短柄草柄锈菌在感病寄主二穗短柄草上发育过程的组织学研究

本研究采用荧光染色和荧光显微镜技术,系统研究了短柄草柄锈菌Puccinia brachypodii (分离系F-Co和K-Ki)在感病二穗短柄草Brachypodium distachyon自交系Bd21-3叶片中的发育过程。荧光显微镜观察结果表明,接种12-18 h时,病原菌通过芽管侵入短柄草叶表皮气孔后形成气孔下囊,产生初生菌丝并形成吸器母细胞,进而侵入植物细胞形成吸器;接种24-48 h后,病原菌初生菌丝分支并形成次生菌丝;接种72 h后,短柄草锈菌开始形成菌落。F-Co的发育过程快于K-Ki,在120-216 h时,F-Co的菌落扩展面积明显高于K-Ki。本研究证实F-Co、K-Ki和二穗短柄草均为亲和互作。     

中国落叶松-杨栅锈菌遗传多样性研究

采用SSR分子标记技术对采自全国19个地区、不同年份的落叶松-杨栅锈菌Melampsora larici-populina（简称MLP）36个单孢子堆菌系的遗传多样性和种群遗传结构进行了研究。用5对SSR多态性引物共检测到62个观察等位基因（Na）,有效等位基因数（Ne）为5.42–9.82,平均有效等位基因数为7.05。供试MLP样本在5个SSR位点上的多态性信息量（PIC）变化范围为0.64–0.89,平均值0.79。平均观察杂合度（Ho）、平均期望杂合度（He）分别为0.36和0.86,不同位点的S     

落叶松-杨栅锈菌基因组密码子使用偏好分析

为了解落叶松‐杨栅锈菌密码子使用模式,并探究影响其密码子偏好形成的因素,本研究利用CondonW对落叶松‐杨栅锈菌标准菌株98AG31基因组中14 650个基因进行分析,计算基因的有效密码子数,及64个密码子的相对使用度等偏好性参数。结果表明,落叶松‐杨栅锈菌全基因组水平的密码子偏好程度较低,只有少数基因呈现出高偏好性。落叶松‐杨栅锈菌的高频密码子多以A或T结尾,而最优密码子则倾向以G或C结尾。PR2-plot分析及ENC-plot曲线与中性绘图分析显示,落叶松‐杨栅锈菌基因密码子使用模式受到选择压力和突变压力等多重因素的影响,相较于选择压力,落叶松‐杨栅锈菌基因密码子的偏好更多地受到突变压力的影响。相关性分析表明,密码子碱基组成会对密码子偏好性产生影响,其他因素如序列长度等均不会影响密码子偏好性。     

落叶松-杨栅锈菌基因复制事件及共线性分析

落叶松-杨栅锈菌是一种分布广且危害严重的林木病原真菌.了解基因组内发生的基因复制事件及基因组间的共线性关系,能为最终理解落叶松-杨栅锈菌适应性进化等生物学问题提供帮助.落叶松-杨栅锈菌全基因组水平上基因复制相关研究未见报道,共线性研究报道也较少.本研究利用落叶松-杨栅锈菌全基因组序列分析其基因复制模式.结果表明,落叶松...     

三裂叶豚草锈菌侵染寄主叶片的显微和超微观察

【背景】三裂叶豚草是我国重要的外来入侵植物之一,其传播速度快,已给我国造成巨大的经济损失。近年来发现的三裂叶豚草锈菌是一种对其具有生物防治潜力的病原菌。【方法】本文利用显微技术研究了三裂叶豚草锈菌的侵染过程及其对寄主结构的影响。【结果】三裂叶豚草锈菌菌丝可从多处侵入同一个叶肉细胞,胞间菌丝与叶肉细胞相接触可使部分细胞壁增厚。锈菌侵染使三裂叶豚草叶脉末梢导管分枝增多,造成三裂叶豚草水分代谢失调;叶片细胞内膜系统破碎化,细胞器结构受到不同程度的破坏,导致细胞内膜系统紊乱,细胞器结构稳定性降低。【结论与意义】豚草锈菌侵染破坏了三裂叶豚草叶片的细胞结构。本研究为深入研究豚草锈菌的致病机理奠定了基础。     

松杨栅锈菌遗传多样性初步分析

采用ITS-nrDNA-RELP、测序技术、RAPD(随机扩增多态性DNA)分子标记技术,对我国松杨栅锈菌不同地域的5个生理小种11个菌系进行了遗传多样性分化研究.结果表明,该菌在我国的遗传分化与地理来源相关,可分为西部地理群和北方地理群.西部地理群又可分为高山森林生态型(HMF)和平原生态型(WPL).小种遗传分化不一定与致病性分化一致.t检验表明,各生理小种RAPD遗传多样性指数无明显差异,高山森林小种遗传多样性指数(0.5172)略高于平原小种遗传多样性指数(0.5089).核糖体基因转录间隔区高度保守,不适合该菌种内群体遗传多样性分化研究.     

