泾河沿岸景观格局梯度变化及驱动力分析

以MODIS影像数据为基础,利用Fragstats为工具,对泾河主干沿岸做10 km缓冲区(Buffer) ,从景观水平和类型水平上,分析河岸带景观格局的梯度变化,同时对产生这种梯度变化的驱动力进行分析。结果表明泾河自上游而下,景观水平上的景观指数有3种不同的变化类型:(1)上升型(2 )下降型(3)无明显趋势,表现出斑块数量、丰富度、连接度的递增,形状指数、分维数和斑块大小的递减;类型水平上以农田、草地和农草交错类为主,这3种类型的景观指数表现突出,具有明显的峰值。景观格局的梯度变化受到温度、降水、土壤等影响,同时,人为干扰也是不可忽视的重要因素,经济发展,人口增加使景观类型及其分布格局发生巨大的变化。景观格局的数量化对生态系统评估、监测起重要的作用。     

小波变换在岷江上游杂古脑流域径流时间序列分析中的应用

采用Dmey小波函数对杂古脑(岷江的一个重要流域)水文站41年(1962～2002)的月径流时间序列进行了多尺度分析和周期性分析.结果表明,无论在64月(5.4年)还是在128月(10.7年)的时间尺度上,1962～1978年期间杂古脑流域植被虽然破坏严重,但其径流相对稳定,并略低于多年历史平均;1986～1997年期间径流明显处于上升趋势,表明全球变暖对岷江上游水文动态规律具有重要影响.周期性分析发现,在最近40多年间,杂古脑流域径流出现了多次丰枯交替,次数与时间尺度有关(5年尺度7次,10年尺度3次).这表明在流域尺度上研究土地利用/土地覆盖变化的水文效应时应考虑全球气候变化的影响.     

Reprograming of gut microbiome energy metabolism by the FUT2 Crohn's disease risk polymorphism

Fucosyltransferase 2 (FUT2) is an enzyme that is responsible for the synthesis of the H antigen in body fluids and on the intestinal mucosa. The H antigen is an oligosaccharide moiety that acts as both an attachment site and carbon source for intestinal bacteria. Non-secretors, who are homozygous for the loss-of-function alleles of FUT2 gene (sese), have increased susceptibility to Crohn''s disease (CD). To characterize the effect of FUT2 polymorphism on the mucosal ecosystem, we profiled the microbiome, meta-proteome and meta-metabolome of 75 endoscopic lavage samples from the cecum and sigmoid of 39 healthy subjects (12 SeSe, 18 Sese and 9 sese). Imputed metagenomic analysis revealed perturbations of energy metabolism in the microbiome of non-secretor and heterozygote individuals, notably the enrichment of carbohydrate and lipid metabolism, cofactor and vitamin metabolism and glycan biosynthesis and metabolism-related pathways, and the depletion of amino-acid biosynthesis and metabolism. Similar changes were observed in mice bearing the FUT2^−/− genotype. Metabolomic analysis of human specimens revealed concordant as well as novel changes in the levels of several metabolites. Human metaproteomic analysis indicated that these functional changes were accompanied by sub-clinical levels of inflammation in the local intestinal mucosa. Therefore, the colonic microbiota of non-secretors is altered at both the compositional and functional levels, affecting the host mucosal state and potentially explaining the association of FUT2 genotype and CD susceptibility.     

