暖温带森林生态系统主要树种若干水分参数的季节变化

本文通过PV技术对暖温带落叶阔叶林主要树种辽东栎(Quercus liaotungensis)、棘桦(Betula dahurica)、五角枫(Acer mono)、大叶白蜡(Fraxinus rhychophylla)及其林下灌木六道木(Abelia biflora)、山地针叶林的主要树种油松(Pinus tabulaeformis)以及次生灌丛主要树种山杏(Prunus armeniaca var.ansu)、山桃(Prunus davidiana)、大果榆(Ulmus macrocarpa)、北京丁香(Syringa pekinensis)的日最低叶水势Ψmin、饱和含水量时的最大渗透势Ψs sat、初始质壁分离时渗透势Ψs tlp、初始质壁分离的渗透水的相对含量(ROWCtlp)、相对含水量(RWCtlp)、质外体水的相对含量(AWC)6种水分生理指标的季节变化进行了研究。结果表明：1)所研究的10种树种叶水势Ψw min的季节进程基本与土壤湿度的变化一致。乔木Ψw min季节均值由低到高的顺序为油松<辽东栎<大叶白蜡<棘皮桦<五角枫。次生灌丛4种树种Ψw min季节均值由低到高依次为：山杏<山桃<北京丁香<大果榆。在生长季的不同时期,同为灌木、生长于落叶阔叶林下的六道木Ψw min均高于灌丛样地4类树种的同期值,且季节变幅较小。2)各树种饱和含水量时的最大渗透势Ψs sat和初始质壁分离时渗透势Ψs tlp,表现出随季节进程而不断降低的趋势;Ψs tlp和Ψs sat的季节变化并未表现出与土壤水分状况变化的一致关系,而与树木自身生长发育的物候节律有关。从Ψs tlp和Ψs sat指标所反映的树木耐旱能力的季节变化来看,表现为随季节进程不断上升的趋势。一般在展叶和随后的生长旺盛期,上述树种的耐旱能力较弱。3)初始质壁分离的渗透水的相对含量(ROWCtlp)和相对含水量 (RWCtlp)的季节变化在各树种间呈现大体相同的趋势,5月下旬的生长高峰期,达到生长季中的最高值。而后随林木当年生叶的成熟和嫩枝的木质化,ROWCtlp和RWCtlp呈下降趋势。4)各树种质外体水的相对含量(AWC)表现为随季节进程而上升的趋势。     

gPGA: GPU Accelerated Population Genetics Analyses

Background

The isolation with migration (IM) model is important for studies in population genetics and phylogeography. IM program applies the IM model to genetic data drawn from a pair of closely related populations or species based on Markov chain Monte Carlo (MCMC) simulations of gene genealogies. But computational burden of IM program has placed limits on its application.

Methodology

With strong computational power, Graphics Processing Unit (GPU) has been widely used in many fields. In this article, we present an effective implementation of IM program on one GPU based on Compute Unified Device Architecture (CUDA), which we call gPGA.

Conclusions

Compared with IM program, gPGA can achieve up to 52.30X speedup on one GPU. The evaluation results demonstrate that it allows datasets to be analyzed effectively and rapidly for research on divergence population genetics. The software is freely available with source code at https://github.com/chunbaozhou/gPGA.     

Proteomic and Metabolic Analyses of S49 Lymphoma Cells Reveal Novel Regulation of Mitochondria by cAMP and Protein Kinase A

Cyclic AMP (cAMP), acting via protein kinase A (PKA), regulates many cellular responses, but the role of mitochondria in such responses is poorly understood. To define such roles, we used quantitative proteomic analysis of mitochondria-enriched fractions and performed functional and morphologic studies of wild-type (WT) and kin⁻ (PKA-null) murine S49 lymphoma cells. Basally, 75 proteins significantly differed in abundance between WT and kin⁻ S49 cells. WT, but not kin⁻, S49 cells incubated with the cAMP analog 8-(4-chlorophenylthio)adenosine cAMP (CPT-cAMP) for 16 h have (a) increased expression of mitochondria-related genes and proteins, including ones in pathways of branched-chain amino acid and fatty acid metabolism and (b) increased maximal capacity of respiration on branched-chain keto acids and fatty acids. CPT-cAMP also regulates the cellular rate of ATP-utilization, as the rates of both ATP-linked respiration and proton efflux are decreased in WT but not kin⁻ cells. CPT-cAMP protected WT S49 cells from glucose or glutamine deprivation, In contrast, CPT-cAMP did not protect kin⁻ cells or WT cells treated with the PKA inhibitor H89 from glutamine deprivation. Under basal conditions, the mitochondrial structure of WT and kin⁻ S49 cells is similar. Treatment with CPT-cAMP produced apoptotic changes (i.e. decreased mitochondrial density and size and loss of cristae) in WT, but not kin⁻ cells. Together, these findings show that cAMP acts via PKA to regulate multiple aspects of mitochondrial function and structure. Mitochondrial perturbation thus likely contributes to cAMP/PKA-mediated cellular responses.     

