Comment on "Atomic Scale Structure and Chemical Composition across Order-Disorder Interfaces"

Interfaces have long been known to be the key to many mechanical and electric properties. To nickel base superalloys which have perfect creep and fatigue properties and have been widely used as materials of turbine blades, interfaces determine the strengthening capacities in high temperature. By means of high resolution scanning transmission electron microscopy (HRSTEM) and 3D atom probe (3DAP) tomography, Srinivasan et al. proposed a new point that in nickel base superalloys there exist two different interfacial widths across the {\gamma}/{\gamma}' interface, one corresponding to an order-disorder transition, and the other to the composition transition. We argue about this conclusion in this comment

Wheat powdery mildew resistance: from gene identification to immunity deployment

Powdery mildew is one of the most devastating diseases on wheat and is caused by the obligate biotrophic phytopathogen Blumeria graminis f. sp. tritici (Bgt). Due to the complexity of the large genome of wheat and its close relatives, the identification of powdery mildew resistance genes had been hampered for a long time until recent progress in large-scale sequencing, genomics, and rapid gene isolation techniques. Here, we describe and summarize the current advances in wheat powdery mildew resistance, emphasizing the most recent discoveries about the identification of genes conferring powdery mildew resistance and the similarity, diversity and molecular function of those genes. Multilayered resistance to powdery mildew in wheat could be used for counteracting Bgt, including durable, broad spectrum but partial resistance, as well as race-specific and mostly complete resistance mediated by nucleotide-binding and leucine rich repeat domain (NLR) proteins. In addition to the above mentioned layers, manipulation of susceptibility (S) and negative regulator genes may represent another layer that can be used for durable and broad-spectrum resistance in wheat. We propose that it is promising to develop effective and durable strategies to combat powdery mildew in wheat by simultaneous deployment of multilayered immunity

Mutation of the Glucosinolate Biosynthesis Enzyme Cytochrome P450 83A1 Monooxygenase Increases Camalexin Accumulation and Powdery Mildew Resistance

Small secondary metabolites, including glucosinolates and the major phytoalexin camalexin, play important roles in immunity in Arabidopsis thaliana. We isolated an Arabidopsis mutant with increased resistance to the powdery mildew fungus Golovinomyces cichoracearum and identified a mutation in the gene encoding cytochrome P450 83A1 monooxygenase (CYP83A1), which functions in glucosinolate biosynthesis. The cyp83a1-3 mutant exhibited enhanced defense responses to G. cichoracearum and double mutant analysis showed that this enhanced resistance requires NPR1, EDS1, and PAD4, but not SID2 or EDS5. In cyp83a1-3 mutants, the expression of genes related to camalexin synthesis increased upon G. cichoracearum infection. Significantly, the cyp83a1-3 mutant also accumulated higher levels of camalexin. Decreasing camalexin levels by mutation of the camalexin synthetase gene PAD3 or the camalexin synthesis regulator AtWRKY33 compromised the powdery mildew resistance in these mutants. Consistent with these observations, overexpression of PAD3 increased camalexin levels and enhanced resistance to G. cichoracearum. Taken together, our data indicate that accumulation of higher levels of camalexin contributes to increased resistance to powdery mildew

Regulation of Plant Disease Resistance, Stress Responses, Cell Death, and Ethylene Signaling in Arabidopsis by the EDR1 Protein Kinase

ENHANCED DISEASE RESISTANCE 1 (EDR1) encodes a CTR1-like kinase and was previously reported to function as a negative regulator of disease resistance and ethylene-induced senescence. Here, we report that the edr1 mutant displays enhanced stress responses and spontaneous necrotic lesions under drought conditions in the absence of pathogen, suggesting that EDR1 is also involved in stress response signaling and cell death regulation. Double mutant analysis revealed that these drought-induced phenotypes require salicylic acid but not ethylene signaling pathways. In addition, the edr1-mediated ethylene-induced senescence phenotype was suppressed by mutations in EIN2, but not by mutations in SID2, PAD4, EDS1, or NPR1, suggesting that EDR1 functions at a point of cross talk between ethylene and salicylic acid signaling that impinges on senescence and cell death. Two edr1-associated phenotypes, drought-induced growth inhibition and ethylene-induced senescence, were suppressed by mutations in ORE9, implicating ubiquitin-mediated protein degradation in the regulation of these phenotypes. However, the ore9 mutation did not suppress edr1-mediated enhanced disease resistance to powdery mildew or spontaneous lesions, indicating that these phenotypes are controlled by separate signaling pathways. To investigate the function of the EDR1 kinase domain, we expressed the C-terminal third of EDR1 in wild-type Columbia and edr1 backgrounds under the control of a dexamethasone-inducible promoter. Overexpression of the EDR1 kinase domain in an edr1 background had no obvious effect on edr1-associated phenotypes. However, overexpression of the EDR1 kinase domain in a wild-type Columbia background caused dominant negative phenotypes, including enhanced disease resistance to powdery mildew and enhanced ethylene-induced senescence; thus, the overexpressed EDR1 kinase domain alone does not exert EDR1 function, but rather negatively affects the function of native EDR1 protein

A self-assembled DNA nanostructure-amplified quartz crystal microbalance with dissipation biosensing platform for nucleic acids

A self-assembled DNA nanostructure as an efficient signal amplifier was introduced to create a simple and label-free quartz crystal microbalance with dissipation monitoring (QCM-D) biosensing platform for highly sensitive and selective detection of nucleic acids