泰国中-新生代热带植物木化石研究

泰国东北部柯叻府及邻区中-新生代木化石非常丰富并保存有完好的解剖构造,是探究热带植被历史、古气候演化以及古环境变迁等问题的重要实证材料.最近的野外调查和专题研究确认该地区中-新生代木化石11科19属约50个种或种级分类单元,分别隶属于裸子植物和被子植物两大分类群,其中有5科7属20种(包括未定种)为前人在泰国未曾报道的类型.当前木材化石群揭示出在中生代后期,泰国东北部热带针叶树植被以南洋杉科为主;在中新世-更新世时期,该地区主要发育落叶和常绿阔叶树植被,代表热带气候环境.     

Bypassing genomic imprinting allows seed development

In developing progeny of mammals the two parental genomes are differentially expressed according to imprinting marks, and embryos with only a uniparental genetic contribution die. Gene expression that is dependent on the parent of origin has also been observed in the offspring of flowering plants, and mutations in the imprinting machinery lead to embryonic lethality, primarily affecting the development of the endosperm-a structure in the seed that nourishes the embryo, analogous to the function of the mammalian placenta. Here we have generated Arabidopsis thaliana seeds in which the endosperm is of uniparental, that is, maternal, origin. We demonstrate that imprinting in developing seeds can be bypassed and viable albeit smaller seedlings can develop from seeds lacking a paternal contribution to the endosperm. Bypassing is only possible if the mother is mutant for any of the FIS-class genes, which encode Polycomb group chromatin-modifying factors. Thus, these data provide functional evidence that the action of the FIS complex balances the contribution of the paternal genome. As flowering plants have evolved a special reproduction system with a parallel fusion of two female with two male gametes, our findings support the hypothesis that only with the evolution of double fertilization did the action of the FIS genes become a requirement for seed development. Furthermore, our data argue for a gametophytic origin of endosperm in flowering plants, thereby supporting a hypothesis raised in 1900 by Eduard Strasburger.     

Non-volcanic tremor driven by large transient shear stresses

Non-impulsive seismic radiation or 'tremor' has long been observed at volcanoes and more recently around subduction zones. Although the number of observations of non-volcanic tremor is steadily increasing, the causative mechanism remains unclear. Some have attributed non-volcanic tremor to the movement of fluids, while its coincidence with geodetically observed slow-slip events at regular intervals has led others to consider slip on the plate interface as its cause. Low-frequency earthquakes in Japan, which are believed to make up at least part of non-volcanic tremor, have focal mechanisms and locations that are consistent with tremor being generated by shear slip on the subduction interface. In Cascadia, however, tremor locations appear to be more distributed in depth than in Japan, making them harder to reconcile with a plate interface shear-slip model. Here we identify bursts of tremor that radiated from the Cascadia subduction zone near Vancouver Island, Canada, during the strongest shaking from the moment magnitude M(w) = 7.8, 2002 Denali, Alaska, earthquake. Tremor occurs when the Love wave displacements are to the southwest (the direction of plate convergence of the overriding plate), implying that the Love waves trigger the tremor. We show that these displacements correspond to shear stresses of approximately 40 kPa on the plate interface, which suggests that the effective stress on the plate interface is very low. These observations indicate that tremor and possibly slow slip can be instantaneously induced by shear stress increases on the subduction interface-effectively a frictional failure response to the driving stress.     

Structural basis for cofactor-independent dioxygenation in vancomycin biosynthesis

Enzyme-catalysed oxidations are some of the most common transformations in primary and secondary metabolism. The vancomycin biosynthetic enzyme DpgC belongs to a small class of oxygenation enzymes that are not dependent on an accessory cofactor or metal ion. The detailed mechanism of cofactor-independent oxygenases has not been established. Here we report the first structure of an enzyme of this oxygenase class in complex with a bound substrate mimic. The use of a designed, synthetic substrate analogue allows unique insights into the chemistry of oxygen activation. The structure confirms the absence of cofactors, and electron density consistent with molecular oxygen is present adjacent to the site of oxidation on the substrate. Molecular oxygen is bound in a small hydrophobic pocket and the substrate provides the reducing power to activate oxygen for downstream chemical steps. Our results resolve the unique and complex chemistry of DpgC, a key enzyme in the biosynthetic pathway of an important class of antibiotics. Furthermore, mechanistic parallels exist between DpgC and cofactor-dependent flavoenzymes, providing information regarding the general mechanism of enzymatic oxygen activation.     

