草坪草育种研究进展 (综述)

介绍草坪草传统育种和转基因育种的历史与现状,概述草坪转基因育种的操作过程,对植物特别是草坪草转基因过程中存在的一些问题如基因丢失,基因沉默,基因流引起的转基因安全性等进行评述。     

冷季型草坪草对高温胁迫的生理生态适应机理研究进展

高温是制约草坪草(尤其是冷季型草坪草)生长的重要生态因子之一。然而,草坪草本身都具有一定的耐热性,特别是通过其体内的一些生理和生化机制能够抵御和适应一定程度和时间的热胁迫,比如通过植物体内细胞膜膜脂组分的变化、抗氧化系统对氧自由基的清除、热激蛋白的合成以及一些其它物质代谢的渗透调节以获得耐热性,从而缓减高温对其的伤害。本文结合作者数年的研究成果,就这两个方面综述了国内外的研究进展并提出了目前有关这些方面研究的不足以及今后研究的重点,以便为揭示冷季型草坪草在夏季所受高温伤害机理以及热适应机理提供科学的理论依据和实践指导。     

我国暖季型草坪草锈病的研究进展

锈病是暖季型草坪草上的一种重要病害,可明显降低暖季型草坪草的观赏价值和使用价值.综述了目前我国暖季型草坪草锈病的病原物、症状及发生情况、发病规律以及防治方面的研究进展,对目前我国暖季型草坪草锈病研究中存在的问题加以分析,并对暖季型草坪草锈病研究前景加以展望.     

水肥对草坪草影响的研究进展

施肥和灌溉作为草坪日常养护管理的两大重要措施,是建成高质量草坪的重要保障.从施肥措施中的N、P、K及其三元素配施对草坪草的影响以及灌溉措施中的灌溉频率和灌溉水量对草坪草生长发育的影响等方面,综述近年来草坪草施肥和灌溉研究的热点问题,探讨理想草坪草所需的适合施肥水平和灌溉水平,阐明施肥和灌溉两个措施对草坪草的影响存在一定的互助关系.通过对施肥和灌溉对草坪草生长发育影响的研究作简要的概述,为制定适宜的草坪施肥与灌溉计划,节约水资源利用,减少过量肥料对环境与草坪草生长的不利影响,同时为获得理想的草坪质量提供参考依据.     

浅析北方草坪的养护管理

草坪作为环境绿化的基色,在城市广场、在街道、在园林景点特别是体育运动场等场地,随处都可以看到绿化草坪。然而草坪如果管理不当,就会出行草荒甚至退化,草坪草作为绿化植物的重要组成部分,养护管理非常重要。     

入侵植物野胡萝卜浸提液对4种草坪草的化感效应

【目的】明确入侵植物野胡萝卜水浸提液对4种草坪草的化感效应。【方法】采用培养皿滤纸法,观察记录不同浓度(0、10、20、30、40 g·L^-1)的野胡萝卜根、茎、叶水浸提液对4种草坪草种子萌发的影响,根据化感综合效应指数分析野胡萝卜水浸提液的化感作用。【结果】野胡萝卜不同部位浸提液对受体种子的发芽率、发芽势、发芽指数、活力指数、根长和芽长均有一定的影响。化感综合效应指数表明,随着野胡萝卜浸提液浓度的增加,对白三叶、黑麦草、翦股颖的化感抑制作用均增强,对高羊茅的化感作用表现为“低促高抑”的双重效应。4种草坪草的耐受强弱顺序为:高羊茅＞黑麦草＞翦股颖＞白三叶;野胡萝卜叶浸提液对4种草坪草的化感作用强于根和茎。【结论】入侵植物野胡萝卜浸提液对4种草坪草的化感效应较为显著,在入侵严重地区,可选用耐受力强的草坪草建坪。     

运动场草坪的药剂修剪

运动场草坪的药剂修剪黄天芳为了维持运动场草坪的品质,使草坪草保持整齐一致的高度,提高草坪的致密性和增加其覆盖度,在培育管理中往往需要对草坪经常进行刈剪。运动场草坪除了通常使用剪草机进行修剪外,也可使用植物生长抑制剂进行药剂修剪。例如,对用高羊茅建植的...     

