A new indolic antiauxin, α-(5,7-dichloroindole-3-)isobutyric acid: its chemical synthesis and biological activity

Summary A new potent antiauxin, -(5,7-dichloroindole-3-)isobutyric acid has been synthesized and shown to inhibit auxin-mediated elongation ofAvena coleoptiles and to stimulate root growth of rice seedlings. Its activity is stronger than -(p-chlorophenoxy)isobutyric acid and is comparable to that of 2,3,5-triiodobenzoic acid, which are typical antiauxins.     

中国苏北预先导孔CCSD-PP2片麻岩中锆石的矿物包裹体及其超高压变质作用的证据

采用激光Raman及阴极发光技术,确认中国大陆科学钻探工程预选预先导孔CCSD－PP2几乎所有类型片麻岩中的锆石均保存典型的柯石英包体以及绿辉石、硬玉、石榴石、多硅白云母等矿物包体,表明片麻岩类岩石曾普遍经历了超高压变质作用,该成果对于重新探讨苏鲁超高压变质带的俯冲－折返机制和对中国大陆科学钻探工程的选址有重要的科学意义。     

Phosphorylation by aurora kinase A induces Mdm2-mediated destabilization and inhibition of p53

Aurora kinase A (also called STK15 and BTAK) is overexpressed in many human cancers. Ectopic overexpression of aurora kinase A in mammalian cells induces centrosome amplification, chromosome instability and oncogenic transformation, a phenotype characteristic of loss-of-function mutations of p53. Here we show that aurora kinase A phosphorylates p53 at Ser315, leading to its ubiquitination by Mdm2 and proteolysis. p53 is not degraded in the presence of inactive aurora kinase A or ubiquitination-defective Mdm2. Destabilization of p53 by aurora kinase A is abrogated in the presence of mutant Mdm2 that is unable to bind p53 and after repression of Mdm2 by RNA interference. Silencing of aurora kinase A results in less phosphorylation of p53 at Ser315, greater stability of p53 and cell-cycle arrest at G2-M. Cells depleted of aurora kinase A are more sensitive to cisplatin-induced apoptosis, and elevated expression of aurora kinase A abolishes this response. In a sample of bladder tumors with wild-type p53, elevated expression of aurora kinase A was correlated with low p53 concentration. We conclude that aurora kinase A is a key regulatory component of the p53 pathway and that overexpression of aurora kinase A leads to increased degradation of p53, causing downregulation of checkpoint-response pathways and facilitating oncogenic transformation of cells.     

A first-order liquid-liquid phase transition in phosphorus

First-order structural phase transitions are common in crystalline solids, whereas first-order liquid-liquid phase transitions (that is, transitions between two distinct liquid forms with different density and entropy) are exceedingly rare in pure substances. But recent theoretical and experimental studies have shown evidence for such a transition in several materials, including supercooled water and liquid carbon. Here we report an in situ X-ray diffraction observation of a liquid-liquid transition in phosphorus, involving an abrupt, pressure-induced structural change between two distinct liquid forms. In addition to a known form of liquid phosphorus--a molecular liquid comprising tetrahedral P4 molecules--we have found a polymeric form at pressures above 1 GPa. Changing the pressure results in a reversible transformation from the low-pressure molecular form into the high-pressure polymeric form. The transformation is sharp and rapid, occurring within a few minutes over a pressure range of less than 0.02 GPa. During the transformation, the two forms of liquid coexist. These features are strongly suggestive of a first-order liquid-liquid phase transition.     

(S)-(+)-4,4,4-Trifluoro-3-(indole-3-)butyric acid,a novel fluorinated plant growth regulator

Racemic 4,4,4-trifluoro-3-(indole-3-)butyric acid (TFIBA) has been synthesized and shown to inhibitAvena coleoptile elongation. (S)-(+)-TFIBA (fig. 1), which was prepared by an enzymatic method and markedly promotes root growth of Chinese cabbage, lettuce and rice plants, is a novel fluorinated plant growth regulator. Activity of the (S)-(+)-enantiomer of TFIBA was 10-fold greater than that of the (R)-(–)-enantiomer in the first two plant species and 5-fold greater in rice.     

