Stoichiometry determination of chalcogenide superlattices by means of X-ray diffraction and its limits

In this paper we explore the potential of stoichiometry determination for chalcogenide superlattices, promising candidates for next-generation phase-change memory, via X-ray diffraction. To this end, a set of epitaxial GeTe/Sb2Te3 superlattice samples with varying layer thicknesses is sputter-deposited. Kinematical scattering theory is employed to link the average composition with the diffraction features. The observed lattice constants of the superlattice reference unit cell follow Vegard's law, enabling a straight-forward and non-destructive stoichiometry determination.Comment: physica status solidi (RRL) - Rapid Research Letters (2019

Two-color STED microscopy reveals different degrees of colocalization between hexokinase-I and the three human VDAC isoforms

The voltage-dependent anion channel (VDAC, also known as mitochondrial porin) is the major transport channel mediating the transport of metabolites, including ATP, across the mitochondrial outer membrane. Biochemical data demonstrate the binding of the cytosolic protein hexokinase-I to VDAC, facilitating the direct access of hexokinase-I to the transported ATP. In human cells, three hVDAC isoforms have been identified. However, little is known on the distribution of these isoforms within the outer membrane of mitochondria and to what extent they colocalize with hexokinase-I. In this study we show that whereas hVDAC1 and hVDAC2 are localized predominantly within the same distinct domains in the outer membrane, hVDAC3 is mostly uniformly distributed over the surface of the mitochondrion. We used two-color stimulated emission depletion (STED) microscopy enabling a lateral resolution of ~40 nm to determine the detailed sub-mitochondrial distribution of the three hVDAC isoforms and hexokinase-I. Individual hVDAC and hexokinase-I clusters could thus be resolved which were concealed in the confocal images. Quantitative colocalization analysis of two-color STED images demonstrates that within the attained resolution, hexokinase-I and hVDAC3 exhibit a higher degree of colocalization than hexokinase-I with either hVDAC1 or hVDAC2. Furthermore, a substantial fraction of the mitochondria-bound hexokinase-I pool does not colocalize with any of the three hVDAC isoforms, suggesting a more complex interplay of these proteins than previously anticipated. This study demonstrates that two-color STED microscopy in conjunction with quantitative colocalization analysis is a powerful tool to study the complex distribution of membrane proteins in organelles such as mitochondria

Mdm31 and Mdm32 are inner membrane proteins required for maintenance of mitochondrial shape and stability of mitochondrial DNA nucleoids in yeast

The MDM31 and MDM32 genes are required for normal distribution and morphology of mitochondria in the yeast Saccharomyces cerevisiae. They encode two related proteins located in distinct protein complexes in the mitochondrial inner membrane. Cells lacking Mdm31 and Mdm32 harbor giant spherical mitochondria with highly aberrant internal structure. Mitochondrial DNA (mtDNA) is instable in the mutants, mtDNA nucleoids are disorganized, and their association with Mmm1-containing complexes in the outer membrane is abolished. Mutant mitochondria are largely immotile, resulting in a mitochondrial inheritance defect. Deletion of either one of the MDM31 and MDM32 genes is synthetically lethal with deletion of either one of the MMM1, MMM2, MDM10, and MDM12 genes, which encode outer membrane proteins involved in mitochondrial morphogenesis and mtDNA inheritance. We propose that Mdm31 and Mdm32 cooperate with Mmm1, Mmm2, Mdm10, and Mdm12 in maintenance of mitochondrial morphology and mtDNA

Disorder control in crystalline GeSb2Te4 and its impact on characteristic length scales