No extreme bipolar glaciation during the main Eocene calcite compensation shift

Major ice sheets were permanently established on Antarctica approximately 34 million years ago, close to the Eocene/Oligocene boundary, at the same time as a permanent deepening of the calcite compensation depth in the world's oceans. Until recently, it was thought that Northern Hemisphere glaciation began much later, between 11 and 5 million years ago. This view has been challenged, however, by records of ice rafting at high northern latitudes during the Eocene epoch and by estimates of global ice volume that exceed the storage capacity of Antarctica at the same time as a temporary deepening of the calcite compensation depth approximately 41.6 million years ago. Here we test the hypothesis that large ice sheets were present in both hemispheres approximately 41.6 million years ago using marine sediment records of oxygen and carbon isotope values and of calcium carbonate content from the equatorial Atlantic Ocean. These records allow, at most, an ice budget that can easily be accommodated on Antarctica, indicating that large ice sheets were not present in the Northern Hemisphere. The records also reveal a brief interval shortly before the temporary deepening of the calcite compensation depth during which the calcite compensation depth shoaled, ocean temperatures increased and carbon isotope values decreased in the equatorial Atlantic. The nature of these changes around 41.6 million years ago implies common links, in terms of carbon cycling, with events at the Eocene/Oligocene boundary and with the 'hyperthermals' of the Early Eocene climate optimum. Our findings help to resolve the apparent discrepancy between the geological records of Northern Hemisphere glaciation and model results that indicate that the threshold for continental glaciation was crossed earlier in the Southern Hemisphere than in the Northern Hemisphere.     

p15Ink4b is a critical tumour suppressor in the absence of p16Ink4a

The CDKN2b-CDKN2a locus on chromosome 9p21 in human (chromosome 4 in mouse) is frequently lost in cancer. The locus encodes three cell cycle inhibitory proteins: p15INK4b encoded by CDKN2b, p16INK4a encoded by CDKN2a and p14ARF (p19Arf in mice) encoded by an alternative reading frame of CDKN2a (ref. 1). Whereas the tumour suppressor functions for p16INK4a and p14ARF have been firmly established, the role of p15INK4b remains ambiguous. However, many 9p21 deletions also remove CDKN2b, so we hypothesized a synergistic effect of the combined deficiency for p15INK4b, p14ARF and p16INK4a. Here we report that mice deficient for all three open reading frames (Cdkn2ab-/-) are more tumour-prone and develop a wider spectrum of tumours than Cdkn2a mutant mice, with a preponderance of skin tumours and soft tissue sarcomas (for example, mesothelioma) frequently composed of mixed cell types and often showing biphasic differentiation. Cdkn2ab-/- mouse embryonic fibroblasts (MEFs) are substantially more sensitive to oncogenic transformation than Cdkn2a mutant MEFs. Under conditions of stress, p15Ink4b protein levels are significantly elevated in MEFs deficient for p16Ink4a. Our data indicate that p15Ink4b can fulfil a critical backup function for p16Ink4a and provide an explanation for the frequent loss of the complete CDKN2b-CDKN2a locus in human tumours.     

Global warming and climate forcing by recent albedo changes on Mars

For hundreds of years, scientists have tracked the changing appearance of Mars, first by hand drawings and later by photographs. Because of this historical record, many classical albedo patterns have long been known to shift in appearance over time. Decadal variations of the martian surface albedo are generally attributed to removal and deposition of small amounts of relatively bright dust on the surface. Large swaths of the surface (up to 56 million km2) have been observed to darken or brighten by 10 per cent or more. It is unknown, however, how these albedo changes affect wind circulation, dust transport and the feedback between these processes and the martian climate. Here we present predictions from a Mars general circulation model, indicating that the observed interannual albedo alterations strongly influence the martian environment. Results indicate enhanced wind stress in recently darkened areas and decreased wind stress in brightened areas, producing a positive feedback system in which the albedo changes strengthen the winds that generate the changes. The simulations also predict a net annual global warming of surface air temperatures by approximately 0.65 K, enhancing dust lifting by increasing the likelihood of dust devil generation. The increase in global dust lifting by both wind stress and dust devils may affect the mechanisms that trigger large dust storm initiation, a poorly understood phenomenon, unique to Mars. In addition, predicted increases in summertime air temperatures at high southern latitudes would contribute to the rapid and steady scarp retreat that has been observed in the south polar residual ice for the past four Mars years. Our results suggest that documented albedo changes affect recent climate change and large-scale weather patterns on Mars, and thus albedo variations are a necessary component of future atmospheric and climate studies.     

