scholarly journals Amino acid substitutions responsible for different QoI and SDHI sensitivity patterns in Puccinia horiana , the causal agent of chrysanthemum white rust

2020 ◽  
Vol 70 (2) ◽  
pp. 377-386
Author(s):  
Yuichi Matsuzaki ◽  
Toshiyuki Harada ◽  
Fukumatsu Iwahashi
Keyword(s):  
Amino Acid ◽  
Causal Agent ◽  
Amino Acid Substitutions ◽  
White Rust ◽  
Puccinia Horiana

scholarly journals Cladosporium cladosporioides and Cladosporium pseudocladosporioides as potential new fungal antagonists of Puccinia horiana Henn., the causal agent of chrysanthemum white rust

PLoS ONE ◽  
2017 ◽  
Vol 12 (1) ◽  
pp. e0170782 ◽  
Author(s):  
David Eduardo Torres ◽  
Reyna Isabel Rojas-Martínez ◽  
Emma Zavaleta-Mejía ◽  
Patricia Guevara-Fefer ◽  
G. Judith Márquez-Guzmán ◽  
...  
Keyword(s):  
Cladosporium Cladosporioides ◽  
Causal Agent ◽  
White Rust ◽  
Puccinia Horiana

Fungicide Impact on in vitro Germination of Basidiospores of Puccinia horiana, the Causal Agent of Chrysanthemum White Rust

2015 ◽  
Vol 16 (2) ◽  
pp. 73-76 ◽  
Author(s):  
C. L. Palmer ◽  
M. R. Bonde ◽  
S. E. Nester ◽  
J. M. Revell ◽  
D. G. Luster
Keyword(s):  
Mode Of Action ◽  
Causal Agent ◽  
In Vitro Germination ◽  
Resistance Development ◽  
Fungicide Sensitivity ◽  
White Rust ◽  
Petri Plate ◽  
Puccinia Horiana ◽  
Over Time

Puccinia horiana is an actionable pathogen that, upon diagnosis, triggers an eradication protocol combining destruction of symptomatic chrysanthemums and a strict fungicide regime for asymptomatic plants. Symptoms typically appear during the fall as growers prepare to ship their crops. To expand the list of effective fungicides and develop fungicide sensitivity baselines, we screened in vitro germination of P. horiana basidiospores in 0.05% water agar solution amended with varying concentrations of 14 fungicides: azoxystrobin, boscalid + pyraclostrobin, fluoxastrobin, mancozeb, mandestrobin, metconazole, myclobutanil, propiconazole, tebuconazole, triadimefon, trifloxystrobin, trifloxystrobin + triadimefon, and triticonazole. Leaves with pustules ready to sporulate were affixed to petri plate lids over bases containing fungicide-amended agar. After 2 days in the dark, percent basidiospore germination was assessed. Concentrations required for 50% germination (EC50) grouped according to fungicide mode of action. Benzimidazoles exhibited EC50 values ranging from 9 to 244 ppm, while strobilurins ranged from 2 to 27 ppb. Mancozeb exhibited an EC50 of 7 ppm, and chlorothalonil was 205 ppb. Combinations of strobilurins with other modes of action exhibited EC50 values in the same range as the strobilurins. These data provide a baseline for monitoring resistance development to P. horiana over time. Accepted for publication 15 January 2015. Published 7 April 2015.

scholarly journals First Confirmed Report that Puccinia horiana, Causal Agent of Chrysanthemum White Rust, Can Overwinter in Pennsylvania

Plant Disease ◽  
2012 ◽  
Vol 96 (9) ◽  
pp. 1381-1381 ◽  
Author(s):  
G. O'Keefe ◽  
D. D. Davis
Keyword(s):  
United States ◽  
Molecular Analysis ◽  
Tap Water ◽  
Signs And Symptoms ◽  
The United States ◽  
Causal Agent ◽  
Controlled Environment ◽  
White Rust ◽  
Environment Chamber ◽  
Puccinia Horiana

Chrysanthemum white rust (CWR) is a quarantine-significant pest in the United States (Title 7, Code of Federal Regulations, Part 319.37-2). The causal agent of CWR, Puccinia horiana Henn., is an autoecious, microcyclic rust that is pathogenic on chrysanthemum species (Chrysanthemum spp.) and close relatives within the family Asteraceae. CWR is indigenous to Japan, where it was first reported in 1895 (4). By the 1960s, CWR was found throughout Europe and later spread to Africa, Oceana, South America, and other parts of Asia. In North America, CWR was reported in Mexico and in the United States (New Jersey and Pennsylvania [1977], Oregon and Washington [1990], and California [1991]). Additional detections of CWR were later reported in 22 Pennsylvania counties (2004, 2006 to 2010) (3). These later Pennsylvania reports stated that eradication was attempted at some sites, but unconfirmed observations suggested that the rust pathogen might overwinter in volunteer plants (3). Since “CWR is known to overwinter in Europe where chrysanthemums overwinter (average minimum temperatures ranging from –10°F to 10°F)” (2), the unconfirmed Pennsylvania observations prompted us to determine if P. horiana can overwinter in Pennsylvania. During October 2010, we identified CWR on perennial mums planted at six outdoor garden locations in University Park, PA. Symptomatic plants were quarantined and eradication attempted. Eradicated sites were routinely surveyed and CWR confirmed in July 2011 on volunteer plants at two of the originally infested sites. An additional outdoor garden site with CWR was observed in State College, PA, during October 2011 and eradication attempted. The three infested sites were surveyed throughout the fall and winter of 2011 to 2012. During February 2012, two asymptomatic volunteer plants arising from root pieces were collected from each of the three sites. Each sample was washed with tap water to remove excess soil, examined morphologically, surface sterilized with 10% bleach, and divided into two subsamples. One subsample from each site was divided into crown and root portions and DNA extracted using a Qiagen DNeasy Plant Mini Kit. Molecular analysis was performed using modifications of published primers ITS 5 and Rust1 (1,4). Puccinia horiana was detected in plant roots from one site and in plant crowns from two sites. The remaining two subsamples from each site were transplanted into sterilized potting soil and placed in a clean controlled environment chamber at 18°C and 85% relative humidity (RH). After 6 weeks, six actively growing plants were transferred to a second clean controlled environment chamber at 17°C and 90 to 100% RH. On 6 April 2012, CWR symptoms and signs were confirmed morphologically on two plants that had been removed from one site. On 19 April 2012, CWR signs and symptoms were confirmed morphologically and by molecular analysis on leaves of volunteer plants at one University Park site. DNA extractions were sequenced and shared a 100% maximum identity to a known P. horiana accession (EU816920.1) in GenBank. To our knowledge, this is the first confirmed report of P. horiana overwintering in Pennsylvania. References: (1) H. Alaei et al. Mycol. Res. 113:668, 2009. (2) Anon. Chrysanthemum White Rust Bulletin, Syngenta Flowers Inc., Gilroy, CA, 2010. (3) S. Kim et al. Phytopathology 101:S91, 2011. (4) K. Pedley. Plant Dis. 93:1252, 2009.

