scholarly journals Bright-Field and Fluorescence Microscopic Study of Development of Erysiphe polygoni in Susceptible and Resistant Bigleaf Hydrangea

Plant Disease ◽  
2009 ◽  
Vol 93 (2) ◽  
pp. 130-134 ◽  
Author(s):  
Yonghao Li ◽  
Mark T. Windham ◽  
Robert N. Trigiano ◽  
Sandra M. Reed ◽  
James M. Spiers ◽  
...  
Keyword(s):  
Powdery Mildew ◽  
Hyphal Growth ◽  
Early Response ◽  
Resistance Mechanisms ◽  
Colony Development ◽  
Susceptible Cultivar ◽  
Bright Field ◽  
Erysiphe Polygoni ◽  
Infected Cells ◽  
Germ Tubes

Temporal development of Erysiphe polygoni and responses of bigleaf hydrangeas (Hydrangea macrophylla) to the fungal attack were investigated using bright-field and fluorescence microscopy. Conidia germinated 2 h after inoculation (HAI) and formed primary appressoria at the tip of the primary germ tubes within 4 HAI. Secondary germ tubes were initiated from primary appressoria or other parts of conidia 12 HAI. Hyphae developed through elongation of secondary germ tubes, and paired lateral appressoria were formed along hyphae within 2 days after inoculation (DAI). Conidiophores and conidia were formed 5 DAI. In the susceptible cultivar Nikko Blue and the resistant cultivar Veitchii, the fungus established a parasitic relationship, which was indicated by the formation of haustoria under primary appressoria and development of secondary germ tubes at 1 DAI. A hypersensitive response (HR) and accumulation of callose were detected in both resistant and susceptible cultivars at 3 DAI. Resistance to powdery mildew in Veitchii was evident by manifestation of early accumulation of callose, relatively high percentage of necrotic infected cells, and restricted colony development compared to the susceptible cultivar Nikko Blue. Restricting hyphal growth and sporulation by early response of callose accumulation and HR are important resistance mechanisms that could be used in screening hydrangeas for resistance to powdery mildew.

scholarly journals Identification of Race-Specific Resistance in North American Vitis spp. Limiting Erysiphe necator Hyphal Growth

2012 ◽  
Vol 102 (1) ◽  
pp. 83-93 ◽  
Author(s):  
David W. Ramming ◽  
Franka Gabler ◽  
Joseph L. Smilanick ◽  
Dennis A. Margosan ◽  
Molly Cadle-Davidson ◽  
...  
Keyword(s):  
Powdery Mildew ◽  
Resistance Genes ◽  
Specific Resistance ◽  
Hyphal Growth ◽  
Resistance Mechanisms ◽  
Hybrid Breeding ◽  
Erysiphe Necator ◽  
Vitis Rotundifolia ◽  
Resistance Sources

Race-specific resistance against powdery mildews is well documented in small grains but, in other crops such as grapevine, controlled analysis of host–pathogen interactions on resistant plants is uncommon. In the current study, we attempted to confirm powdery mildew resistance phenotypes through vineyard, greenhouse, and in vitro inoculations for test cross-mapping populations for two resistance sources: (i) a complex hybrid breeding line, ‘Bloodworth 81-107-11', of at least Vitis rotundifolia, V. vinifera, V. berlandieri, V. rupestris, V. labrusca, and V. aestivalis background; and (ii) Vitis hybrid ‘Tamiami’ of V. aestivalis and V. vinifera origin. Statistical analysis of vineyard resistance data suggested the segregation of two and three race-specific resistance genes from the two sources, respectively. However, in each population, some resistant progeny were susceptible in greenhouse or in vitro screens, which suggested the presence of Erysiphe necator isolates virulent on progeny segregating for one or more resistance genes. Controlled inoculation of resistant and susceptible progeny with a diverse set of E. necator isolates clearly demonstrated the presence of fungal races differentially interacting with race-specific resistance genes, providing proof of race specificity in the grape powdery mildew pathosystem. Consistent with known race-specific resistance mechanisms, both resistance sources were characterized by programmed cell death of host epidermal cells under appressoria, which arrested or slowed hyphal growth; this response was also accompanied by collapse of conidia, germ tubes, appressoria, and secondary hyphae. The observation of prevalent isolates virulent on progeny with multiple race-specific resistance genes before resistance gene deployment has implications for grape breeding strategies. We suggest that grape breeders should characterize the mechanisms of resistance and pyramid multiple resistance genes with different mechanisms for improved durability.

