小麦雪霉叶枯病菌侵染过程中的细胞学研究

采用电镜技术研究了小麦雪霉叶枯病（Ｇｅｒｌａｃｈｉａｎｉｖａｌｉｓ）侵染过程的细胞学特征,电镜观察发现,分子孢子萌发产生的芽管由孢子细胞壁内层延伸而成,病菌侵入寄主体内后,胞间菌丝先在寄主细胞间扩展,随后胞间菌丝侵入坏死的寄主细胞,形成细胞内菌丝;胞间菌丝和胞内菌丝在形态结构上无明显差异,在病菌扩展过程中,寄生细胞发生了一系列的病理变化,并最终坏死消解,寄主细胞的变化可能与病菌分泌的毒素有关。     

小麦纹枯病菌侵染过程的组织学研究

本文报道了小麦纹枯病菌侵染小麦的过程,病菌在穿透寄主之前产生侵染热 丝圈以及形态简单的单附着胞等侵染结构,由染垫基部丝或附产丰胞产生的侵染菌丝直接或通过气孔侵入寄主,也可见菌丝直接侵入寄主;菌丝侵入寄主表皮后,迅速在受侵细胞内呈网状产扩展,并直接穿透毗邻细胞壁,向其它细胞纵横扩展,受病组织出现细胞变形,变空;接近菌丝的质膜发生质壁分离,质膜断裂,叶绿体有,变小或接近消失,类本被破坏,叶绿体内嗜颗粒     

小麦纹枯病菌侵染过程的组织学研究

本文报道了小麦纹枯病菌(Rhizoctonia cerealis)侵染小麦的过程。病菌在穿透寄主之前产生侵染垫、菌丝圈以及形态简单的单附着胞等侵染结构。由侵染垫基部菌丝或附着胞产生的侵染菌丝直接或通过气孔侵入寄主,也可见菌丝直接侵入寄主;菌丝侵入寄主表皮后,迅速在受侵细胞内呈网状扩展,并直接穿透毗邻细胞壁,向其它细胞纵横扩展。受病组织出现细胞变形、变空;接近菌丝的质膜发生质壁分离,质膜断裂：叶绿体变形、变小或接近消失,类囊体被破坏,叶绿体内嗜饿颗料减少或无;线粒体解体等系列组织病变。     

苜蓿假盘菌侵染苜蓿叶片的细胞学研究

采用微分干涉相差显微镜、扫描和透射电镜技术系统研究了苜蓿假盘菌Pseudopeziza medicaginis在苜蓿叶片的侵染过程及超微结构特征。结果表明,接种4h后,子囊孢子萌发产生芽管;12h后,芽管以直接侵入的方式进入表皮细胞形成侵染菌丝;24h后,表皮细胞中侵染菌丝向相邻表皮细胞扩展,同时侵入到叶肉细胞以胞内生长方式扩展;接种72h后,侵染菌丝在表皮细胞下的叶肉组织中形成初始菌落;第5d后,菌丝扩展至整个叶片组织,大量菌丝聚集形成子座组织,并进一步形成子囊盘与子囊。病菌菌丝在侵入寄主细胞初期,并不穿透寄主质膜与原生质,而是被其所包围。但随着菌丝进一步扩展,叶片组织发生了一系列的病理变化,其中包括叶肉细胞肿胀、细胞质消解、叶绿体等细胞器解体以及寄主细胞坏死塌陷,并最终在叶表面产生典型的褐斑病症状。     

苜蓿假盘菌侵染苜蓿叶片的细胞学研究

采用微分干涉相差显微镜、扫描和透射电镜技术系统研究了苜蓿假盘菌Pseudopeziza medicaginis在苜蓿叶片的侵染过程及超微结构特征。结果表明,接种4h后,子囊孢子萌发产生芽管;12h后,芽管以直接侵入的方式进入表皮细胞形成侵染菌丝;24h后,表皮细胞中侵染菌丝向相邻表皮细胞扩展,同时侵入到叶肉细胞以胞内生长方式扩展;接种72h后,侵染菌丝在表皮细胞下的叶肉组织中形成初始菌落;第5d后,菌丝扩展至整个叶片组织,大量菌丝聚集形成子座组织,并进一步形成子囊盘与子囊。病菌菌丝在侵入寄主细胞初期,并不     