A mycorrhiza-specific H+-ATPase is essential for arbuscule development and symbiotic phosphate and nitrogen uptake

Most land plants can form symbiosis with arbuscular mycorrhizal (AM) fungi to enhance uptake of mineral nutrients, particularly phosphate (Pi) and nitrogen (N), from the soil. It is established that transport of Pi from interfacial apoplast into plant cells depends on the H⁺ gradient generated by the H⁺-ATPase located on the periarbuscular membrane (PAM); however, little evidence regarding the potential link between mycorrhizal N transport and H⁺-ATPase activity is available to date. Here, we report that a PAM-localized tomato H⁺-ATPase, SlHA8, is indispensable for arbuscule development and mycorrhizal P and N uptake. Knockout of SlHA8 resulted in truncated arbuscule morphology, reduced shoot P and N accumulation, and decreased H⁺-ATPase activity and acidification of apoplastic spaces in arbusculated cells. Overexpression of SlHA8 in tomato promoted both P and N uptake, and increased total colonization level, but did not affect arbuscule morphology. Heterogeneous expression of SlHA8 in the rice osha1 mutant could fully complement its defects in arbuscule development and mycorrhizal P and N uptake. Our results propose a pivotal role of the SlHA8 in energizing both the symbiotic P and N transport, and highlight the evolutionary conservation of the AM-specific H⁺-ATPase orthologs in maintaining AM symbiosis across different mycorrhizal plant species.     

The Plant Exocyst

The exocyst is an octameric vesicle tethering complex that functions upstream of SNARE mediated exocytotic vesicle fusion with the plasma membrane. All proteins in the complex have been conserved during evolution, and genes that encode the exocyst subunits are present in the genomes of all plants investigated to date. Although the plant exocyst has not been studied in great detail, it is likely that the basic function of the exocyst in vesicle tethering is conserved. Nevertheless, genomic and genetic studie...     

NF-kappaB is required for UV-induced JNK activation via induction of PKCdelta

Ultraviolet (UV) exerts its biological activities by activating downstream effectors, including NF-kappaB, JNK, and caspases. Activation of JNK is required for UV-induced apoptosis. It is unknown whether any crosstalk occurs between NF-kappaB and JNK in response to UV and, if so, how it affects UV killing. Here we report that NF-kappaB promotes UV-induced JNK activation, thereby contributing to UV-induced apoptosis. UV-induced JNK activation is impaired in RelA/NF-kappaB null murine embryonic fibroblasts. In resting cells, the preexisting nuclear RelA has already been recruited to PKCdelta promoter and is essential for its expression. UV-induced rapid and robust activation of JNK requires PKCdelta, which augments JNK phosphorylation-activation by its upstream kinases. The RelA/NF-kappaB-PKCdelta-JNK pathway is critical for UV-induced apoptosis, as it induces the immediate expression of the proapoptotic Fas ligand. Thus, our results demonstrate that RelA/NF-kappaB via PKCdelta positively regulates UV-induced JNK activation and provide a mechanism by which NF-kappaB promotes UV-induced apoptosis.     

Hydrogen peroxide promotes Abeta production through JNK-dependent activation of gamma-secretase

Accumulation of senile plaques composed of amyloid beta-peptide (Abeta) is a pathological hallmark of Alzheimer disease (AD), and Abeta is generated through the sequential cleavage of amyloid precursor protein (APP) by beta- and gamma-secretase. Although oxidative stress has been implicated in the AD pathogenesis by inducing Abeta production, the underlying mechanism remains elusive. Here we show that the pro-oxidant H(2)O(2) promotes Abeta production through c-Jun N-terminal kinase (JNK)-dependent activation of gamma-secretase. Treatment with H(2)O(2) induced significant increase in the levels of intracellular and secreted Abeta in human neuroblastoma SH-SY5Y cells. Although gamma-secretase-mediated cleavage of APP or C99 was enhanced upon H(2)O(2) treatment, expression of APP or its alpha/beta-secretase-mediated cleavage was not affected. Silencing of the stress-activated JNK by small interfering RNA or the specific JNK inhibitor SP600125 reduced H(2)O(2)-induced gamma-secretase-mediated cleavage of APP. JNK activity was augmented in human brain tissues from AD patients and active JNK located surrounding the senile plaques in the brain of AD model mouse. Our data suggest that oxidative stress-activated JNK may contribute to senile plaque expansion through the promotion of gamma-secretase-mediated APP cleavage and Abeta production.