Discrete Change in Magnetization by Chiral Soliton Lattice Formation in the Chiral Magnet Cr1/3NbS2

In the chiral magnet Cr1/3NbS2, discrete changes in the magnetization (M) caused by the formation of a chiral soliton lattice (CSL) were observed in magnetization curve measurements using a single crystal of submillimeter thickness. When M is measured with a minimal increment of the magnetic field H, 0.15 Oe, discrete changes in M are observed in the H region that exhibits definite magnetic hysteresis. In particular, enormous discrete changes in M are observed as H decreases from the field above the saturation field, while fine M steps are also found in the intermediate H range independently of the sweeping direction of the field. The former is considered as a type of enormous Barkhausen effect associated with the CSL formation. The latter originates from the change in soliton number during the CSL formation

Geometrical protection of topological magnetic solitons in microprocessed chiral magnets

A chiral soliton lattice stabilized in a monoaxial chiral magnet CrNb3S6 is a magnetic superlattice consisting of magnetic kinks with a ferromagnetic background. The magnetic kinks are considered to be topological magnetic solitons (TMSs). Changes in the TMS number yield discretized responses in magnetization and electrical conductivity, and this effect is more prominent in smaller crystals. We demonstrate that, in microprocessed CrNb3S6 crystals, TMSs are geometrically protected through element-selected micromagnetometry using soft x-ray magnetic circular dichroism (MCD). A series of x-ray MCD data is supported by mean-field and micromagnetic analyses. By designing the microcrystal geometry, TMS numbers can be successfully changed and fixed over a wide range of magnetic fields

Starvation Induced Cell Death in Autophagy-Defective Yeast Mutants Is Caused by Mitochondria Dysfunction

Autophagy is a highly-conserved cellular degradation and recycling system that is essential for cell survival during nutrient starvation. The loss of viability had been used as an initial screen to identify autophagy-defective (atg) mutants of the yeast Saccharomyces cerevisiae, but the mechanism of cell death in these mutants has remained unclear. When cells grown in a rich medium were transferred to a synthetic nitrogen starvation media, secreted metabolites lowered the extracellular pH below 3.0 and autophagy-defective mutants mostly died. We found that buffering of the starvation medium dramatically restored the viability of atg mutants. In response to starvation, wild-type (WT) cells were able to upregulate components of the respiratory pathway and ROS (reactive oxygen species) scavenging enzymes, but atg mutants lacked this synthetic capacity. Consequently, autophagy-defective mutants accumulated the high level of ROS, leading to deficient respiratory function, resulting in the loss of mitochondria DNA (mtDNA). We also showed that mtDNA deficient cells are subject to cell death under low pH starvation conditions. Taken together, under starvation conditions non-selective autophagy, rather than mitophagy, plays an essential role in preventing ROS accumulation, and thus in maintaining mitochondria function. The failure of response to starvation is the major cause of cell death in atg mutants