A second generation human haplotype map of over 3.1 million SNPs

We describe the Phase II HapMap, which characterizes over 3.1 million human single nucleotide polymorphisms (SNPs) genotyped in 270 individuals from four geographically diverse populations and includes 25-35% of common SNP variation in the populations surveyed. The map is estimated to capture untyped common variation with an average maximum r2 of between 0.9 and 0.96 depending on population. We demonstrate that the current generation of commercial genome-wide genotyping products captures common Phase II SNPs with an average maximum r2 of up to 0.8 in African and up to 0.95 in non-African populations, and that potential gains in power in association studies can be obtained through imputation. These data also reveal novel aspects of the structure of linkage disequilibrium. We show that 10-30% of pairs of individuals within a population share at least one region of extended genetic identity arising from recent ancestry and that up to 1% of all common variants are untaggable, primarily because they lie within recombination hotspots. We show that recombination rates vary systematically around genes and between genes of different function. Finally, we demonstrate increased differentiation at non-synonymous, compared to synonymous, SNPs, resulting from systematic differences in the strength or efficacy of natural selection between populations.     

Genome-wide detection and characterization of positive selection in human populations

With the advent of dense maps of human genetic variation, it is now possible to detect positive natural selection across the human genome. Here we report an analysis of over 3 million polymorphisms from the International HapMap Project Phase 2 (HapMap2). We used 'long-range haplotype' methods, which were developed to identify alleles segregating in a population that have undergone recent selection, and we also developed new methods that are based on cross-population comparisons to discover alleles that have swept to near-fixation within a population. The analysis reveals more than 300 strong candidate regions. Focusing on the strongest 22 regions, we develop a heuristic for scrutinizing these regions to identify candidate targets of selection. In a complementary analysis, we identify 26 non-synonymous, coding, single nucleotide polymorphisms showing regional evidence of positive selection. Examination of these candidates highlights three cases in which two genes in a common biological process have apparently undergone positive selection in the same population:LARGE and DMD, both related to infection by the Lassa virus, in West Africa;SLC24A5 and SLC45A2, both involved in skin pigmentation, in Europe; and EDAR and EDA2R, both involved in development of hair follicles, in Asia.     

14-3-3sigma controls mitotic translation to facilitate cytokinesis

14-3-3 proteins are crucial in a wide variety of cellular responses including cell cycle progression, DNA damage checkpoints and apoptosis. One particular 14-3-3 isoform, sigma, is a p53-responsive gene, the function of which is frequently lost in human tumours, including breast and prostate cancers as a result of either hypermethylation of the 14-3-3sigma promoter or induction of an oestrogen-responsive ubiquitin ligase that specifically targets 14-3-3sigma for proteasomal degradation. Loss of 14-3-3sigma protein occurs not only within the tumours themselves but also in the surrounding pre-dysplastic tissue (so-called field cancerization), indicating that 14-3-3sigma might have an important tumour suppressor function that becomes lost early in the process of tumour evolution. The molecular basis for the tumour suppressor function of 14-3-3sigma is unknown. Here we report a previously unknown function for 14-3-3sigma as a regulator of mitotic translation through its direct mitosis-specific binding to a variety of translation/initiation factors, including eukaryotic initiation factor 4B in a stoichiometric manner. Cells lacking 14-3-3sigma, in marked contrast to normal cells, cannot suppress cap-dependent translation and do not stimulate cap-independent translation during and immediately after mitosis. This defective switch in the mechanism of translation results in reduced mitotic-specific expression of the endogenous internal ribosomal entry site (IRES)-dependent form of the cyclin-dependent kinase Cdk11 (p58 PITSLRE), leading to impaired cytokinesis, loss of Polo-like kinase-1 at the midbody, and the accumulation of binucleate cells. The aberrant mitotic phenotype of 14-3-3sigma-depleted cells can be rescued by forced expression of p58 PITSLRE or by extinguishing cap-dependent translation and increasing cap-independent translation during mitosis by using rapamycin. Our findings show how aberrant mitotic translation in the absence of 14-3-3sigma impairs mitotic exit to generate binucleate cells and provides a potential explanation of how 14-3-3sigma-deficient cells may progress on the path to aneuploidy and tumorigenesis.