Pnpla3/Adiponutrin deficiency in mice does not contribute to fatty liver disease or metabolic syndrome

PNPLA3 (adiponutrin, calcium-independent phospholipase A(2) epsilon [iPLA(2)ε]) is an adipose-enriched, nutritionally regulated protein that belongs to the patatin-like phospholipase domain containing (PNPLA) family of lipid metabolizing proteins. Genetic variations in the human PNPLA3 gene (i.e., the rs738409 I148M allele) has been strongly and repeatedly associated with fatty liver disease. Although human PNPLA3 has triacylglycerol (TAG) hydrolase and transacylase activities in vitro, its in vivo function and physiological relevance remain controversial. The objective of this study was to determine the metabolic consequences of global targeted deletion of the Pnpla3 gene in mice. We found that Pnpla3 mRNA expression is altered in adipose tissue and liver in response to acute and chronic nutritional challenges. However, global targeted deletion of the Pnpla3 gene in mice did not affect TAG hydrolysis, nor did it influence energy/glucose/lipid homoeostasis or hepatic steatosis/injury. Experimental interventions designed to increase Pnpla3 expression (refeeding, high-sucrose diet, diet-induced obesity, and liver X receptor agonism) likewise failed to reveal differences in the above-mentioned metabolic phenotypes. Expression of the Pnpla3 paralog, Pnpla5, was increased in adipose tissue but not in liver of Pnpla3-deficient mice, but compensatory regulation of genes involved in TAG metabolism was not identified. Together these data argue against a role for Pnpla3 loss-of-function in fatty liver disease or metabolic syndrome in mice.     

Effect of LNA- and OMeN-modified oligonucleotide probes on the stability and discrimination of mismatched base pairs of duplexes

Locked nucleic acid (LNA) and 2'-O-methyl nucleotide (OMeN) are the most extensively studied nucleotide analogues. Although both LNA and OMeN are characterized by the C3'-endo sugar pucker conformation, which is dominant in A-form DNA and RNA nucleotides, they demonstrate different binding behaviours. Previous studies have focused attention on their properties of duplex stabilities, hybridization kinetics and resistance against nuclease digestion; however, their ability to discriminate mismatched hybridizations has been explored much less. In this study, LNA- and OMeN-modified oligonucleotide probes have been prepared and their effects on the DNA duplex stability have been examined: LNA modifications can enhance the duplex stability, whereas OMeN modifications reduce the duplex stability. Next, we studied how the LNA:DNA and OMeN:DNA mismatches reduced the duplex stability. Melting temperature measurement showed that different LNA:DNA or OMeN:DNA mismatches indeed influence the duplex stability differently. LNA purines can discriminate LNA:DNA mismatches more effectively than LNA pyrimidines as well as DNA nucleotides. Furthermore, we designed five LNA- and five OMeN-modified oligonucleotide probes to simulate realistic situations where target-probe duplexes contain a complementary LNA:DNA or OMeN:DNA base pairs and a DNA:DNA mismatch simultaneously. The measured collective effect showed that the duplex stability was enhanced by the complementary LNA:DNA base pair but decreased by the DNA:DNA mismatch in a position-dependent manner regardless of the chemical identity and position of the complementary LNA:DNA base pair. On the other hand, the OMeN-modified probes also showed that the duplex stability was reduced by both the OMeN modification and the OMeN:DNA mismatch in a position-dependent manner.     

Interleukin-6 signaling regulates anchorage-independent growth, proliferation, adhesion and invasion in human ovarian cancer cells

It has been widely reported that Interleukin-6 (IL-6) is overexpressed in the serum and ascites of ovarian cancer (OVCA) patients, and elevated IL-6 level correlates with poor prognosis and survival. However, the exact role that IL-6 plays in this malignancy or whether IL-6 can regulate tumorigenic properties has not been established. Here we demonstrate that overexpression of IL-6 in non-IL-6-expressing A2780 cells (by transfecting with plasmid encoding for sense IL-6) increases anchorage-independent growth, proliferation, adhesion and invasion, while depletion of endogenous IL-6 expression in IL-6-overexpressing SKOV-3 cells (by transfecting with plasmid encoding for antisense IL-6) decreases. Further investigation indicates that IL-6 promotes OVCA cell proliferation by altering cell cycle distribution rather than inhibiting apoptosis and that IL-6-enhanced OVCA cell invasive may be associated with increased matrix metalloproteinase (MMP)-9 but not MMP-2 proteolytic activity. In addition, overexpressing or deleting of IL-6 in OVCA cells enhances or reduces its receptor (IL-6Rα and gp130) expression and basal phosphorylation levels of both ERK and Akt, and additional treatment with specific inhibitor of the ERK or Akt signaling pathway significantly inhibits the proliferation of IL-6-overexpressing A2780 cells. Our data suggest that the autocrine production of IL-6 by OVCA cells regulates tumorigenic properties of these cells by inducing IL-6 signaling pathways. Thus, regulation of IL-6 expression or its related signaling pathway may be a promising strategy for controlling the progression of OVCA.