苜蓿假盘菌侵染苜蓿叶片的细胞学研究

采用微分干涉相差显微镜、扫描和透射电镜技术系统研究了苜蓿假盘菌Pseudopeziza medicaginis在苜蓿叶片的侵染过程及超微结构特征。结果表明,接种4h后,子囊孢子萌发产生芽管：12h后,芽管以直接侵入的方式进入表皮细胞形成侵染菌丝：24h后,表皮细胞中侵染菌丝向相邻表皮细胞扩展,同时侵入到叶肉细胞以胞内生长方式扩展：接种72h后,侵染菌丝在表皮细胞下的叶肉组织中形成初始菌落;第5d后,菌丝扩展至整个叶片组织,大量菌丝聚集形成子座组织,并进一步形成子囊盘与子囊。病菌菌丝在侵入寄主细胞初期,并不穿透寄主质膜与原生质,而是被其所包围。但随着菌丝进一步扩展,叶片组织发生了一系列的病理变化,其中包括叶肉细胞肿胀、细胞质消解、叶绿体等细胞器解体以及寄主细胞坏死塌陷,并最终在叶表面产生典型的褐斑病症状。     

内吸杀菌剂甲霜灵对向日葵霜霉菌发育的影响

利用电镜技术研究了内吸杀菌剂甲霜灵对向日葵霜霉菌在寄主向日葵上发育的影响。观察发现甲霜灵引起病菌发生一系列的变化。病菌胞间菌丝细胞内液泡、电子致密体增加,线粒体肿胀畸形;菌丝细胞壁不规则地加厚,部分极度加厚的细胞壁构成了假隔膜,并且在菌丝上还有不规则的突起形成。病菌吸器外间质明显不规则地变宽,其中充满大量电子致密度高的物质：部分吸器体不能正常扩张膨大,发育受阻而成畸形。向日葵霜霉菌的以上变化导致菌丝细胞和吸器的坏死,从而抑制了病菌的进一步发育。     

冠盘二胞Marssonina coronaria侵染不同抗性苹果叶片的组织病理学研究

利用光学和电子显微镜,从组织细胞学水平系统研究了冠盘二胞Marssonina coronaria在苹果抗、感病品种叶片上的侵染过程及侵染后寄主细胞的超微结构特征。结果表明：冠盘二胞的侵入和定殖过程可以分为6个阶段：孢子萌发与芽管形成、附着胞形成、侵入细胞角质层、在叶肉细胞内产生吸器、菌丝在叶肉细胞间和细胞内扩展、分生孢子盘形成。随着菌丝扩展,受侵寄主细胞出现细胞壁加厚,细胞壁降解,质壁分离,叶绿体内淀粉粒、嗜饿颗粒积累,叶绿体基粒片层瓦解,线粒体空泡化等现象。在不同抗性的苹果品种上,分生孢子萌发率差别不明     

小麦条锈菌吸器母细胞入侵菌丝现象的进一步研究

应用电镜技术对小麦条锈菌吸器母细胞入侵自身菌丝的现象进行了研究,观察发现,在吸器母细胞与寄主细胞和菌丝细胞同时相接触的情况下,入侵栓可在与寄主细胞接触处形成,也可在与菌丝接触处形成;在菌落中心部位,吸器母细胞虽然未与寄主细胞接触,但同样可在与菌丝细胞接触处产生入侵栓;吸器母细胞在与菌丝接触处形成的人侵栓,其超微结构正常,并且可侵入到菌丝细胞壁内,但是未能穿透菌丝细胞壁。本文观察结果表明,小麦条锈菌吸器母细胞和人侵栓形成所需诱导因子可能是物理接触作用,而不涉及到化学作用,并且该病菌与寄主间的识别作用可能发生在入侵栓形成之后。     

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。     

Ultrastructural characterisation of the host–pathogen interface in white blister-infected Arabidopsis leaves

