Single-crystal ZrN films, 830 nm thick, are grown on MgO(001) at 450 °C by magnetically unbalanced reactive magnetron sputtering. The combination of high-resolution x-ray diffraction reciprocal lattice maps, high-resolution cross-sectional transmission electron microscopy, and selected-area electron diffraction shows that ZrN grows epitaxially on MgO(001) with a cube-on-cube orientational relationship, (001)ZrN‖(001)MgO and [100]ZrN‖[100]MgO. The layers are essentially fully relaxed with a lattice parameter of 0.4575 nm, in good agreement with reported results for bulk ZrN crystals. X-ray reflectivity results reveal that the films are completely dense with smooth surfaces (roughness = 1.3 nm, consistent with atomic-force microscopy analyses). Based on temperature-dependent electronic transport measurements, epitaxial ZrN/MgO(001) layers have a room-temperature resistivity ρ300K of 12.0 μΩ-cm, a temperature coefficient of resistivity between 100 and 300 K of 5.6 × 10−8 Ω-cm K−1, a residual resistivity ρo below 30 K of 0.78 μΩ-cm (corresponding to a residual resistivity ratio ρ300Κ/ρ15K = 15), and the layers exhibit a superconducting transition temperature of 10.4 K. The relatively high residual resistivity ratio, combined with long in-plane and out-of-plane x-ray coherence lengths, ξ‖ = 18 nm and ξ⊥ = 161 nm, indicates high crystalline quality with low mosaicity. The reflectance of ZrN(001), as determined by variable-angle spectroscopic ellipsometry, decreases slowly from 95% at 1 eV to 90% at 2 eV with a reflectance edge at 3.04 eV. Interband transitions dominate the dielectric response above 2 eV. The ZrN(001) nanoindentation hardness and modulus are 22.7 ± 1.7 and 450 ± 25 GPa.
36The crystalline surface layer (S-layer), consisting of two glycoproteins SlaA and SlaB, is 37 considered to be the exclusive component of the cell envelope outside of the cytoplasmic 38 membrane in Sulfolobus species. Although biochemically and structurally characterized, the S-39 layer in vivo functions remain largely elusive in Archaea. Here, we investigate how the S-layer 40 genes contribute to the S-layer architecture and affect cellular physiology in a crenarchaeal 41 model, Sulfolobus islandicus M.16.4. Electron micrographs of mutant cells lacking slaA or both 42 slaA and slaB confirm the absence of the outermost layer (SlaA), whereas cells with intact, 43 partially, or completely detached SlaA are observed for the ΔslaB mutant. Importantly, we 44 identify a novel S-layer-associated protein M164_1049, which does not functionally replace its 45 homolog SlaB but likely assists SlaB to stabilize SlaA. Additionally, we find that mutants 46 deficient in SlaA form large cell aggregates and the individual cell size varies significantly. The 47 slaB gene deletion also causes noticeable cellular aggregation, but the size of those aggregates 48 is smaller when compared to ΔslaA and ΔslaAB mutants. We further show the ΔslaA mutant 49 cells exhibit more sensitivity to hyperosmotic stress but are not reduced to wild-type cell size. 50Finally, we demonstrate that the ΔslaA mutant contains aberrant chromosome copy numbers 51 not seen in wild-type cells where the cell cycle is tightly regulated. Together these data suggest 52 that the lack of slaA results in either cell fusion or irregularities in cell division. Our studies 53 provide novel insights into the physiological and cellular functions of the S-layer in Archaea. 55Significance 56Rediscovery of the ancient evolutionary relationship between archaea and eukaryotes has 57 revitalized interest in archaeal cell biology. Key to understanding the archaeal cell is the S-58 layer which is ubiquitous in Archaea but whose in vivo function is unknown. In this study, we 59 genetically dissect how the two well-known S-layer genes as well as a newly identified S-layer-60 associated-protein-encoding gene contribute to the S-layer architecture in a hyperthermophilic 61 crenarchaeal model S. islandicus. We provide genetic evidence for the first time showing that 62 the slaA gene is a key cell morphology determinant and may play a role in Sulfolobus cell 63 division or cell fusion.64 65 66 67 68 69 70 71 72The primary interface between the cell and its environment is a multi-functional cellular 73 envelope. Comprised in this structure in some bacterial and most archaeal cells is a 74 proteinaceous 2D-crystalline matrix coating the outside of the cell called the surface layer (S-75 layer). Despite its broad distribution in cells from two domains, a generalized function of the 76 S-layer has not been identified. One unifying concept suggests the S-layer functions as an 77 exoskeleton that interacts with other proteins in the cell membrane to coordinate diverse 78 internal and externa...
Obesity is a major epidemic and is associated with metabolic dysfunction leading to excess accumulation of fat. Bile acids (BAs) are body's natural detergents that facilitate fat digestion. Additionally, BAs act as signaling molecules regulating metabolism and can protect against obesity. Despite, several studies have demonstrated that elevated BAs promote energy expenditure, it remains unknown if BAs are present in brown adipose tissue (BAT) and can they directly affect BAT function. Here, we show that BAs, BA transporters and de novo synthetic enzymes are detected in BAT. Notably, the global farnesoid X receptor; small heterodimer partner double knockout (DKO) mice, a model for BA overload, exhibit higher BAs levels in BAT than the control mice. DKO mice exhibit lower body temperature, decreased mitochondrial DNA content, and altered activities of oxidative phosphorylation enzyme complexes. Consistent with this phenotype, we find that excess BAs impair BAT mitochondrial function and can cause thermogenic dysfunction. Importantly, when low physiological BA levels are used to treat brown adipocytes, we do not find mitochondrial defects. However, upon treatment with pathological BA concentrations, differentiated primary brown adipocytes in vitro show reduced mitochondrial membrane potential and concomitant reduction in thermogenic gene expression profile. We have shown that DKO mice are resistant to fat accumulation both on normal chow and when challenged with a high‐fat diet. This protection is significantly lost when the mice are housed at thermoneutral conditions indicating that by having leaky mitochondria and poor thermoregulation, DKO mice are protected against accumulating fat. Overall, we show for the first time the presence of BA metabolic machinery in the BAT and identify that elevated levels of BAs can cause thermogenic dysfunctions. Weinan Zhou and Philip VanDuyne contributed equally to this work.Support or Funding InformationStartup funds from the University of Illinois at Urbana‐Champaign, and R01 DK113080 from NIDDK.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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