The essence of turbulent flow is the conveyance of kinetic energy through the formation, interaction, and destruction of eddies over a wide range of spatial scalesfrom the largest scales where energy is injected, down to the smallest scales where it is dissipated through viscosity. For nearly a century, this universal energy cascade has been the foundation of our understanding for how turbulent flows function. However, a mechanistic description of how ensembles of vortices interact to drive this energy cascade remains elusive. Here we introduce one essential mechanism for turbulence. We show that a sequence of the elliptical instability, arising from the close interaction between counter-rotating vortices, leads to the emergence of turbulent flow. We demonstrate how the nonlinear development of the elliptical instability generates an ordered array of antiparallel secondary filaments, which are perpendicular to the original vortex tubes. These secondary filaments interact with one another, leading to the generation of even smaller tertiary filaments. This iterated cascade of the elliptical instability produces vortices of smaller and smaller sizes, until viscosity damps out all motion. In our experiments and simulations, we clearly observe two and three iterations of this cascade, respectively. Our observations indicate that the elliptical instability could be a fundamental mechanism by which the turbulent cascade develops and is sustained.

When vortex rings collide head-on at high enough Reynolds numbers, they ultimately annihilate through a violent interaction which breaks down their cores into a turbulent cloud. We experimentally show that this very strong interaction, which leads to the production of fluid motion at very fine scales, uncovers direct evidence of a novel iterative cascade of instabilities in a bulk fluid. When the coherent vortex cores approach each other, they deform into tent-like structures, and the mutual strain causes them to locally flatten into extremely thin vortex sheets. These sheets then break down into smaller secondary vortex filaments, which themselves rapidly flatten and break down into even smaller tertiary filaments. By performing numerical simulations of the full Navier-Stokes equations, we also resolve one iteration of this instability and highlight the subtle role that viscosity must play in the rupturing of a vortex sheet. The concurrence of this observed iterative cascade of instabilities over various scales with those of recent theoretical predictions could provide a new mechanistic framework in which the evolution of turbulent flows can be examined in real-time as a series of discrete dynamic instabilities. arXiv:1802.09973v3 [physics.flu-dyn]

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DNA double-strand breaks (DSBs), one of the most cytotoxic forms of DNA damage, can be repaired by the tightly regulated nonhomologous end joining (NHEJ) machinery (Stinson and Loparo and Zhao et al. ). Core NHEJ factors form an initial long-range (LR) synaptic complex that transitions into a DNA-PKcs (DNA-dependent protein kinase, catalytic subunit)–free, short-range state to align the DSB ends (Chen et al. ). Using single-particle cryo–electron microscopy, we have visualized three additional key NHEJ complexes representing different transition states, with DNA-PKcs adopting distinct dimeric conformations within each of them. Upon DNA-PKcs autophosphorylation, the LR complex undergoes a substantial conformational change, with both Ku and DNA-PKcs rotating outward to promote DNA break exposure and DNA-PKcs dissociation. We also captured a dimeric state of catalytically inactive DNA-PKcs, which resembles structures of other PIKK (Phosphatidylinositol 3-kinase-related kinase) family kinases, revealing a model of the full regulatory cycle of DNA-PKcs during NHEJ.

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