Histone H3 serine 10 phosphorylation by Aurora B causes HP1 dissociation from heterochromatin

Histones are subject to numerous post-translational modifications. Some of these 'epigenetic' marks recruit proteins that modulate chromatin structure. For example, heterochromatin protein 1 (HP1) binds to histone H3 when its lysine 9 residue has been tri-methylated by the methyltransferase Suv39h (refs 2-6). During mitosis, H3 is also phosphorylated by the kinase Aurora B. Although H3 phosphorylation is a hallmark of mitosis, its function remains mysterious. It has been proposed that histone phosphorylation controls the binding of proteins to chromatin, but any such mechanisms are unknown. Here we show that antibodies against mitotic chromosomal antigens that are associated with human autoimmune diseases specifically recognize H3 molecules that are modified by both tri-methylation of lysine 9 and phosphorylation of serine 10 (H3K9me3S10ph). The generation of H3K9me3S10ph depends on Suv39h and Aurora B, and occurs at pericentric heterochromatin during mitosis in different eukaryotes. Most HP1 typically dissociates from chromosomes during mitosis, but if phosphorylation of H3 serine 10 is inhibited, HP1 remains chromosome-bound throughout mitosis. H3 phosphorylation by Aurora B is therefore part of a 'methyl/phos switch' mechanism that displaces HP1 and perhaps other proteins from mitotic heterochromatin.     

Blood-brain barrier damage and prolonged cerebral hyperemia following changes in cerebral perfusion pressure; an experimental EEG study

Résumé En expérimentant sur le chien, l'on peut produire des lésions de la barrière hémo-encéphalique aussi bien en diminuant qu'en élevant la pression de perfusion cérébrale. Ainsi l'administration d'un produit épileptogène tel que la Pénicilline déclenche des crises comitiales alors que celle-ci est normalement arrêtée par la barrière hémoencéphalique lorsque cette dernière est intacte. En clinique, des cas d'épilepsie de même mécanisme ont été demontrés.     

Sm(Ⅲ)(BCB)3与DNA的相互作用机理

以中性红(NR)作探针,利用光谱法研究钐(Ⅲ)与灿烂甲酚蓝(BCB)形成的配合物Sm(Ⅲ)(BCB)3与鲱鱼精脱氧核糖核酸(DNA)的相互作用.研究结果表明Sm(Ⅲ)(BCB)3与鲱鱼精DNA结合比n(Sm(Ⅲ)(BCB)3)n(DNA)=41,其结合常数为2.30×105L/mol.Sm(Ⅲ)(BCB)3与鲱鱼精DNA之间的作用方式主要为沟槽作用方式,△rH☉m和△rS☉m都有利于Sm(Ⅲ)(BCB)3-DNA超分子复合物的形成,但主要影响因素是△rS☉m.     

Environmental determinants of extinction selectivity in the fossil record

The causes of mass extinctions and the nature of biological selectivity during extinction events remain central questions in palaeobiology. Although many different environmental perturbations have been invoked as extinction mechanisms, it has long been recognized that fluctuations in sea level coincide with many episodes of biotic turnover. Recent work supports the hypothesis that changes in the areas of epicontinental seas have influenced the macroevolution of marine animals, but the extent to which differential environmental turnover has contributed to extinction selectivity remains unknown. Here I use a new compilation of the temporal durations of sedimentary rock packages to show that carbonate and terrigenous clastic marine shelf environments have different spatio-temporal dynamics and that these dynamics predict patterns of genus-level extinction, extinction selectivity and diversity among Sepkoski's Palaeozoic and modern evolutionary faunae. These results do not preclude a role for biological interactions or unusual physical events as drivers of macroevolution, but they do suggest that the turnover of marine shelf habitats and correlated environmental changes have been consistent determinants of extinction, extinction selectivity and the shifting composition of the marine biota during the Phanerozoic eon.     

超声导波波包宽度与管材内径-壁厚比的关系

在自由管材的情况下,在各传播距离、各频厚积和各激发脉冲周数上,分析了内径-壁厚比和管材中较低阶纵向导波模式波包宽度的关系.分析结果表明:当内径-壁厚比较小时,内径-壁厚比的变化对各导波模式的波包宽度有较大影响,但随内径-壁厚比的增加,这种影响将减小;内径-壁厚比对导波波包宽度的影响随导波模式阶次的增加而减小.另一方面,对于不同内径-壁厚比的管材,检测中应当用不同的导波模式,所用的激发脉冲周数和频厚积也应当不同.     

Modulation of γδ T cell responses by TLR ligands

Toll-like receptors (TLR) are pattern-recognition receptors that recognize a broad variety of structurally conserved molecules derived from microbes. The recognition of TLR ligands functions as a primary sensor of the innate immune system, leading to subsequent indirect activation of the adaptive immunity as well as none-immune cells. However, TLR are also expressed by several T cell subsets, and the respective ligands can directly modulate their effector functions. The present review summarizes the recent findings of γδ T cell modulation by TLR ligands. TLR1/2/6, 3, and 5 ligands can act directly in combination with T cell receptor (TCR) stimulation to enhance cytokine/chemokine production of freshly isolated human γδ T cells. In contrast to human γδ T cells, murine and bovine γδ T cells can directly respond to TLR2 ligands with increased proliferation and cytokine production in a TCR-independent manner. Indirect stimulatory effects on IFN-γ production of human and murine γδ T cells via TLR-ligand activated dendritic cells have been described for TLR2, 3, 4, 7, and 9 ligands. In addition, TLR3 and 7 ligands indirectly increase tumor cell lysis by human γδ T cells, whereas ligation of TLR8 abolishes the suppressive activity of human tumor-infiltrating Vδ1 γδ T cells on αβ T cells and dendritic cells. Taken together, these data suggest that TLR-mediated signals received by γδ T cells enhance the initiation of adaptive immune responses during bacterial and viral infection directly or indirectly. Moreover, TLR ligands enhance cytotoxic tumor responses of γδ T cells and regulate the suppressive capacity of γδ T cells.