scholarly journals Conidial Germination, Infection Structure Formation, and Early Colony Development of Powdery Mildew on Poinsettia

1998 ◽  
Vol 88 (2) ◽  
pp. 105-113 ◽  
Author(s):  
G. J. Celio ◽  
M. K. Hausbeck
Keyword(s):  
United States ◽  
Powdery Mildew ◽  
Incubation Temperature ◽  
The United States ◽  
Conidial Germination ◽  
Colony Development ◽  
Euphorbia Pulcherrima ◽  
Basal Cells ◽  
Northern United States ◽  
Germ Tubes

Powdery mildew disease on poinsettias (Euphorbia pulcherrima) growing in commercial greenhouses was first observed in the United States in 1990 and has become an economically significant problem for poinsettia growers in the Midwest and northern United States since 1992. The temporal development of infection structures produced by conidial germ tubes of the pathogen (Oidium sp.) and the effect of high temperature on their development were investigated using poinsettia leaf disks placed in humidity chambers. Observations were made using light microscopy and scanning electron microscopy. At 20°C (85% relative humidity), conidia germinated and formed an appressorium within 6 h of inoculation. Germination over time followed a monomolecular curve (r2 = 0.77, P ≤ 0.0001). Within 24 h postinoculation, germinated conidia had formed secondary germ tubes and a haustorium. The percentage of germinated conidia with appressoria and one or more secondary germ tubes increased linearly with time (r2 = 0.92, P ≤ 0.0001), while the percentage of germinated conidia with appressoria and haustoria increased mono-molecularly (r2 = 0.93, P ≤ 0.0001). Conidia had an ornamented appearance, and all conidiophores had arced basal cells. When the incubation temperature was 30°C, conidial germination and development of secondary germ tubes and a haustorium were reduced.

Microscopy studies of powdery mildew on summer squash

1991 ◽  
Vol 49 ◽  
pp. 520-521
Author(s):  
John S. Gardner ◽  
W. M. Hess
Keyword(s):  
Powdery Mildew ◽  
Tip Growth ◽  
Hyphal Growth ◽  
Plant Tissues ◽  
Vegetative Hypha ◽  
Powdery Mildews ◽  
Summer Squash ◽  
Conidial Formation ◽  
Polar Tip Growth ◽  
Short Conidiophore

Powdery mildews are characterized by the appearance of spots or patches of a white to grayish, powdery, mildewy growth on plant tissues, entire leaves or other organs. Ervsiphe cichoracearum, the powdery mildew of cucurbits is among the most serious parasites, and the most common. The conidia are formed similar to the process described for Ervsiphe graminis by Cole and Samson. Theconidial chains mature basipetally from a short, conidiophore mother-cell at the base of the fertile hypha which arises holoblastically from the conidiophore. During early development it probably elongates by polar-tip growth like a vegetative hypha. A septum forms just above the conidiophore apex. Additional septa develop in acropetal succession. However, the conidia of E. cichoracearum are more doliform than condia from E. graminis. The purpose of these investigations was to use scanning electron microscopy (SEM) to demonstrate the nature of hyphal growth and conidial formation of E. cichoracearum on field-grown squash leaves.