scholarly journals Evidence for Systemic Infection by Puccinia horiana, Causal Agent of Chrysanthemum White Rust, in Chrysanthemum

2015 ◽  
Vol 105 (1) ◽  
pp. 91-98 ◽  
Author(s):  
M. R. Bonde ◽  
C. A. Murphy ◽  
G. R. Bauchan ◽  
D. G. Luster ◽  
C. L. Palmer ◽  
...  
Keyword(s):  
United States ◽  
Cell Walls ◽  
Vascular Tissue ◽  
Mesophyll Cell ◽  
The United States ◽  
Causal Agent ◽  
Control Measures ◽  
Mesophyll Cells ◽  
White Rust ◽  
Puccinia Horiana

Puccinia horiana, causal agent of the disease commonly known as chrysanthemum white rust (CWR), is a quarantine-significant fungal pathogen of chrysanthemum in the United States and indigenous to Asia. The pathogen was believed to have been eradicated in the United States but recently reappeared on several occasions in northeastern United States. The objective of the study presented here was to determine whether P. horiana could systemically infect chrysanthemum plants, thus providing a means of survival through winters. Scanning and transmission electron microscopy revealed the development of P. horiana on the surface and within leaves, stems, or crowns of inoculated chrysanthemum plants artificially exposed to northeastern U.S. winter temperatures. P. horiana penetrated leaves directly through the cuticle and then colonized the mesophyll tissue both inter- and intracellularly. An electron-dense material formed at the interface between fungal and host mesophyll cells, suggesting that the pathogen adhered to the plant cells. P. horiana appeared to penetrate mesophyll cell walls by enzymatic digestion, as indicated by the absence of deformation lines in host cell walls at penetration sites. The fungus was common in vascular tissue within the infected crown, often nearly replacing the entire contents of tracheid cell walls. P. horiana frequently passed from one tracheid cell to an adjacent tracheid cell by penetration either through pit pairs or nonpitted areas of the cell walls. Individual, presumed, fungal cells in mature tracheid cells of the crown and stems arising from infected crowns suggested that the pathogen might have been moving at least partially by means of the transpiration stream. The demonstration that chrysanthemum plants can be systemically infected by P. horiana suggests that additional disease control measures are required to effectively control CWR.

Recombinant Variants of Tissue-Type Plasminogen Activator Containing Amino Acid Substitutions in the Finger Domain

1992 ◽  
Vol 68 (06) ◽  
pp. 672-677 ◽  
Author(s):  
Hitoshi Yahara ◽  
Keiji Matsumoto ◽  
Hiroyuki Maruyama ◽  
Tetsuya Nagaoka ◽  
Yasuhiro Ikenaka ◽  
...  
Keyword(s):  
Amino Acid ◽  
Plasminogen Activator ◽  
Half Life ◽  
Tissue Type ◽  
Clot Lysis ◽  
Amino Acid Substitutions ◽  
Wild Type ◽  
Plasma Clot ◽  
Tissue Type Plasminogen Activator ◽  
Type Plasminogen Activator

SummaryTissue-type plasminogen activator (t-PA) is a fibrin-specific agent which has been used to treat acute myocardial infarction. In an attempt to clarify the determinants for its rapid clearance in vivo and high affinity for fibrin clots, we produced five variants containing amino acid substitutions in the finger domain, at amino acid residues 7–9, 10–14, 15–19, 28–33, and 37–42. All the variants had a prolonged half-life and a decreased affinity for fibrin of various degrees. The 37–42 variant demonstrated about a 6-fold longer half-life with a lower affinity for fibrin. Human plasma clot lysis assay estimated the fibrinolytic activity of the 37–42 variant to be 1.4-fold less effective than that of the wild-type rt-PA. In a rabbit jugular vein clot lysis model, doses of 1.0 and 0.15 mg/kg were required for about 70% lysis in the wild-type and 37–42 variant, respectively. Fibrinogen was degraded only when the wild-type rt-PA was administered at a dose of 1.0 mg/kg. These findings suggest that the 37–42 variant can be employed at a lower dosage and that it is a more fibrin-specific thrombolytic agent than the wild-type rt-PA.

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