真菌反硝化过程及其驱动的N2O产生机制研究进展

真菌反硝化过程的发现打破了反硝化过程只发生在原核生物中的传统认识,是对全球微生物氮循环过程的重要补充。真菌参与的反硝化过程由于缺乏N_2O还原酶,其终产物为具有强辐射效应的温室气体N_2O。真菌在环境中分布广泛,生物量巨大,故真菌反硝化作用对全球N_2O释放通量的贡献是不容忽视的。近年来许多研究表明,真菌反硝化过程是自然环境中N_2O产生的重要途径。本文对反硝化真菌的发现、多样性及分布、产生N_2O的机制和活性测定方法等几个方面进行综述,并对未来的研究提出展望。     

植物病原真菌过氧化物酶体的发生机制及功能

过氧化物酶体（peroxisome,P）是真核细胞中普遍存在的细胞器,参与多种重要的代谢过程。P的产生、增殖及降解是细胞器发生机理研究的重要部分。到目前已知的P发生相关基因有30多个,但其机制仍不完全清楚。作为一种多细胞真核生物,丝状真菌在P发生机制的研究中有重要价值。近年来,随着基因组序列的应用和真菌生物技术的进展,丝状真菌中P功能及发生机制的研究取得了较大进展。同时,作为丝状真菌真菌中的重要类群,植物病原真菌P在致病过程中的作用也引起关注。本文对P发生机制、在丝状真菌中的研究概况,以及与植物病原真菌致病性的关系进行了 综述。     

中国环柄菇类真菌新组合（英文）

在中国真菌志编研中,作者发现有必要对其中几种环柄菇类真菌进行必要的分类处理。根据形态特征和部分ITS和n LSU序列分析结果,本文提出6个新组合,即红鳞囊小伞Cystolepiota squamulosa、暗色锥鳞环柄菇Lepiota ompnera、黑鳞白环蘑Leucoagaricus atrosquamulosus、滴泪白环蘑Leucoagaricus lacrymans、雪白小白环蘑Leucoagaricus nivalis和紫红白环蘑Leucoagaricus purpureoruber。     

鬼臼类植物内生真菌的分离及其抗癌活性研究

通过对三属四种鬼臼类植物地下茎内生真菌的分离,发现鬼臼类植物地下茎中内生真菌的物种类型极其丰富,主要分布在地下茎的表皮层和维管组织中,来源于外界环境.通过对包括鬼臼类植物在内的7种植物内生真菌的抗癌活性测定,发现内生真菌的抗癌活性与宿主有密切有关系,鬼臼类植物地下茎内生真菌含有较高比例的抗癌活性菌株.宿主种类、地理位置都会影响内生真菌的分布,进而影响活性菌株出现的频率.通过对所有鬼臼类植物地下茎内生真菌次生代谢产物的深入分析,并没有发现产生鬼臼毒素的内生真菌,鬼臼类植物地下茎内生真菌的抗癌活性成分是独立产生的.     

茶树品种、叶片生育期和茶叶化学成份对内生真菌的影响

通过茶树品种、叶片龄期及叶片化学成份对茶树内生真菌分布影响的研究,发现:(1)在供试的4个茶树品种中,黄旦的内生真菌分离频率达100%,而福云六号只有7.5%,表明茶树品种不同或遗传背景不同,其叶片中内生真菌的发生存在明显差异。(2)随着茶树叶片的成熟,叶片中内生真菌的种类与数量逐渐增多,与叶片龄期呈正相关,叶片龄期影响茶树内生真菌的种群结构。(3)不同龄期叶片水浸提液对Colletotrichum、Pestalotiopsis、Guignardia三种茶树上的主要内生真菌的生长产生不同的影响;在PDA培养基中添加15%的茶多酚,对此3种内生真菌均有一定的抑制作用,但抑制程度有所不同,表明茶树叶片的化学成份是影响内生真菌分布的重要因素之一。     

谈谈低等植物的接合生殖

生物的有性生殖是实现其遗传物质重组的重要途径。遗传物质的突变和重组是生物变异产生的基础,是生物多样性和适应性形成的渊源。某些尚未出现有性生殖的低等植物,如细菌及部分真菌,在生活史中,亦有遗传物质重组的现象,“接合”便是实现这种重组的方式之一。低等植物的几种不同的接合类型细菌的接合细菌是原核生物,细胞内尚未形成真正的细胞核。细菌的繁殖主要靠直接分裂,因此,过去曾与蓝藻一起被称为裂殖植物。迄今还没有发现细菌有真正的有性生殖过程。但在不同的个体间遗传物质发生交换和重     