Crystalline GeSb2Te4 (GST) is remarkable material, as it allows to continuously tune the electrical resistance by orders of magnitude without involving a phase transition or stoichiometric changes, just by altering the short-range order. While well-ordered specimen are metallic, increasing amounts of disorder can eventually lead to an insulating state with vanishing conductivity in the 0K limit, but a similar number of charge carriers. These observations make disordered GST one of the most promising candidates for the realization of a true Anderson insulator. While so far the low-temperature properties have mostly been studied in films of small grain size, here a sputter-deposition process is employed that enables preparation of a large variety of these GST states including metallic and truly insulating ones. By growing films of GST on mica substrates, biaxially textured samples with huge grain sizes are obtained. A series of these samples is employed for transport measurements, as their electron mean free path can be altered by a factor of 20. Yet, the mean free path always remains more than an order of magnitude smaller than the lateral grain size. This proves unequivocally that grain boundaries play a negligible role for electron scattering, while intragrain scattering, presumably by disordered vacancies, dominates. Most importantly, these findings underline that the Anderson insulating state as well as the system's evolution towards metallic conductivity are indeed intrinsic properties of the material

The inner membrane protein Mdm33 controls mitochondrial morphology in yeast

Mitochondrial distribution and morphology depend on MDM33, a Saccharomyces cerevisiae gene encoding a novel protein of the mitochondrial inner membrane. Cells lacking Mdm33 contain ring-shaped, mostly interconnected mitochondria, which are able to form large hollow spheres. On the ultrastructural level, these aberrant organelles display extremely elongated stretches of outer and inner membranes enclosing a very narrow matrix space. Dilated parts of Δmdm33 mitochondria contain well-developed cristae. Overexpression of Mdm33 leads to growth arrest, aggregation of mitochondria, and generation of aberrant inner membrane structures, including septa, inner membrane fragments, and loss of inner membrane cristae. The MDM33 gene is required for the formation of net-like mitochondria in mutants lacking components of the outer membrane fission machinery, and mitochondrial fusion is required for the formation of extended ring-like mitochondria in cells lacking the MDM33 gene. The Mdm33 protein assembles into an oligomeric complex in the inner membrane where it performs homotypic protein–protein interactions. Our results indicate that Mdm33 plays a distinct role in the mitochondrial inner membrane to control mitochondrial morphology. We propose that Mdm33 is involved in fission of the mitochondrial inner membrane

Topological States on the Gold Surface

Gold surfaces host special electronic states that have been understood as a prototype of Shockley surface states (SSs). These SSs are commonly employed to benchmark the capability of angle-resolved photoemission spectroscopy (ARPES) and scanning tunneling spectroscopy. We find that these Shockley SSs can be reinterpreted as topologically derived surface states (TDSSs) of a topological insulator (TI), a recently discovered quantum state. Based on band structure calculations, the Z2 topological invariant can be well defined to characterize the nontrivial features of gold that we detect by ARPES. The same TDSSs are also recognized on surfaces of other well-known noble metals (e.g., silver, copper, platinum, and palladium). Besides providing a new understanding of noble metal SSs, finding topological states on late transition metals provokes interesting questions on the role of topological effects in surface-related processes, such as adsorption and catalysis.Comment: 21 pages, 3 figure

The class V myosin motor protein, Myo2, plays a major role in mitochondrial motility in Saccharomyces cerevisiae

The actin cytoskeleton is essential for polarized, bud-directed movement of cellular membranes in Saccharomyces cerevisiae and thus ensures accurate inheritance of organelles during cell division. Also, mitochondrial distribution and inheritance depend on the actin cytoskeleton, though the precise molecular mechanisms are unknown. Here, we establish the class V myosin motor protein, Myo2, as an important mediator of mitochondrial motility in budding yeast. We found that mutants with abnormal expression levels of Myo2 or its associated light chain, Mlc1, exhibit aberrant mitochondrial morphology and loss of mitochondrial DNA. Specific mutations in the globular tail of Myo2 lead to aggregation of mitochondria in the mother cell. Isolated mitochondria lacking functional Myo2 are severely impaired in their capacity to bind to actin filaments in vitro. Time-resolved fluorescence microscopy revealed a block of bud-directed anterograde mitochondrial movement in cargo binding–defective myo2 mutant cells. We conclude that Myo2 plays an important and direct role for mitochondrial motility and inheritance in budding yeast