In this study transmission electron microscopy (TEM) was used to examine details of the host–pathogen interface in Arabidopsis thaliana cotyledons infected by Albugo candida, causal agent of white blister. After successful entry through stomatal pores, the pathogen developed a substomatal vesicle and subsequently produced intercellular hyphae. TEM observations revealed that coenocytic intercellular hyphae ramified and spread intercellularly throughout the host tissue forming several haustoria in host mesophyll cells. Intracellular haustoria were spherical and 4.5 μm in diameter. Each haustorium was connected to intercellular hyphae by a narrow, slender haustorium neck. The cytoplasm of the haustorium included the organelles characteristic of the pathogen. No obvious response was observed in host cells following formation of haustoria. Most of the mesophyll cells contained normal haustoria and the host cytoplasm displayed a high degree of structural integrity. Absence of host cell wall alteration and cell death in penetrated host cells suggest that the pathogen exerts considerable control over basic cellular processes and in this respect, response to this biotrophic Oomycete differs considerably from responses to other pathogens such as necrotrophs. Modification of the host plasma membrane (PM) along the cell wall and around the haustoria, was detected by applying the periodic acid-chromic acid-phosphotungstic acid (PACP) staining technique. After staining with PACP, the host PM was found to be intensely electron dense where it was adjacent to the host cell wall and the distal region of the haustorial neck. By contrast, the extrahaustorial membrane, where the host PM surrounded the haustorium, was consistently very lightly stained.     

The infection biology of Fusarium graminearum: defining the pathways of spikelet to spikelet colonisation in wheat ears

Fusarium graminearum is one of the main causal agents of Fusarium Ear Blight on wheat. How the pathogen colonises the entire ear is not known. There is controversy over whether this mycotoxin producing pathogenic fungus invades wheat floral tissue using a necrotrophic or another mode of nutrition. A detailed microscopic investigation has revealed how wild-type fungal hyphae, of the sequenced strain PH-1, colonised susceptible wheat ears and spread from spikelet to spikelet. At the advancing infection front, colonisation of the host cortex occurred ahead of any vascular colonisation and the hyphae adapted to the available intercellular space between host cells. Intercellular hyphae then became abundant and host cells lost their entire cellular contents just prior to intracellular colonisation. No host cells died ahead of the infection. However, while these deep cortex infections progressed, just below the surface the highly photosynthetic chlorenchyma cells were observed to have died prior to colonisation. Behind the infection front, hyphae were abundant in the vasculature and the cortex, often growing through the pit fields of thick walled cells. This high level of inter- and intracellular fungal colonisation resulted in the collapse of the non-lignified cell-types. In this middle zone of infection, hyphal diameters were considerably enlarged. Far behind the infection front inter- and intracellular hyphae were devoid of contents and had often collapsed. At later stages of infection, the pathogen switched from predominately vertical to lateral growth and accumulated below the surface of the rachis. Here the lignified host cell walls became heavily degraded and hyphae ruptured the epidermis and produced an aerial mycelium.     

Light and Electron Microscopy of the Compatible Interaction Between Arabidopsis and the Downy Mildew Pathogen Peronospora parasitica

In this study, we focused on compatible interactions between Peronospora parasitica isolate Emoy‐2 and wild‐type (Oy‐0) and mutant (Ws‐eds1) Arabidopsis thaliana accessions by using light and transmission electron microscopy (TEM). Light microscopy of compatible interactions revealed that conidia germinated and penetrated through the anticlinal cell walls of two epidermal cells. Rapid spreading of the hyphal growth with formation of numerous haustoria within the mesophyll cells was subsequently followed by profuse sporulation in the absence of host cell necrosis on both wild‐type and mutant accessions. TEM observations revealed that coenocytic intercellular hyphae ramified and spread intercellularly throughout the host tissue forming several haustoria in host mesophyll cells. Intracellular haustoria were lobed with the diameter of 6–7 μm. Each haustorium was connected to intercellular hyphae in the absence of apparent haustorial neck. The cytoplasm of the haustorium included the organelles characteristic of the pathogen. Callose‐like deposits were frequently observed at sites of penetration around the proximal region of the haustorial neck. Apart from a few callose ensheatments, no obvious response was observed in host cells following formation of haustoria. Most of mesophyll cells contained normal haustoria and the host cytoplasm displayed a high degree of structural integrity. Absence of host cell wall alteration and cell death in penetrated host cell of both accessions suggest that the pathogen exerts considerable control over basic cellular processes and in this respect, response to this biotroph oomycete differs considerably from responses to other pathogens such as necrotrophs.     

