Enhancing Durability and Capacity Retention of Ultrafine-Grained Aluminum Foil Anodes in Lithium-Ion Batteries.

In this study, we present our successful fabrication of commercial-grade pure aluminum anode foil (99.5%, 2NAl) with an ultrafine-grained (UFG) microstructure and high hardness, achieved through cold rolling. Under identical rolling conditions, a coarse-grained microstructure with a low hardness was attained from the high-purity Al foil (99.99%, 4NAl). The UFG 2NAl foil exhibited enhanced lithium-ion diffusivity and reduced nucleation and activation overpotentials for forming the ß-LiAl phase compared to the 4NAl foil. The high-density grain boundaries in the UFG 2NAl foil facilitated the rapid formation of a uniform ß-LiAl phase layer on its surface, thereby mitigating mechanical damage within the ß-LiAl phase layer caused by volume changes during the lithiation and delithiation processes. The high hardness of the UFG 2NAl sample effectively prevented macroscopic plastic deformation during cycling, thus preserving the integrity of the ß-LiAl phase layer and inhibiting the formation of cracks within the unreacted Al matrix. The collective advantages of reduced overpotential, enhanced Li-ion diffusivity, and high resistance to mechanical damage and plastic deformation in UFG 2NAl contribute to its superior durability and capacity retention compared to the high-purity Al in electrochemical cycling.

Deformation Mechanisms and Processing Maps for High Entropy Alloys (Presentation of Processing Maps in Terms of Zener-Hollomon Parameter): Review.

In this review paper, the hot compressive deformation mechanisms and processing maps of high-entropy alloys (HEAs) with different chemical compositions and crystal structures are analyzed. The stress exponent (n1) values measured from the series of compression tests for the HEAs performed at different temperatures and strain rates are distributed between 3 and 35, and they are most populated between 3 and 7. Power law breakdown (PLB) is found to typically occur at T/Tm ≤ 0.6 (where T is the testing temperature and Tm is the melting temperature). In AlxCrMnFeCoNi (x = 0-1) and AlxCrFeCoNi (x = 0-1) HEAs, n1 tends to decrease as the concentration of Al increases, suggesting that Al acts as a solute atom that exerts a drag force on dislocation slip motion at high temperatures. The values of activation energy for plastic flow (Qc) for the HEAs are most populated in the range between 300 and 400 kJ/mol. These values are close to the activation energy of the tracer diffusivity of elements in the HEAs ranging between 240 and 408 kJ/mol. The power dissipation efficiency η of the HEAs is shown to follow a single equation, which is uniquely related to n1. Flow instability for the HEAs is shown to occur near n1 = 7, implying that the onset of flow instability occurs at the transition from power law creep to PLB. Processing maps for the HEAs are demonstrated to be represented by plotting η as a function of the Zener-Hollomon parameter (Z = expQcRT, where R is the gas constant). Flow stability prevails at Z ≤ 1012 s-1, while flow instability does at Z ≥ 3 × 1014 s-1.

Regulation of Ras localization and cell transformation by evolutionarily conserved palmitoyltransferases.

Ras can act on the plasma membrane (PM) to mediate extracellular signaling and tumorigenesis. To identify key components controlling Ras PM localization, we performed an unbiased screen to seek Schizosaccharomyces pombe mutants with reduced PM Ras. Five mutants were found with mutations affecting the same gene, S. pombe erf2 (sp-erf2), encoding sp-Erf2, a palmitoyltransferase, with various activities. sp-Erf2 localizes to the trans-Golgi compartment, a process which is mediated by its third transmembrane domain and the Erf4 cofactor. In fission yeast, the human ortholog zDHHC9 rescues the phenotypes of sp-erf2 null cells. In contrast, expressing zDHHC14, another sp-Erf2-like human protein, did not rescue Ras1 mislocalization in these cells. Importantly, ZDHHC9 is widely overexpressed in cancers. Overexpressing ZDHHC9 promotes, while repressing it diminishes, Ras PM localization and transformation of mammalian cells. These data strongly demonstrate that sp-Erf2/zDHHC9 palmitoylates Ras proteins in a highly selective manner in the trans-Golgi compartment to facilitate PM targeting via the trans-Golgi network, a role that is most certainly critical for Ras-driven tumorigenesis.

Moc3, a novel Zn finger type protein involved in sexual development, ascus formation, and stress response of Schizosaccharomyces pombe.