草坪的冬季管理

冬季来临,草坪草进入休眠期。草坪草的冬季管理好坏,直接影响来年草坪的生长和提高草坪的观赏性。多年来,根据我们绿化养护的经验,并根据草坪草的类型,分别介绍其冬季养护管理的具体措施。 一、暖季型草坪的管理 暖季型草坪草一般有马尼拉草、台湾青和天鹅绒草等。进入冬季,此类草坪草处于休眠状态,地上部分已枯萎,它们除了自身微     

三种草坪草的茎、叶解剖结构及其坪用性状

利用石蜡片法,对台湾草（Zoysia tenuifoia Willd.ex Trin.)、海雀稗（Paspalum vaginatum Sw.）、狗牙根[Cnodon dactylon(L.)Pers．]三种细叶暖季型草坪草的叶片有茎的解剖结构进行了研究。结果表明：叶片及茎的解剖结构与植物的耐旱性、耐践踏性和弹性等坪用特性有着密切联系。三种植物中,台湾草因叶片表皮细胞、泡状细胞、维管束鞘、机械组织有茎中纤维带的特征,而在耐旱性、耐踏踏性和弹性等坪用特性上表现出优于其他二种草坪草;狗牙根的耐旱性较强,耐踏踏性和弹性一般,海雀稗则在这几项坪用特征上均较弱。     

中国的草坪草资源及其开发利用

中国的草坪草资源相当丰富。文章初步分析了草坪草的一般特性、我国草坪草的分类以及主要的草坪草种类,并简要介绍了我国草坪草资源的现状。最后,就如何开发利用我国的草坪草资源并走草坪国产化道路提出建议。     

The Arabidopsis receptor kinase FLS2 binds flg22 and determines the specificity of flagellin perception

Flagellin, the main building block of the bacterial flagellum, acts as a pathogen-associated molecular pattern triggering the innate immune response in animals and plants. In Arabidopsis thaliana, the Leu-rich repeat transmembrane receptor kinase FLAGELLIN SENSITIVE2 (FLS2) is essential for flagellin perception. Here, we demonstrate the specific interaction of the elicitor-active epitope flg22 with the FLS2 protein by chemical cross-linking and immunoprecipitation. The functionality of this receptor was further tested by heterologous expression of the Arabidopsis FLS2 gene in tomato (Lycopersicon esculentum) cells. The perception of flg22 in tomato differs characteristically from that in Arabidopsis. Expression of Arabidopsis FLS2 conferred an additional flg22-perception system on the cells of tomato, which showed all of the properties characteristic of the perception of this elicitor in Arabidopsis. In summary, these results show that FLS2 constitutes the pattern-recognition receptor that determines the specificity of flagellin perception.     

DYNAMIN-RELATED PROTEIN DRP1A functions with DRP2B in plant growth,flg22-immune responses,and endocytosis

Ligand-induced endocytosis of the immune receptor FLAGELLIN SENSING2 (FLS2) is critical for maintaining its proper abundance in the plasma membrane (PM) to initiate and subsequently down regulate cellular immune responses to bacterial flagellin or flg22-peptide. The molecular components governing PM abundance of FLS2, however, remain mostly unknown. Here, we identified Arabidopsis (Arabidopsis thaliana) DYNAMIN-RELATED PROTEIN1A (DRP1A), a member of a plant-specific family of large dynamin GTPases, as a critical contributor to ligand-induced endocytosis of FLS2 and its physiological roles in flg22-signaling and immunity against Pseudomonas syringae pv. tomato DC3000 bacteria in leaves. Notably, drp1a single mutants displayed similar flg22-defects as those previously reported for mutants in another dynamin-related protein, DRP2B, that was previously shown to colocalize with DRP1A. Our study also uncovered synergistic roles of DRP1A and DRP2B in plant growth and development as drp1a drp2b double mutants exhibited severely stunted roots and cotyledons, as well as defective cell shape, cytokinesis, and seedling lethality. Furthermore, drp1a drp2b double mutants hyperaccumulated FLS2 in the PM prior to flg22-treatment and exhibited a block in ligand-induced endocytosis of FLS2, indicating combinatorial roles for DRP1A and DRP1B in governing PM abundance of FLS2. However, the increased steady-state PM accumulation of FLS2 in drp1a drp2b double mutants did not result in increased flg22 responses. We propose that DRP1A and DRP2B are important for the regulation of PM-associated levels of FLS2 necessary to attain signaling competency to initiate distinct flg22 responses, potentially through modulating the lipid environment in defined PM domains.

A plant-specific large dynamin GTPase is required for plant responses against bacterial pathogens and, with another dynamin, regulates the cell surface composition for plant growth and defense.     

