Specific inhibition of a calcium dependent activation of brain cyclic AMP phosphodiesterase activity by vinblastine.

Vinblastine selectively inhibits the activation of brain cyclic AMP phosphodiesterase activity by Ca++-protein activator (50% inhibition by 2 x 10(-5) M). This inhibitory effect was reversed by excessive amounts of the activator, whereas large quantities of Ca++ caused only a slight suppression of the vinblastine effect. This result of vinblastine suggests a new site of its action and also suggests the possible role of protein activator, phosphodiesterase proteins or cyclic nucleotides in the previously known effects of vinblastine in vivo and in vitro.     

Protein synthesis during germination of heterothallic yeast ascospores.

Protein synthesis during ascospore germination of the heterothallic Saccharomyces cerevisiae strain AP-3 was investigated. Protein synthesis in the germinating ascospores appeared to begin approximately 20 min following glucose initiation. Since RNA synthesis did not start until approximately 70 min after the onset of germination, strain AP-3 ascospores must contain RNA which is ready for immediate translation. Both trehalase and glyceraldehyde-3-phosphate dehydrogenase activities were found to be affected by the onset of germination. Trehalase activity was found to increase severalfold following 60 min of spore germination but remained relatively constant over the subsequent 120 min examined. Dehydrogenase activity was not detectable in AP-3 ascospores but was measurable in germinating ascospores.     

Aberrant chromosome morphology in human cells defective for Holliday junction resolution

In somatic cells, Holliday junctions can be formed between sister chromatids during the recombinational repair of DNA breaks or after replication fork demise. A variety of processes act upon Holliday junctions to remove them from DNA, in events that are critical for proper chromosome segregation. In human cells, the BLM protein, inactivated in individuals with Bloom's syndrome, acts in combination with topoisomerase IIIα, RMI1 and RMI2 (BTR complex) to promote the dissolution of double Holliday junctions. Cells defective for BLM exhibit elevated levels of sister chromatid exchanges (SCEs) and patients with Bloom's syndrome develop a broad spectrum of early-onset cancers caused by chromosome instability. MUS81-EME1 (refs 4-7), SLX1-SLX4 (refs 8-11) and GEN1 (refs 12, 13) also process Holliday junctions but, in contrast to the BTR complex, do so by endonucleolytic cleavage. Here we deplete these nucleases from Bloom's syndrome cells to analyse human cells compromised for the known Holliday junction dissolution/resolution pathways. We show that depletion of MUS81 and GEN1, or SLX4 and GEN1, from Bloom's syndrome cells results in severe chromosome abnormalities, such that sister chromatids remain interlinked in a side-by-side arrangement and the chromosomes are elongated and segmented. Our results indicate that normally replicating human cells require Holliday junction processing activities to prevent sister chromatid entanglements and thereby ensure accurate chromosome condensation. This phenotype was not apparent when both MUS81 and SLX4 were depleted from Bloom's syndrome cells, suggesting that GEN1 can compensate for their absence. Additionally, we show that depletion of MUS81 or SLX4 reduces the high frequency of SCEs in Bloom's syndrome cells, indicating that MUS81 and SLX4 promote SCE formation, in events that may ultimately drive the chromosome instabilities that underpin early-onset cancers associated with Bloom's syndrome.     

褐飞虱空间格局的地统计学分析

褐飞虱Nilaparvata lugens(Stl)是我国重要的迁飞性水稻害虫,对我国的水稻生产造成严重危害.为研究其迁入后田间的聚集与扩散的动态过程和空间分布规律,为综合防治提供理论依据,作者根据2009年在秀山县的田间系统调查资料,运用地统计学中的半方差函数,建立了褐飞虱发生期的空间变异曲线模型,并利用Surfer8.0软件对空间分布数据进行插值和模拟.结果表明,在本研究尺度下,褐飞虱各时间段均呈聚集分布,空间依赖范围约为49-132 m,变程随时间先减小,后增大;自水稻插秧开始,褐飞虱密度逐渐增大,8月20日达到最高峰,即该时段应是本地区防治褐飞虱的关键时期.     

Long-term interactions of climate, productivity, species richness, and growth form in relictual sagebrush steppe plant communities

Vegetation trends due to climatic changes are difficult to separate from disturbances caused by varying land uses. To separate climatic influences from livestock grazing and fire disturbances within sagebrush steppe, we compared vegetation structure and productivity during 2 periods (10-year sequences of data from the late 1950s to the late 1960s and 3 years in the early 1990s) at 12 stands within 3 relict areas in or near the Great Rift of southern Idaho. Yearto- year fluctuations in annual net aboveground phytomass accumulation (ANAPA) were considerable in response to varying climate during both periods. More importantly, an apparently significant increase in ANAPA was observed during the latter study period. However, this apparent increase may have been due to the unusually wet conditions of 1993. Throughout both study periods, ANAPA was even more positively correlated with species richness than with precipitation, although both influences were statistically significant. Aggregation of these data by plant growth forms showed that shrubs, particularly sagebrushes, have progressively increased their proportion relative to herbaceous understory. This directional (successional) change in the proportional contributions of growth forms to ANAPA was probably due more to long-term absence of fire at these isolated locations than to any detectable climate change or lack of grazing. This finding reduces our confidence in the use of such areas as reference sites for monitoring or as living examples for restoration efforts, but it does increase our understanding of vegetation dynamics within sagebrush steppe. ACRONYMS. ANAPA—annual net aboveground phytomass accumulations, ANOVA—analysis of variance, ANPP—aboveground net primary production, COV—coefficient of variation, CY—crop year, CYP—crop-year precipitation, ES—ecological site, MANOVA—multivariate analysis of variance, MAT—mean annual temperature, NRCS—Natural Resources Conservation Service, PDSI—Palmer Drought Severity Index, RUE—rainfall use efficiency.     