安徽清凉峰自然保护区大型真菌的生态分布

清凉峰北坡的大型真菌十分丰富,经初步调查,发现清凉峰北坡共有大型真菌2纲10目38科72属160种,它们广泛分布于常绿阔叶林、马尾松林、常绿-落叶混交林、落叶阔叶林和黄山松林等林带中。按经济价值分有食用菌72种,药用菌55种,毒菌19种;依生态习性分有木生菌68种,土生菌84种,菌根真菌21种。本文论述了该地区大型真菌自然发生的常见种类和分布,并对该区大型真菌资源进行了评价,大型真菌在各林带下的分布有一定规律性,种群的组成和分布与植被类型、林中小生境、土壤类型、海拔高度等相关。该区有多种具有经济价值的大型真菌,是主要的自然资源之一,它们在食用、药用、营林等方面有着较大的利用潜力。     

青蒿内生真菌研究进展

植物内生真菌可以产生与宿主植物相同或相似的次生代谢产物,已成为活性化合物生产和发现新化合物的重要来源。为了解青蒿内生真菌的潜在应用价值,介绍了青蒿内生真菌的生物多样性、生物活性和部分次生代谢产物,并展望了未来的研究方向,以期为进一步开发利用青蒿内生真菌提供参考。     

甲壳质脱乙酰基酶的研究概况及进展

甲壳质脱乙酰基酶（ｃｈｉｔｉｎｄｅａｃｅｔｙｌａｓｅ）最初是从真菌毛霉（Ｍｕｃｏｒ．ｒｏｕｘｉ）分离纯化的一种乙酰基转移酶。这种酶可以催化脱去甲壳质分子中Ｎ－乙酰葡糖胺链上的乙酰基,而使之变成壳多糖［１］。除几种真菌外,在昆虫中也发现了这种酶的存在［２］。真菌的甲壳质脱乙酰基酶主要参与真菌细胞壁的形成［３］,还与真菌自溶的过程中的细胞壁裂解有关［４］。最近又发现它参与植物和病原微生物的相互作...     

菌寄生真菌与寄主相互作用的生化研究进展*

菌寄生真菌是指生长于其它真菌上,并从其它真菌获得营养的一类真菌。早在两百多年以前菌物学家就发现了这类真菌,但真正对其研究则始于19世纪60年代。近年来,随着对菌寄生真菌和寄主相互作用研究的不断深入,发现菌寄生真菌、其基因产物及其与寄主相互作用过程中产生的抗真菌次生代谢物在植物病害的防治上具有巨大的应用潜力而受到越来越多菌物研究者的重视。 菌寄生的过程是由许多步级联反应 (cascade reaction ) 所组成,非常复杂。菌寄生真菌或许能遥感到寄主并朝其生长。随后菌寄生真菌和寄主接触,这一步说明它们之间发生了识别,可…     

Specific association of a small protein with the telomeric DNA-protein complex during the onset of leaf senescence in Arabidopsis thaliana

Telomeres and their changes in length throughout the life span of cells have been intensively investigated in different organisms. Telomere length is assumed to control replicative senescence in mammalian cells. However, only very few data are available on the developmental dynamics of plant telomeres. Here, changes of telomere length and DNA-protein structure of Arabidopsis thaliana telomeres were analysed in different stages of development, with the main focus resting on the transition from pre-senescent to senescent leaves. The lengths of the telomeres, ranging from ca. 2.0 to 6.5 kb, do not significantly change during plant development indicating that telomere length is not involved in differentiation and replicative senescence nor in post-mitotic senescence of A. thaliana. In dedifferentiated cultured cells a slight increase in length can be determined. The nucleoprotein structure of the telomeric DNA was investigated by gel mobility shift assays, with synthetic oligonucleotides and nuclear protein extracts derived from four defined stages of post-mitotic leaf senescence. In all four stages, a highly salt-resistant DNA-protein complex was formed with the double-stranded as well as with the single-stranded G-rich telomeric DNA. An additional DNA-protein complex was identified in nuclear protein extracts isolated from plants in the transition stage from pre-senescence to senescence. The protein components of the DNA-protein complexes were analysed on native PAGE and SDS-PAGE gels. A protein of 67 kDa (ATBP1) bound to the telomeric DNA in all developmental stages. An additional protein of merely 22 kDa (ATBP2) was associated via protein-protein interaction with ATBP1 to form a higher-order complex exclusively during the onset of senescence. DNA interaction of this higher-order protein complex seems to be restricted to double-stranded telomeric DNA. The defined period of ATBP1/ATBP2 complex formation with the telomeric DNA probably indicates that ATBP2 is involved in the onset of post-mitotic leaf senescence by either disturbing an established or establishing an additional function exhibited by the telomeres in the interphase nuclei.     