Shugoshin collaborates with protein phosphatase 2A to protect cohesin

Sister chromatid cohesion, mediated by a complex called cohesin, is crucial--particularly at centromeres--for proper chromosome segregation in mitosis and meiosis. In animal mitotic cells, phosphorylation of cohesin promotes its dissociation from chromosomes, but centromeric cohesin is protected by shugoshin until kinetochores are properly captured by the spindle microtubules. However, the mechanism of shugoshin-dependent protection of cohesin is unknown. Here we find a specific subtype of serine/threonine protein phosphatase 2A (PP2A) associating with human shugoshin. PP2A colocalizes with shugoshin at centromeres and is required for centromeric protection. Purified shugoshin complex has an ability to reverse the phosphorylation of cohesin in vitro, suggesting that dephosphorylation of cohesin is the mechanism of protection at centromeres. Meiotic shugoshin of fission yeast also associates with PP2A, with both proteins collaboratively protecting Rec8-containing cohesin at centromeres. Thus, we have revealed a conserved mechanism of centromeric protection of eukaryotic chromosomes in mitosis and meiosis.     

Monitoring and phenomena observation during YAG laser lap welding of Zn-coated steel sheets

1　IntroductionZn coatedsteelsareusedinvariousindustryfieldsbecauseoflowpricesandhighcorrosionresistance .ItisalsoknownthatZncausesspattersorporosityeasilyinlaserlapwelding[1～ 3] .ItisthusexpectedtounderstandlaserweldingphenomenonofZn coatedsteels,tointe…     

The neuronal sortilin-related receptor SORL1 is genetically associated with Alzheimer disease

The recycling of the amyloid precursor protein (APP) from the cell surface via the endocytic pathways plays a key role in the generation of amyloid beta peptide (Abeta) in Alzheimer disease. We report here that inherited variants in the SORL1 neuronal sorting receptor are associated with late-onset Alzheimer disease. These variants, which occur in at least two different clusters of intronic sequences within the SORL1 gene (also known as LR11 or SORLA) may regulate tissue-specific expression of SORL1. We also show that SORL1 directs trafficking of APP into recycling pathways and that when SORL1 is underexpressed, APP is sorted into Abeta-generating compartments. These data suggest that inherited or acquired changes in SORL1 expression or function are mechanistically involved in causing Alzheimer disease.     

TMP21 is a presenilin complex component that modulates gamma-secretase but not epsilon-secretase activity

The presenilin proteins (PS1 and PS2) and their interacting partners nicastrin, aph-1 (refs 4, 5) and pen-2 (ref. 5) form a series of high-molecular-mass, membrane-bound protein complexes that are necessary for gamma-secretase and epsilon-secretase cleavage of selected type 1 transmembrane proteins, including the amyloid precursor protein, Notch and cadherins. Modest cleavage activity can be generated by reconstituting these four proteins in yeast and Spodoptera frugiperda (sf9) cells. However, a critical but unanswered question about the biology of the presenilin complexes is how their activity is modulated in terms of substrate specificity and/or relative activities at the gamma and epsilon sites. A corollary to this question is whether additional proteins in the presenilin complexes might subsume these putative regulatory functions. The hypothesis that additional proteins might exist in the presenilin complexes is supported by the fact that enzymatically active complexes have a mass that is much greater than predicted for a 1:1:1:1 stoichiometric complex (at least 650 kDa observed, compared with about 220 kDa predicted). To address these questions we undertook a search for presenilin-interacting proteins that differentially affected gamma- and epsilon-site cleavage events. Here we report that TMP21, a member of the p24 cargo protein family, is a component of presenilin complexes and differentially regulates gamma-secretase cleavage without affecting epsilon-secretase activity.