Identification of a major locus conferring resistance to powdery mildew (Erysiphe polygoni DC) in mungbean (Vigna radiata L. Wilczek) by QTL analysis

Genome ◽  
2003 ◽  
Vol 46 (5) ◽  
pp. 738-744 ◽  
Author(s):  
M E Humphry ◽  
T Magner ◽  
C L McIntyre ◽  
E A.B Aitken ◽  
C J Liu
Keyword(s):  
Powdery Mildew ◽  
Linkage Map ◽  
Qtl Analysis ◽  
Vigna Radiata ◽  
Mapping Population ◽  
Susceptible Variety ◽  
Resistance Response ◽  
Causal Organism ◽  
Major Locus ◽  
Erysiphe Polygoni

A major locus conferring resistance to the causal organism of powdery mildew, Erysiphe polygoni DC, in mungbean (Vigna radiata L. Wilczek) was identified using QTL analysis with a population of 147 recombinant inbred individuals. The population was derived from a cross between 'Berken', a highly susceptible variety, and ATF 3640, a highly resistant line. To test for response to powdery mildew, F7 and F8 lines were inoculated by dispersing decaying mungbean leaves with residual conidia of E. polygoni amongst the young plants to create an artificial epidemic and assayed in a glasshouse facility. To generate a linkage map, 322 RFLP clones were tested against the two parents and 51 of these were selected to screen the mapping population. The 51 probes generated 52 mapped loci, which were used to construct a linkage map spanning 350 cM of the mungbean genome over 10 linkage groups. Using these markers, a single locus was identified that explained up to a maximum of 86% of the total variation in the resistance response to the pathogen.Key words: mungbean, powdery mildew, Erysiphe polygoni, QTL, molecular markers.

scholarly journals First Report of Powdery Mildew Caused by Erysiphe polygoni on Rumex obtusifolius in Korea

Plant Disease ◽  
2019 ◽  
Vol 103 (5) ◽  
pp. 1043-1043
Author(s):  
S. H. Hong ◽  
Y. H. Lee ◽  
Y. J. Choi ◽  
H. D. Shin
Keyword(s):  
Powdery Mildew ◽  
First Report ◽  
Rumex Obtusifolius ◽  
Erysiphe Polygoni

scholarly journals Activation and Antagonism of the OAS–RNase L Pathway

Proceedings ◽  
2020 ◽  
Vol 50 (1) ◽  
pp. 14
Author(s):  
Susan R. Weiss
Keyword(s):  
Cell Death ◽  
Antiviral Activity ◽  
Apoptotic Cell ◽  
Early Response ◽  
Apoptotic Cell Death ◽  
Rnase L ◽  
Oligoadenylate Synthetase ◽  
Viral Genomes ◽  
L System ◽  
Infected Cells

The oligoadenylate synthetase–ribonuclease L (OAS–RNase L) system is a potent antiviral pathway that severely limits the pathogenesis of many viruses. Upon sensing dsRNA, OASs produce 2′,5′-oligoadenylates (2-5A) that activate RNase L to cleave both host and viral single-stranded RNA, thereby limiting protein production, virus replication and spread, leading to apoptotic cell death. Endogenous host dsRNA, which accumulates in the absence of adenosine deaminase acting on RNA (ADAR)1, can also activate RNase L and lead to apoptotic cell death. RNase L activation and antiviral activity during infections with several types of viruses in human and bat cells is dependent on OAS3 but independent of virus-induced interferon (IFN) and, thus, RNase L can be activated even in the presence of IFN antagonists. Differently from other human viruses examined, Zika virus is resistant to the antiviral activity of RNase L and instead utilizes RNase L to enhance its replication factories to produce more infectious virus. Some betacoronaviruses antagonize RNase L activation by expressing 2′,5′-phosphodiesterases (PDEs) that cleave 2-5A and thereby antagonize activation of RNase L. The best characterized of these PDEs is the murine coronavirus (MHV) NS2 accessory protein. Enzymatically active NS2 is required for replication in myeloid cells and in the liver. Interestingly, while wild type mice clear MHV from the liver by 7–10 days post-infection, RNase L knockout mice fail to effectively clear MHV, probably due to diminished apoptotic death of infected cells. We suggest that RNase L antiviral activity stems from direct cleavage of viral genomes and cessation of protein synthesis as well as through promoting death of infected cells, limiting the spread of virus. Importantly, OASs are pattern recognition receptors and the OAS–RNase L pathway is a primary innate response pathway to viruses, capable of early response, coming into play before IFN is induced or when the virus shuts down IFN signaling.

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