小麦条锈菌胞间菌丝的超微结构和细胞化学研究

本文应用电镜技术和细胞化学方法,对小麦条锈菌寄主胞间菌丝的超微结构进行了研究。观察发现:小麦条锈菌胞间菌丝有两种类型,即具隔膜菌丝和无隔膜菌丝。在胞间菌丝中,多核现象极为普遍。常规染色和细胞化学染色结果表明:胞间菌丝的细胞壁由四层组成,隔膜由三层构成,细胞壁的内层与隔膜的外层相连,细胞壁和隔膜中含有蛋白质和多糖物质。隔膜的发育可分三个阶段,即隔膜突的形成,隔膜壁的延伸和隔膜孔结构的形成。本研究中还观察到胞间菌丝间的融合现象。本文的研究结果表明:小麦条锈菌胞间菌丝的一些特征显然不同于其它锈菌。     

Ultrastructure of the Host-Pathogen Relationship in Entomosporium Leaf Spot Disease of Photinia

Entomosporium mespili appears to be a hemibiotroph on infected Photinia leaves. This fungal pathogen produced distinctive haustoria in living host cells in young lesions. Each haustorium possessed a long slender neck with a single septum and an enlarged distal body that contained a single nucleus. A collar of host cell wall material was associated with the haustorial neck. Intact haustoria also were found in necrotic cells of older lesions. However, by this stage of disease development, the pathogen also possessed an extensive system of branched, septate hyphae that grew indiscriminately between and through dead and dying host cells. These hyphae eventually gave rise to a subcutaneous layer of sporogenous cells that formed conidia.     

ELECTRON MICROSCOPY OF THE HOST-PARASITE RELATIONSHIPS IN STEM RUST OF WHEAT

Ehrlich , H. G., and Mary A. Ehrlich . (Duquesne U., Pittsburgh, Pa.) Electron microscopy of the host-parasite relationships in stem rust of wheat.—Amer. Jour. Bot. 50(2): 123–130. Illus. 1963.—A series of micrographs showing intercellular dikaryotic mycelium, haustorial mother cells, stages in haustorial formation, and haustoria within host cells are presented in the present report. Of special interest and potential significance in a study of obligate parasitism is an encapsulation ranging from 800 to 3400 A in thickness which surrounds the haustorium, but which is not present around the intercellular hyphae. The encapsulation completely encases the haustorium proper; it is bounded on the inside by the cell wall of the haustorium, and its thin membranous outer margin abuts directly on the protoplast of the host cell. The nature of the material composing the encapsulation is uncertain, but it appears to originate from the haustorial protoplast, and at least a portion of it may be fungal cytoplasm. This newly described structure represents the actual interface between the host and pathogen. Small vesicles which seem to originate from the outer margin of the encapsulation are sometimes found in the host cytoplasm surrounding apparently vigorous haustoria. The vesicles are bounded by a membrane and contain particulate material.     

柿树炭疽菌侵染寄主的细胞学研究*

超微结构研究表明,柿树炭疽菌(Colletotrichum gloeosporioides)侵染后在寄主细胞中形成初生菌丝和次生菌丝,寄主细胞膜外沉积了一层厚的电子不透明物质,初生菌丝与具有沉积物的寄主原生质膜之间有一层界面基质(interfacial matrix)。当初生菌丝扩张并侵染相邻细胞时, 围绕着初生菌丝层的界面基质消失,具有沉积物的原生质膜被逐步降解。初生菌丝在穿透寄主细胞壁过程中形成一个漏斗状的菌丝锥,然后穿透寄主细胞壁并迅速膨大, 然后形成厚壁的初生菌丝。初生菌丝在寄主细胞壁中收缩狭窄处产生一个隔膜,隔膜两边菌丝中细胞质的电子密度明显不同,菌丝锥中有浓密的电子密度。死体营养的次生菌丝在死的细胞中繁殖和扩展,并产生分枝。次生菌丝可直接穿透较薄的寄主细胞壁,无缢缩或任何变形现象,菌丝顶端部分未见隔膜产生;在穿透较厚的细胞壁时,靠近顶端处产生隔膜,顶端细胞膨大,使寄主细胞壁撕裂。接种90h后分生孢子盘在枝条表面形成。柿树炭疽菌其侵染过程有两个阶段,即初生菌丝的活体营养阶段和次生菌丝的死体营养阶段。     