杨树抗锈性研究现状

综述了落叶松一杨栅锈菌生理小种分化、寄主杨树抗锈性、抗锈病基因分子标记和抗病基因连锁遗传图谱构建技术;分析了我国杨树抗锈病育种研究的现状和亟待解决的问题。     

杨树叶锈病研究

松杨栅锈菌（Melampsora larici-populina）导致的杨树叶锈病是杨树病害中分布最广、危害最大的一种病害,它造成杨树林的材积损失和材质下降,严重制约着杨树商品林和生态林的发展。该文从病原菌的分布和寄主种类、病原菌生理分化、寄主抗锈性及分子标记、防治措施等几方面介绍了杨树叶锈病的研究。     

葡萄座腔菌Botryosphaeria dothidea侵染及其对苹果果实影响的组织细胞学研究

利用光镜和电镜技术系统研究了苹果轮纹病菌葡萄座腔菌在成熟果实上的侵染扩展过程及其细胞学特征。扫描电镜观察发现,接种后3h位于皮孔处的分生孢子开始萌发,萌发后的孢子从一端或两端产生芽管直接侵入皮孔细胞,接种后9h完成侵入。30d后果面接种部位表现症状,45d后产生子实体。对接种部位取样进行光镜和透射电镜观察发现,病菌菌丝主要存在于寄主细胞壁、细胞内、细胞间隙及细胞壁与细胞膜之间。菌丝呈丝状,分枝,具隔膜。菌丝细胞内含有细胞核、线粒体、液泡等细胞器;菌丝外散发出一些高电子密度的颗粒物质,这些物质以菌丝为中心,呈放射状分布。病菌在果肉细胞生长扩展过程中,果肉细胞发生一系列变化。果肉细胞壁膨胀、变形,胞间层分离、破裂。与菌丝接触或相邻的果肉细胞细胞壁电子致密度降低,被降解成为如散发状的胞壁纤维束丝。果肉细胞的液泡破裂,质壁分离,细胞质凝结坏死并沉积于细胞壁周围,或通过受损的细胞壁胞间连丝从一个细胞转移到另一个细胞。后期菌丝在表皮下聚集生长、发育成分生孢子器。分生孢子器内壁细胞排列紧密,细胞中含有由数条丝状物平行排列而成的细胞器。该细胞器形状多样,周围总是分布着丰富的脂肪粒,推测可能与营养的运输与积累有关。     

指状青霉Penicillium digitatum侵染柑橘果实的细胞学研究

采用电子显微镜技术系统研究了指状青霉Penicillium digitatum对柑橘果实的侵染过程及超微结构特征。结果表明室温条件下,接种12h后,伤口附近的分生孢子开始萌发产生芽管;然后从伤口处直接侵入果实表皮细胞内;接种24h后,受侵染果实细胞中的菌丝向相邻细胞扩展蔓延,寄主细胞壁开始消解,质壁分离,细胞内含物及各类细胞器凝集,颜色加深,最后完全消解,伤口部位的果皮开始变软,伤口处的菌丝向外生长;84h后伤口处病斑软化,部分长出白色的霉层;96h后病斑软化面积直径达3cm,白色霉层面积逐渐扩大;120h后白色霉层中间伤口处霉层颜色加深变为灰绿色;144h后整个果实变软腐烂。果胶质标记结果表明,菌丝侵入果实后产生果胶酶并降解柑橘细胞壁中的果胶,使得细胞壁松弛,软化腐烂。     

Ultrastructural studies on the fungus,Nomuraea rileyi,infecting the velvetbean caterpillar,Anticarsia gemmatalis

Combined scanning and transmission electron microscopy was used to study the fine structure of the developmental stages of Nomuraea rileyi infecting host larvae of Anticarsia gemmatalis. Larvae were dusted with large numbers of fungal conidia, which germinated and penetrated the cuticle within 6 hr post-treatment. Within 24 hr, penetration hyphae had reached the cuticular epidermis and, via a budding process, initiated the hyphal body stage in the hemocoel. The hyphal bodies, suspended in hemolymph, multiplied and spread throughout the host larvae. By 6–7 days post-treatment, the majority of larvae were mummified. Within 12 hr postmortem numerous conidiophores emerged producing a confluent mycelial mat over the entire cuticular surface. Numerous hydrophobic conidia were formed on phialides present on the aerial conidiophores.     

Cytological Observations of the Infection Process by Phomopsis helianthi (Munt.-Cvet) in Leaves of Sunflower

The infection process of Phomopsis helianthi and the specific degradation of infected tissue were studied in detail using light and transmission electron microscopy. In comparison with other vascular pathogens, the infection and degradation process was in some aspects different. The favourite tissue for the pathogen to grow in was the phloem. Parenchymatic cells in and around vascular bundles were extremely sensitive to infection long before hyphae arrived, probably due to a toxin. In the parenchymatic cells the first changes were visible at the chloroplasts where electron-dense material accumulated in the thylakoid space. The chloroplast stroma changed contrast and later the whole cytoplasm also appeared electron dense. In the vascular bundles, first the phloem was destroyed and then hyphae invaded the adjacent mesophyll, the cambium, and finally the vessel elements. In particular, the compact mesophyll of the midvein was severely affected. Vessel elements were lined with electron-dense material and some were filled with flocculent material. Severe wall destruction indicated the action of a complete set of cell wall-degrading enzymes before hyphae entered the tissue; it always started at the innermost wall layer. Wall degradation in vascular tissue and adjacent parenchyma with intercellular spaces was different. Before the degradation of the protoplasts started, the cell walls were completely metabolized and only the secondary walls of the vessels resisted for longer. There were no host–cell reactions visible that could be interpreted as a defence reaction.