The cAMP pathway in Schizosaccharomyces pombe is the major nutrient sensing pathway to initiate sexual development when opposite mating type cells exist. We identified moc1-moc4 as genes that overcome a partially sterile S. pombe strain due to an elevation of cAMP. When we compared the strength of inducing ability of sexual development in the same S. pombe strain, Moc1 had highest, Moc2 had lowest, and both Moc3 and Moc4 had intermediate effects. Moc1/Sds23 and Moc2/Ded1 are known to be a potential regulator of M-phase progression and an essential RNA helicase, respectively. While Moc4 was found to be identical with a Zn-finger protein Zfs1, Moc3 (SPAC821.07c) was a novel protein containing a Zn-finger (Zn(2)-Cys(6)) motif. Deletion mutant of the moc3 gene was constructed and its disruptant was found to be lower in mating efficiency and formed aberrant asci. In addition, unexpectedly, a moc3 disruptant was sensitive to CaCl(2) and DNA damaging agents such as MMS and UV. Those phenotypes were opposite to the phenotypes observed in a zfs1 disruptant, and quite different from the ones in a moc1 disruptant. Moc3 localized in the nucleus as observed for Zfs1. Moc3 bound with Moc4/Zfs1 weakly in the two hybrid system, but no other combination of Moc(s) bound each other in the same analysis. Thus, Moc3 is not only involved in sexual development, but also in ascus formation and DNA integrity in an independent manner with Moc1 and Moc2 in S. pombe.

Interaction between a negative regulator (Msa2/Nrd1) and a positive regulator (Cpc2) of sexual differentiation in Schizosaccharomyces pombe.

The sexual differentiation of Schizosaccharomyces pombe is controlled by many cellular components which have not been fully characterized. We isolated a gene called msa2 as a multi-copy suppressor of a sporulation abnormal mutant (sam1). Msa2p is identical with Nrd1p which has been characterized as a factor that blocks the onset of sexual differentiation. The yeast two-hybrid system was used to identify Cpc2p, a fission yeast homolog of the RACK1 protein, that interacted with Msa2p/Nrd1p. We confirmed that Msa2p/Nrd1p interacted with Cpc2p in S. pombe cells. An epistatic analysis of msa2/nrd1 and cpc2 suggests that Msa2p/Nrd1p was an upstream regulator for Cpc2p. A localization analysis of Cpc2p and Msa2p/Nrd1p indicates that both proteins were predominantly localized in the cytoplasm. The interaction of negative regulator Msa2p/Nrd1p with positive regulator Cpc2p suggests a new regulatory circuit in the sexual differentiation of S. pombe.

A novel gene, msa1, inhibits sexual differentiation in Schizosaccharomyces pombe.

Sexual differentiation in the fission yeast Schizosaccharomyces pombe is triggered by nutrient starvation or by the presence of mating pheromones. We identified a novel gene, msa1, which encodes a 533-aa putative RNA-binding protein that inhibits sexual differentiation. Disruption of the msa1 gene caused cells to hypersporulate. Intracellular levels of msa1 RNA and Msa1 protein diminished after several hours of nitrogen starvation. Genetic analysis suggested that the function of msa1 is independent of the cAMP pathway and stress-responsive pathway. Deletion of the ras1 gene in diploid cells inhibited sporulation and in haploid cells decreased expression of mating-pheromone-induced genes such as mei2, mam2, ste11, and rep1; simultaneous deletion of msa1 reversed both phenotypes. Overexpression of msa1 decreased activated Ras1(Val17)-induced expression of mam2. Phenotypic hypersporulation was similar between cells with deletion of only rad24 and both msa1 and rad24, but simultaneous deletion of msa1 and msa2/nrd1 additively increased hypersporulation. Therefore, we suggest that the primary function of Msa1 is to negatively regulate sexual differentiation by controlling the expression of Ste11-regulated genes, possibly through the pheromone-signaling pathway.

The 14-3-3 proteins Rad24 and Rad25 negatively regulate Byr2 by affecting its localization in Schizosaccharomyces pombe.

In Schizosaccharomyces pombe, rad24 and rad25 have been identified to be homologous to mammalian 14-3-3 genes and found to be involved in many cellular events, including checkpoint and meiosis. In the present study, we present evidences that Rad24 and Rad25 act as negative regulators of Byr2 (mitogen-activated protein kinase [MAPK] kinase kinase). Overexpression of rad24 or rad25 reduced mating and sporulation in homothallic wild-type cells. In contrast, the mating and sporulation efficiency of rad24- or rad25-null cells was higher than that of wild-type cells. Deletion of rad24 or rad25 increased sporulation efficiency in ras1-null diploid cells but not in byr2-, ste4-, byr1-, and spk1-null cells. Rad24 and Rad25 had no effect on the activity of constitutively active Byr1(S214DT218D). Rad24 and Rad25 bound to both the N-terminal and the C-terminal domains of Byr2 when these bacterially expressed proteins were examined. The formation of complexes in vivo between Byr2 and either Rad24 or Rad25 was also confirmed by immunocoprecipitation. Furthermore, we showed negative regulation of Byr2 by Rad25, by monitoring the mRNA level of mam2, which is regulated by both the Ras1/MAPK pathway and ste11, in various combinations of mutants. In addition, the cellular localization of Byr2 in living cells was observed by using fusion to green fluorescent protein. Byr2 was mainly localized in the cytoplasm during vegetative growth and then concentrated at the plasma membrane in response to nitrogen starvation. Deletion of rad24 or rad25 fastened the timing of Byr2 translocation. Our results are consistent with the hypothesis that one of the roles of 14-3-3 is to keep Byr2 in the cytoplasm and to affect the timing of Byr2 translocation in response to sexual developmental signal.