共济失调毛细血管扩张症突变基因与端粒不稳定性关系研究进展

在电离辐射等因素造成的DNA损伤修复信号传导过程中,共济失调毛细血管扩张症突变基因(ATM)起关键作用。同时,ATM属于P13K家族成员,其功能与保持端粒长度有关。端粒是真核细胞内染色体末端的重复的DNA序列,端粒的长短和稳定性决定了细胞的寿命。ATM突变导致端粒的不稳定性,包括端粒连接、端粒染色质结构变化,影响端粒聚集等。     

Negative growth effectors and cellular senescence.

Current studies suggest a genetic program governs the lifespan of each organism. Using cellular senescence as a model system, components of this program for aging have been sought. Human diploid fibroblasts, upon reaching senescence, express active inhibitors of DNA synthesis. It is believed that such inhibitors could be members of a new family of negative growth effectors involved in the pathway to senescence. Factors capable of inhibiting DNA synthesis in a similar manner have also been identified from human quiescent fibroblasts and liver cells as well as from quiescent rodent liver cells. The relationship of these inhibitors to previously identified negative growth effectors and aging are discussed.     

Stochastic mechanism of cellular aging--abrupt telomere shortening as a model for stochastic nature of cellular aging

A strong stochastic component has been described for the appearance of senescent cells in cultures that have not completed their in vitro lifespan. The proliferative potential of individual clones show a bimodal distribution. Additionally, two cells arising from a single mitotic event can exhibit large differences in their doubling capacities. In this report we present a model and a computer simulation of the model that explains the observed stochastic phenomena. The model is based on both gradual and abrupt telomere shortening.Gradual telomere shortening (GTS) occurs during each cell division as a consequence of the inability of DNA polymerase to replicate the very ends of chromosomal DNA. It is responsible for the gradual decline in proliferative potential of a cell culture, but does not explain the stochastic aspects of cellular aging. Abrupt telomere shortening (ATS) occurs either through DNA recombination or nuclease digestion at the subtelomeric/telomeric border region of the chromosome. Recombination involves the invasion of a telomere single-strand three-prime protruding end at this border in the telomere of the same chromosome or in another subtelomeric/telomeric region. Shortening of one or more telomeres in the cell causes a sudden onset of cell senescence, referred to as sudden senescence syndrome (SSS). This is manifested as a stochastic and abrupt transition of cells from the larger to the smaller proliferative potential pool and can cause cell cycle arrest within one cell division. The computer simulation matches well with experimental data supporting the prediction that abrupt telomere shortening underlies the stochastic onset of cell senescence. Sudden senescence syndrome appears to be the most important mechanism in the control of the extent of proliferation of a cell culture because it prevents virtually every cell in the culture from reaching its maximum doubling capacity, that would otherwise be allowed by telomere shortening via the end-replication mechanism alone.     

Ceramide induces endothelial cell senescence

Ceramide has been proposed to be a mediator of replicative senescence. Our aim was to determine whether ceramide induces senescence in vascular endothelial cells. Human umbilical vein endothelial cells were cultured to different population doubling levels and ceramide levels were quantitated. The endogenous levels of ceramide increased 2.4‐fold with senescence onset. Low passage cells were chronically treated with exogenous C₆‐ceramide. This treatment induced a senescent phenotype as measured by an inhibition of cell proliferation and DNA replication while increasing senescence‐associated β‐galactosidase expression. This is the second cell type in which ceramide induces senescence, thus implicating ceramide as a general mediator of cellular senescence. Copyright © 2009 John Wiley & Sons, Ltd.     

DNA double strand break responses and chromatin alterations within the aging cell

Cellular senescence is a state of permanent replicative arrest that allows cells to stay viable and metabolically active but resistant to apoptotic and mitogenic stimuli. Specific, validated markers can identify senescent cells, including senescence-associated β galactosidase activity, chromatin alterations, cell morphology changes, activated p16- and p53-dependent signaling and permanent cell cycle arrest. Senescence is a natural consequence of DNA replication-associated telomere erosion, but can also be induced prematurely by telomere-independent events such as failure to repair DNA double strand breaks. Here, we review the molecular pathways of senescence onset, focussing on the changes in chromatin organization that are associated with cellular senescence, particularly senescence-associated heterochromatin foci formation. We also discuss the altered dynamics of the DNA double strand break response within the context of aging cells. Appreciating how, mechanistically, cellular senescence is induced, and how changes to chromatin organization and DNA repair contributes to this, is fundamental to our understanding of the normal and premature human aging processes associated with loss of organ and tissue function in humans.     

