspots and dynamics in vivo, with potential applications to tissue regeneration and metastasis suppression. Moreover, we anticipate that the analogy between the epithelium and active nematic liquid crystals will trigger further investigations of the link between cellular processes and the material properties of epithelia.

Modern high-power lasers can generate extreme states of matter that are relevant to astrophysics, equation-of-state studies and fusion energy research. Laser-driven implosions of spherical polymer shells have, for example, achieved an increase in density of 1,000 times relative to the solid state. These densities are large enough to enable controlled fusion, but to achieve energy gain a small volume of compressed fuel (known as the 'spark') must be heated to temperatures of about 108 K (corresponding to thermal energies in excess of 10 keV). In the conventional approach to controlled fusion, the spark is both produced and heated by accurately timed shock waves, but this process requires both precise implosion symmetry and a very large drive energy. In principle, these requirements can be significantly relaxed by performing the compression and fast heating separately; however, this 'fast ignitor' approach also suffers drawbacks, such as propagation losses and deflection of the ultra-intense laser pulse by the plasma surrounding the compressed fuel. Here we employ a new compression geometry that eliminates these problems; we combine production of compressed matter in a laser-driven implosion with picosecond-fast heating by a laser pulse timed to coincide with the peak compression. Our approach therefore permits efficient compression and heating to be carried out simultaneously, providing a route to efficient fusion energy production.

Understanding cell morphogenesis during metazoan development requires knowledge of how cells and the extracellular matrix produce and respond to forces. We investigated how apoptosis, which remodels tissue by eliminating supernumerary cells, also contributes forces to a tissue (the amnioserosa) that promotes cell-sheet fusion (dorsal closure) in the Drosophila embryo. We showed that expression in the amnioserosa of proteins that suppress or enhance apoptosis slows or speeds dorsal closure, respectively. These changes correlate with the forces produced by the amnioserosa and the rate of seam formation between the cell sheets (zipping), key processes that contribute to closure. This apoptotic force is used by the embryo to drive cell-sheet movements during development, a role not classically attributed to apoptosis.

Rapid heating of a compressed fusion fuel by a short-duration laser pulse is a promising route to generating energy by nuclear fusion, and has been demonstrated on an experimental scale using a novel fast-ignitor geometry. Here we describe a refinement of this system in which a much more powerful, pulsed petawatt (10(15) watts) laser creates a fast-heated core plasma that is scalable to full-scale ignition, significantly increasing the number of fusion events while still maintaining high heating efficiency at these substantially higher laser energies. Our findings bring us a step closer to realizing the production of relatively inexpensive, full-scale fast-ignition laser facilities.