Oncogenic pathway signatures in human cancers as a guide to targeted therapies

The development of an oncogenic state is a complex process involving the accumulation of multiple independent mutations that lead to deregulation of cell signalling pathways central to the control of cell growth and cell fate. The ability to define cancer subtypes, recurrence of disease and response to specific therapies using DNA microarray-based gene expression signatures has been demonstrated in multiple studies. Various studies have also demonstrated the potential for using gene expression profiles for the analysis of oncogenic pathways. Here we show that gene expression signatures can be identified that reflect the activation status of several oncogenic pathways. When evaluated in several large collections of human cancers, these gene expression signatures identify patterns of pathway deregulation in tumours and clinically relevant associations with disease outcomes. Combining signature-based predictions across several pathways identifies coordinated patterns of pathway deregulation that distinguish between specific cancers and tumour subtypes. Clustering tumours based on pathway signatures further defines prognosis in respective patient subsets, demonstrating that patterns of oncogenic pathway deregulation underlie the development of the oncogenic phenotype and reflect the biology and outcome of specific cancers. Predictions of pathway deregulation in cancer cell lines are also shown to predict the sensitivity to therapeutic agents that target components of the pathway. Linking pathway deregulation with sensitivity to therapeutics that target components of the pathway provides an opportunity to make use of these oncogenic pathway signatures to guide the use of targeted therapeutics.     

Ultra-relativistic electrons in Jupiter's radiation belts

Ground-based observations have shown that Jupiter is a two-component source of microwave radio emission: thermal atmospheric emission and synchrotron emission from energetic electrons spiralling in Jupiter's magnetic field. Later in situ measurements confirmed the existence of Jupiter's high-energy electron-radiation belts, with evidence for electrons at energies up to 20[?]MeV. Although most radiation belt models predict electrons at higher energies, adiabatic diffusion theory can account only for energies up to around 20[?]MeV. Unambiguous evidence for more energetic electrons is lacking. Here we report observations of 13.8[?]GHz synchrotron emission that confirm the presence of electrons with energies up to 50[?]MeV; the data were collected during the Cassini fly-by of Jupiter. These energetic electrons may be repeatedly accelerated through an interaction with plasma waves, which can transfer energy into the electrons. Preliminary comparison of our data with model results suggests that electrons with energies of less than 20[?]MeV are more numerous than previously believed.     

Testing Hamilton's rule with competition between relatives

Hamilton's theory of kin selection suggests that individuals should show less aggression, and more altruism, towards closer kin. Recent theoretical work has, however, suggested that competition between relatives can counteract kin selection for altruism. Unfortunately, factors that tend to increase the average relatedness of interacting individuals--such as limited dispersal--also tend to increase the amount of competition between relatives. Therefore, in most natural systems, the conflicting influences of increased competition and increased relatedness are confounded, limiting attempts to test theory. Fig wasp taxa exhibit varying levels of aggression among non-dispersing males that show a range of average relatedness levels. Thus, across species, the effects of relatedness and competition between relatives can be separated. Here we report that--contrary to Hamilton's original prediction but in agreement with recent theory--the level of fighting between males shows no correlation with the estimated relatedness of interacting males, but is negatively correlated with future mating opportunities.     

Binding of double-strand breaks in DNA by human Rad52 protein

Double-strand breaks (DSBs) in DNA are caused by ionizing radiation. These chromosomal breaks can kill the cell unless repaired efficiently, and inefficient or inappropriate repair can lead to mutation, gene translocation and cancer. Two proteins that participate in the repair of DSBs are Rad52 and Ku: in lower eukaryotes such as yeast, DSBs are repaired by Rad52-dependent homologous recombination, whereas vertebrates repair DSBs primarily by Ku-dependent non-homologous end-joining. The contribution of homologous recombination to vertebrate DSB repair, however, is important. Biochemical studies indicate that Ku binds to DNA ends and facilitates end-joining. Here we show that human Rad52, like Ku, binds directly to DSBs, protects them from exonuclease attack and facilitates end-to-end interactions. A model for repair is proposed in which either Ku or Rad52 binds the DSB. Ku directs DSBs into the non-homologous end-joining repair pathway, whereas Rad52 initiates repair by homologous recombination. Ku and Rad52, therefore, direct entry into alternative pathways for the repair of DNA breaks.