Identification of early senescence-associated genes in rice flag leaves

Leaf senescence is one of the key stages of plant leaf development. It is a highly complex but ordered process involving expression of large scale senescence associated genes, and its molecular mechanisms still remain unclear. By using suppression subtractive hybridization, 815 ESTs that are up-regulated at the onset of rice flag leaf senescence have been isolated. A total of 533 unigenes have been confirmed by macroarray detection and sequencing. 183 of these unigenes have GO annotations, involved in macromolecule metabolism, protein biosynthesis regulation, energy metabolism, gene expression regulations, detoxification, pathogenicity and stress, cytoskeleton organization and flower development. Another 121 unigenes co-localized with previously reported known stay-green QTLS. RT-PCR analysis on the other novel genes indicated that they can be up-regulated in natural early senescence and induced by hormone. Our results indicate that senescence is closely related to various metabolic pathways, thus providing new insight into the onset of leaf senescence mechanism. Electronic supplementary material The online version of this article (doi:) contains supplementary material, which is available to authorized users.     

Nitrogen Metabolism in Senescing Leaves

Leaf senescence is a highly organized process and not a passive decay. Photosynthesizing mesophyll cells lose their functions in an early phase, while the epidermal layer with the stomates and the phloem remains functional throughout senescence. The subcellular compartmentation is maintained and allows the cooperation of different organelles in the remobilization of constituents. Nitrogen metabolism changes at the onset of senescence from assimilation to remobilization. Enzymes involved in nitrate reduction are lost, while some enzymes of intermediary nitrogen metabolism are maintained longer, and some catabolic enzymes reach highest activities during senescence. Chloroplasts are dismantled early, but mitochondria remain active and may fuel remobilization processes. Chloroplast proteins are degraded, and this nitrogen fraction can be translocated via the phloem from senescing leaves to sinks within the same plant. In contrast, chlorophyll is degraded, fragments produced reach the vacuole, and catabolites accumulate there. Nuclear DNA is maintained until a very late phase. The export of nitrogen from senescing plant parts is important for the economic use of this macronutrient. The regulation of senescence at the whole plant level as well as at the molecular level is only rudimentarily known, although interesting new aspects have been presented recently.     

Phospholipase D in cellular senescence

Cellular senescence appears to be an important part of organismal aging. Cellular senescence is characterized by flattened enlarged morphology, inhibition of DNA replication in response to growth factors, inability to phosphorylate the pRb tumor suppressor protein, inability to produce c-fos or AP-1 and overexpression of a variety of genes, notably p21 (CIP-1/WAF-1) and p16^INK. It is now clear that certain early mitotic signals become defective with the onset of senescence. Among these is the PLD/PKC pathway. Evidence suggests that activation of PLD and PKC is critical for mitogenesis. Recent data suggest that the defect in PLD/PKC in cellular senescence is a result of elevated cellular ceramide levels which inhibit PLD activation. It appears that the elevated ceramide is a result of neutral sphingomyelinase activation. Ceramide acts to inhibit the activation of PLD by possibly three mechanisms, inhibiting activation by Rho, translocation to the membrane and gene expression. Addition of ceramide to young cells not only inhibits PLD but also recapitulates all the standard measures of cellular senescence as described above.     

Phospholipase D in cellular senescence.

Cellular senescence appears to be an important part of organismal aging. Cellular senescence is characterized by flattened enlarged morphology, inhibition of DNA replication in response to growth factors, inability to phosphorylate the pRb tumor suppressor protein, inability to produce c-fos or AP-1 and overexpression of a variety of genes, notably p21 (CIP-1/WAF-1) and p16(INK). It is now clear that certain early mitotic signals become defective with the onset of senescence. Among these is the PLD/PKC pathway. Evidence suggests that activation of PLD and PKC is critical for mitogenesis. Recent data suggest that the defect in PLD/PKC in cellular senescence is a result of elevated cellular ceramide levels which inhibit PLD activation. It appears that the elevated ceramide is a result of neutral sphingomyelinase activation. Ceramide acts to inhibit the activation of PLD by possibly three mechanisms, inhibiting activation by Rho, translocation to the membrane and gene expression. Addition of ceramide to young cells not only inhibits PLD but also recapitulates all the standard measures of cellular senescence as described above.