Cleavage of the apoptosis inhibitor DIAP1 by the apical caspase DRONC in both normal and apoptotic drosophila cells

In Drosophila S2 cells, the apical caspase DRONC undergoes a low level of spontaneous autoprocessing. Unintended apoptosis is prevented by the inhibitor of apoptosis DIAP1, which targets the processed form of DRONC for degradation through its E3 ubiquitin protein ligase activity. Recent reports have demonstrated that shortly after the initiation of apoptosis in S2 cells, DIAP1 is cleaved following aspartate residue Asp-20 by the effector caspase DrICE. Here we report a novel caspase-mediated cleavage of DIAP1 in S2 cells. In both living and dying S2 cells, DIAP1 is cleaved by DRONC after glutamate residue Glu-205, located between the first and second BIR domains. The mutation of Glu-205 prevented the interaction of DIAP1 and processed DRONC but had no effect on the interaction with full-length DRONC. The mutation of Glu-205 also had a negative effect on the ability of overexpressed DIAP1 to prevent apoptosis stimulated by the proapoptotic protein Reaper or by UV light. These results expand our knowledge of the events that occur in the Drosophila apoptosome prior to and after receiving an apoptotic signal

The Drosophila DIAP1 protein is required to prevent accumulation of a continuously generated, processed form of the apical caspase DRONC

Although loss of the inhibitor of apoptosis (LAP) protein DIAP1 has been shown to result in caspase activation and spontaneous cell death in Drosophila cells and embryos, the point at which DIAP1 normally functions to inhibit caspase activation is unknown. Depletion of the DIAP1 protein in Drosophila S2 cells or the Sf-IAP protein in Spodoptera frugiperda Sf21 cells by RNA interference (RNAi) or cycloheximide treatment resulted in rapid and widespread caspase-dependent apoptosis. Co-silencing of dronc or dark largely suppressed this apoptosis, indicating that DIAP1 is normally required to inhibit an activity dependent on these proteins. Silencing of dronc also inhibited DRICE processing following stimulation of apoptosis, demonstrating that DRONC functions as an apical caspase in S2 cells. Silencing of diap1 or treatment with UV light induced DRONC processing, which occurred in two steps. The first step appeared to occur continuously even in the absence of an apoptotic signal and to be dependent on DARK because full-length DRONC accumulated when dark was silenced in non-apoptotic cells. In addition, treatment with the proteasome inhibitor MG132 resulted in accumulation of this initially processed form of DRONC, but not full-length DRONC, in non-apoptotic cells. The second step in DRONC processing was observed only in apoptotic cells. These results indicate that the initial step in DRONC processing occurs continuously via a DARK-dependent mechanism in Drosophila cells and that DIAP1 is required to prevent excess accumulation of this first form of processed DRONC, presumably through its ability to act as a ubiquitin-protein ligase

Self-field effects upon the critical current density of flat superconducting strips

We develop a general theory to account self-consistently for self-field effects upon the average transport critical current density Jc of a flat type-II superconducting strip in the mixed state when the bulk pinning is characterized by a field-dependent depinning critical current density Jp(B), where B is the local magnetic flux density. We first consider the possibility of both bulk and edge-pinning contributions but conclude that bulk pinning dominates over geometrical edge-barrier effects in state-of-the-art YBCO films and prototype second-generation coated conductors. We apply our theory using the Kim model, JpK(B) = JpK(0)/(1+|B|/B0), as an example. We calculate Jc(Ba) as a function of a perpendicular applied magnetic induction Ba and show how Jc(Ba) is related to JpK(B). We find that Jc(Ba) is very nearly equal to JpK(Ba) when Ba > Ba*, where Ba* is the value of Ba that makes the net flux density zero at the strip's edge. However, Jc(Ba) is suppressed relative to JpK(Ba) at low fields when Ba < Ba*, with the largest suppression occurring when Ba*/B0 is of order unity or larger.Comment: 9 pages, 4 figures, minor revisions to add four reference

Vortex trapping and expulsion in thin-film YBCO strips

A scanning SQUID microscope was used to image vortex trapping as a function of the magnetic induction during cooling in thin-film YBCO strips for strip widths W from 2 to 50 um. We found that vortices were excluded from the strips when the induction Ba was below a critical induction Bc. We present a simple model for the vortex exclusion process which takes into account the vortex - antivortex pair production energy as well as the vortex Meissner and self-energies. This model predicts that the real density n of trapped vortices is given by n=(Ba-BK)/Phi0 with BK = 1.65Phi0/W^2 and Phi0 = h/2e the superconducting flux quantum. This prediction is in good agreement with our experiments on YBCO, as well as with previous experiments on thin-film strips of niobium. We also report on the positions of the trapped vortices. We found that at low densities the vortices were trapped in a single row near the centers of the strips, with the relative intervortex spacing distribution width decreasing as the vortex density increased, a sign of longitudinal ordering. The critical induction for two rows forming in the 35 um wide strip was (2.89 + 1.91-0.93)Bc, consistent with a numerical prediction

Magnetic field of an in-plane vortex outside a layered superconductor

We present the solution to London's equations for the magnetic fields of a vortex oriented parallel to the plane, and normal to a crystal face, of a layered superconductor. These expressions account for flux spreading at the superconducting surface, which can change the apparent size of the vortex along the planes by as much as 30%. We compare these expressions with experimental results.Comment: 13 pages, 5 figure

Metastability and uniqueness of vortex states at depinning

We present results from numerical simulations of transport of vortices in the zero-field cooled (ZFC) and the field-cooled (FC) state of a type-II superconductor. In the absence of an applied current $I$, we find that the FC state has a lower defect density than the ZFC state, and is stable against thermal cycling. On the other hand, by cycling $I$, surprisingly we find that the ZFC state is the stable state. The FC state is metastable as manifested by increasing $I$ to the depinning current $I_{c}$, in which case the FC state evolves into the ZFC state. We also find that all configurations acquire a unique defect density at the depinning transition independent of the history of the initial states.Comment: 4 pages, 4 figures. Problem of page size correcte

Reducing microwave loss in superconducting resonators due to trapped vortices

Microwave resonators with high quality factors have enabled many recent breakthroughs with superconducting qubits and photon detectors, typically operated in shielded environments to reduce the ambient magnetic field. Insufficient shielding or pulsed control fields can introduce vortices, leading to reduced quality factors, although increased pinning can mitigate this effect. A narrow slot etched into the resonator surface provides a straightforward method for pinning enhancement without otherwise affecting the resonator. Resonators patterned with such a slot exhibited over an order of magnitude reduction in the excess loss due to vortices compared with identical resonators from the same film with no slot