The Arabidopsis leucine-rich repeat receptor-like kinases BAK1/SERK3 and BKK1/SERK4 are required for innate immunity to hemibiotrophic and biotrophic pathogens

Recognition of pathogen-associated molecular patterns (PAMPs) by surface-localized pattern recognition receptors (PRRs) constitutes an important layer of innate immunity in plants. The leucine-rich repeat (LRR) receptor kinases EF-TU RECEPTOR (EFR) and FLAGELLIN SENSING2 (FLS2) are the PRRs for the peptide PAMPs elf18 and flg22, which are derived from bacterial EF-Tu and flagellin, respectively. Using coimmunoprecipitation and mass spectrometry analyses, we demonstrated that EFR and FLS2 undergo ligand-induced heteromerization in planta with several LRR receptor-like kinases that belong to the SOMATIC-EMBRYOGENESIS RECEPTOR-LIKE KINASE (SERK) family, including BRASSINOSTEROID INSENSITIVE1-ASSOCIATED KINASE1/SERK3 (BAK1/SERK3) and BAK1-LIKE1/SERK4 (BKK1/SERK4). Using a novel bak1 allele that does not exhibit pleiotropic defects in brassinosteroid and cell death responses, we determined that BAK1 and BKK1 cooperate genetically to achieve full signaling capability in response to elf18 and flg22 and to the damage-associated molecular pattern AtPep1. Furthermore, we demonstrated that BAK1 and BKK1 contribute to disease resistance against the hemibiotrophic bacterium Pseudomonas syringae and the obligate biotrophic oomycete Hyaloperonospora arabidopsidis. Our work reveals that the establishment of PAMP-triggered immunity (PTI) relies on the rapid ligand-induced recruitment of multiple SERKs within PRR complexes and provides insight into the early PTI signaling events underlying this important layer of plant innate immunity.     

PAMP (Pathogen-associated Molecular Pattern)-induced Changes in Plasma Membrane Compartmentalization Reveal Novel Components of Plant Immunity

Plasma membrane compartmentalization spatiotemporally regulates cell-autonomous immune signaling in animal cells. To elucidate immediate early protein dynamics at the plant plasma membrane in response to the bacterial pathogen-associated molecular pattern (PAMP) flagellin (flg22) we employed quantitative mass spectrometric analysis on detergent-resistant membranes (DRMs) of Arabidopsis thaliana suspension cells. This approach revealed rapid and profound changes in DRM protein composition following PAMP treatment, prominently affecting proton ATPases and receptor-like kinases, including the flagellin receptor FLS2. We employed reverse genetics to address a potential contribution of a subset of these proteins in flg22-triggered cellular responses. Mutants of three candidates (DET3, AHA1, FER) exhibited a conspicuous defect in the PAMP-triggered accumulation of reactive oxygen species. In addition, these mutants showed altered mitogen-activated protein kinase (MAPK) activation, a defect in PAMP-triggered stomatal closure as well as altered bacterial infection phenotypes, which revealed three novel players in elicitor-dependent oxidative burst control and innate immunity. Our data provide evidence for dynamic elicitor-induced changes in the membrane compartmentalization of PAMP signaling components.     

Chemical interference of pathogen-associated molecular pattern-triggered immune responses in Arabidopsis reveals a potential role for fatty-acid synthase type II complex-derived lipid signals

We describe an experimental setup using submerged cultures of Arabidopsis seedlings in 96-well microtiter plates that permits chemical intervention of rapid elicitor-mediated immune responses. Screening of a chemical library comprising 120 small molecules with known biological activities revealed four compounds reducing cellulysin- or flg22-activated gene expression of the early pathogen-associated molecular patterns (PAMP)-responsive ATL2 gene. One chemical, oxytriazine, was found to induce ATL2 gene expression in the absence of PAMP. By monitoring additional flg22-triggered immediate early plant responses, we present evidence that two compounds, triclosan and fluazinam, interfere with the accumulation of reactive oxygen species and internalization of the activated plasma membrane resident FLS2 immune receptor. Using triclosan structure types and enzyme activity inhibition assays, Arabidopsis MOD1 enoyl-acyl carrier protein reductase, a subunit of the fatty-acid synthase type II (FAS II) complex, was identified as a likely cellular target of triclosan. Inhibition of all tested elicitor-triggered early immune responses by triclosan indicates a potential role for signaling lipids in flg22-triggered immunity. Chemical profiling of eca mutants, each showing deregulated ATL2 gene expression, with the identified compounds revealed mutantspecific response patterns and allowed us to deduce tentative action sites of ECA genes relative to the compound targets.     