柿树炭疽菌侵染不同柿树种、品种和部位的细胞学特征

用柿树炭疽病菌Colletotrichumgloeosporioides的分生孢子制备孢子悬浮液,接种无核柿、野柿、冬柿和浙江柿的新梢、叶柄和叶片,并观察致病性、附着胞形成和侵染特性。柿树炭疽菌可以侵染无核柿枝条和叶柄以及野柿枝条,但不侵染无核柿叶片、野柿叶柄和叶片,也不侵染冬柿和浙江柿枝条、叶柄和叶片。室内接种试验与田间自然发病结果一致。柿树炭疽菌在不同柿树表面均能形成附着胞,附着胞产生在寄主表皮背斜细胞壁间结合处(JACWs)或近结合处的百分率达81%~93%。接种12h后,不同柿树表面都有附着胞形成;36h后,无核柿枝条、叶柄中有侵染菌丝存在;48h后,无核柿枝条、叶柄中观察到膨大初生菌丝和较细次生菌丝,初生菌丝可扩展到相邻细胞中,而野柿枝条中仅观察到侵染菌丝;60h后,野柿枝条中也观察到膨大的初生菌丝和较细的次生菌丝,但初生菌丝仅局限在最初侵染的细胞中,无核柿枝条和叶柄以及野柿枝条中都有分枝的次生菌丝在细胞内、细胞间或相邻的细胞中扩展;直到接种90h后,在冬柿和浙江柿上都未观察到侵染菌丝的形成。结果表明,柿树炭疽菌在不同柿树种和品种上侵染菌丝的形成和扩展方式可能是其寄主专化性(或致病性)差异的重要机制之一。     

Compared Anatomy of Young Leaves of Prunus persica (L.) Batsch with Different Degrees of Susceptibility to Taphrina deformans (Berk.) Tul

Anatomical observations of leaves infected by Taphrina deformans were studied in tolerant peach trees (TPT) and in very susceptible (VSPT) ones. Leaves from the first sampling (2nd April) showed hyphae penetrating through the stomata or into the cuticle of the host tissue; anatomical structures of leaf sections were similar for both TPT and VSPT. The ultrastructure of the leaves of TPT showed seemingly normal mesophyll cells. In contrast, mesophyll cells of the VSPT showed important signs of degradation. Cells were organelle‐free and the middle lamella was expanded and invaded by hyphae of T. deformans. In some samples, the leaves of TPT showed deformed epidermal cells, loss of some spongy cells and increase of the intercellular spaces and division of the palisade cells. The pathogen proliferation in the leaves of the VSPT was considerably superior. In this case, stimulation of cell division occurred in the abaxial epidermis. Cells showed periclinal and oblique divisions, with an increased number of plasmodesmata; palisade or spongy cells were not differentiable. Leaves from TPT collected on 26th April showed hyphae with a non‐cylindrical section and with a squashed aspect. The hyphae were very evident in the intercellular spaces, showing abundant endoplasmic reticulum of rough type (RER) in the cytoplasm. On the other hand, epidermis of the leaves of the VSPT had numerous hyphae under the cuticle, which were growing in a thick pectin matrix. Leaves from TPT and VSPT collected on 6th May showed relevant differences. The leaves of TPT had a palisade mesophyll with fewer cells but with active chloroplasts. In contrast, the leaves from VSPT showed empty mesophyll cells, the cytoplasm was collapsed and the adaxial epidermis was covered with the fungus fructification. The observed anatomical and ultrastructural differences of leaves from TPT and VSPT confirm a different behaviour in plant‐host reaction at early stages of infection.