Mutations in FLS2 Ser-938 Dissect Signaling Activation in FLS2-Mediated Arabidopsis Immunity

FLAGELLIN-SENSING 2 (FLS2) is a leucine-rich repeat/transmembrane domain/protein kinase (LRR-RLK) that is the plant receptor for bacterial flagellin or the flagellin-derived flg22 peptide. Previous work has shown that after flg22 binding, FLS2 releases BIK1 kinase and homologs and associates with BAK1 kinase, and that FLS2 kinase activity is critical for FLS2 function. However, the detailed mechanisms for activation of FLS2 signaling remain unclear. The present study initially identified multiple FLS2 in vitro phosphorylation sites and found that Serine-938 is important for FLS2 function in vivo. FLS2-mediated immune responses are abolished in transgenic plants expressing FLS2_S938A, while the acidic phosphomimic mutants FLS2_S938D and FLS2_S938E conferred responses similar to wild-type FLS2. FLS2-BAK1 association and FLS2-BIK1 disassociation after flg22 exposure still occur with FLS2_S938A, demonstrating that flg22-induced BIK1 release and BAK1 binding are not sufficient for FLS2 activity, and that Ser-938 controls other aspects of FLS2 activity. Purified BIK1 still phosphorylated purified FLS2_S938A and FLS2_S938D mutant kinase domains in vitro. Phosphorylation of BIK1 and homologs after flg22 exposure was disrupted in transgenic Arabidopsis thaliana plants expressing FLS2_S938A or FLS2_D997A (a kinase catalytic site mutant), but was normally induced in FLS2_S938D plants. BIK1 association with FLS2 required a kinase-active FLS2, but FLS2-BAK1 association did not. Hence FLS2-BIK1 dissociation and FLS2-BAK1 association are not sufficient for FLS2-mediated defense activation, but the proposed FLS2 phosphorylation site Ser-938 and FLS2 kinase activity are needed both for overall defense activation and for appropriate flg22-stimulated phosphorylation of BIK1 and homologs.     

Within-species flagellin polymorphism in Xanthomonas campestris pv campestris and its impact on elicitation of Arabidopsis FLAGELLIN SENSING2-dependent defenses

Bacterial flagellins have been portrayed as a relatively invariant pathogen-associated molecular pattern. We have found within-species, within-pathovar variation for defense-eliciting activity of flagellins among Xanthomonas campestris pv campestris (Xcc) strains. Arabidopsis thaliana FLAGELLIN SENSING2 (FLS2), a transmembrane leucine-rich repeat kinase, confers flagellin responsiveness. The flg22 region was the only Xcc flagellin region responsible for detectable elicitation of Arabidopsis defense responses. A Val-43/Asp polymorphism determined the eliciting/noneliciting nature of Xcc flagellins (structural gene fliC). Arabidopsis detected flagellins carrying Asp-43 or Asn-43 but not Val-43 or Ala-43, and it responded minimally for Glu-43. Wild-type Xcc strains carrying nonrecognized flagellin were more virulent than those carrying a recognized flagellin when infiltrated into Arabidopsis leaf mesophyll, but this correlation was misleading. Isogenic Xcc fliC gene replacement strains expressing eliciting or noneliciting flagellins grew similarly, both in leaf mesophyll and in hydathode/vascular colonization assays. The plant FLS2 genotype also had no detectable effect on disease outcome when previously untreated plants were infected by Xcc. However, resistance against Xcc was enhanced if FLS2-dependent responses were elicited 1 d before Xcc infection. Prior immunization was not required for FLS2-dependent restriction of Pseudomonas syringae pv tomato. We conclude that plant immune systems do not uniformly detect all flagellins of a particular pathogen species and that Xcc can evade Arabidopsis FLS2-mediated defenses unless the FLS2 system has been activated by previous infections.     

ESCRT-I Mediates FLS2 Endosomal Sorting and Plant Immunity

The plant immune receptor FLAGELLIN SENSING 2 (FLS2) is present at the plasma membrane and is internalized following activation of its ligand flagellin (flg22). We show that ENDOSOMAL SORTING COMPLEX REQUIRED FOR TRANSPORT (ESCRT)-I subunits play roles in FLS2 endocytosis in Arabidopsis. VPS37-1 co-localizes with FLS2 at endosomes and immunoprecipitates with the receptor upon flg22 elicitation. Vps37-1 mutants are reduced in flg22-induced FLS2 endosomes but not in endosomes labeled by Rab5 GTPases suggesting a defect in FLS2 trafficking rather than formation of endosomes. FLS2 localizes to the lumen of multivesicular bodies, but this is altered in vps37-1 mutants indicating compromised endosomal sorting of FLS2 by ESCRT-I loss-of-function. VPS37-1 and VPS28-2 are critical for immunity against bacterial infection through a role in stomatal closure. Our findings identify that VPS37-1, and likewise VPS28-2, regulate late FLS2 endosomal sorting and reveals that ESCRT-I is critical for flg22-activated stomatal defenses involved in plant immunity.