scholarly journals Virulence of Blumeria graminis f. sp. tritici on Winter Wheat in the Eastern United States

Plant Disease ◽  
1998 ◽  
Vol 82 (1) ◽  
pp. 64-68 ◽  
Author(s):  
A. S. Niewoehner ◽  
S. Leath

Samples of perithecia of Blumeria graminis f. sp. tritici from senescing wheat leaves were collected by cooperators from 17 states. Ascospores were discharged from perithecia and single-spore isolates were characterized for virulence genes using a differential host series containing 15 known resistance genes. A total of 520 isolates from 17 states were characterized in 1993 and 1994. Virulence frequencies and complexity and racial composition were examined. The data were analyzed for associations among sets of virulence genes and the geographical distribution of phenotypes. Virulence to Pm3c, Pm3f, pm5, Pm6, and Pm7 was present in all states surveyed. Since 1990, virulence to Pm3a has increased in the northeast, and virulence to Pm1, Pm4b, Pm8, and Pm17 has increased across the area surveyed. The resistance genes Pm12 and Pm16 remain highly effective in the southeastern United States. An increase in virulence frequencies and complexity of isolates was observed.

Plant Disease ◽  
2009 ◽  
Vol 93 (11) ◽  
pp. 1219-1219 ◽  
Author(s):  
C. Cowger ◽  
R. Parks ◽  
D. Marshall

Pm17 is a gene for resistance to powdery mildew caused by Blumeria graminis (DC.) E.O. Speer f. sp. tritici. The gene was first confirmed in the wheat-rye translocation cultivar Amigo (1). In Amigo, the translocation is T1AL-1RS and the 1RS arm has the gene Pm17. In the mid-Atlantic United States, at least two widely deployed soft red winter wheat (Triticum aestivum L.) cultivars, McCormick (2) and Tribute (3), possess Pm17 inherited from Amigo. Before 2009, low frequencies of mostly intermediate virulence to Pm17 were detected among isolates from research plots of highly susceptible cultivars (4), but Pm17-bearing cultivars remained immune to mildew in the field. In April 2009, moderately severe powdery mildew was observed for the first time throughout plots of McCormick, Tribute, and other cultivars in both Kinston and Raleigh, NC. At Kinston, Pm17 virulence was observed at two research sites, separated by approximately 10 km, throughout plots of Amigo, McCormick, Tribute, and the hard red winter wheat cultivar TAM 303, which also contains Pm17. In the same month, virulence to Pm17 was observed in Raleigh throughout rows and plots of Amigo and TAM 303. In Kinston and Raleigh, ratings of powdery mildew severity on the Pm17-containing cultivars were 4 or 5 on a scale of 0 to 9, with 0 being the absence of mildew pustules and 9 the most severe mildew infection. Mildew was observed on leaves of all ages. Mildewed leaves were collected from field plots of all four Pm17-bearing cultivars, and an assay to confirm Pm17 virulence was conducted in the laboratory. Mixed-isolate cultures were derived from the leaves and a detached-leaf assay was performed using Amigo, which is the standard Pm17 differential (4). All tested cultures were fully to moderately virulent on Pm17 and all were fully virulent on the susceptible control Chancellor. In the field, chasmothecia (sexual fruiting bodies) were observed on Pm17-bearing cultivars. Together with the quantitatively varying Pm17 virulence detected in the laboratory assay, this suggests that multiple strains of Pm17-virulent B. graminis f. sp. tritici may be present in the field, although that has not yet been demonstrated. Pm17 has protected wheat from powdery mildew over a substantial area in the mid-Atlantic United States. The loss of Pm17 is the most important virulence shift in the U.S. wheat powdery mildew population since Pm4a became ineffective around 2002. Isolates virulent to Pm17 can be expected to appear and multiply in wheat-producing states of the mid-Atlantic United States, including Delaware, Maryland, Virginia, North Carolina, South Carolina, and Georgia. Thus, the urgency of developing and releasing wheat cultivars with other sources of effective mildew resistance is heightened. References: (1) B. Friebe et al. Euphytica 91:59, 1996. (2) C. A. Griffey et al. Crop Sci. 45:416, 2005. (3) C. A. Griffey et al. Crop Sci. 45:419, 2005. (4) R. Parks et al. Plant Dis. 92:1074, 2008.


Plant Disease ◽  
2016 ◽  
Vol 100 (6) ◽  
pp. 1212-1221 ◽  
Author(s):  
Sierra N. Wolfenbarger ◽  
Stephen T. Massie ◽  
Cynthia Ocamb ◽  
Emily B. Eck ◽  
Gary G. Grove ◽  
...  

Host resistance, both quantitative and qualitative, is the preferred long-term approach for disease management in many pathosystems, including powdery mildew of hop (Podosphaera macularis). In 2012, an epidemic of powdery mildew occurred in Washington and Idaho on previously resistant cultivars whose resistance was putatively based on the gene designated R6. In 2013, isolates capable of causing severe disease on cultivars with R6-based resistance were confirmed in Oregon and became widespread during 2014. Surveys of commercial hop yards during 2012 to 2014 documented that powdery mildew is now widespread on cultivars possessing R6 resistance in Washington and Oregon, and the incidence of disease is progressively increasing. Pathogenic fitness, race, and mating type of R6-virulent isolates were compared with isolates of P. macularis lacking R6 virulence. All isolates were positive for the mating type idiomorph MAT1-1 and were able to overcome resistance genes Rb, R3, and R5 but not R1 or R2. In addition, R6-virulent isolates were shown to infect differential cultivars reported to possess the R6 gene and also the R4 gene, although R4 has not yet been broadly deployed in the United States. R6-virulent isolates were not detected from the eastern United States during 2012 to 2015. In growth chamber studies, R6-virulent isolates of P. macularis had a significantly longer latent period and produced fewer lesions on plants with R6 as compared with plants lacking R6, indicating a fitness cost to the fungus. R6-virulent isolates also produced fewer conidia when compared with isolates lacking R6 virulence, independent of whether the isolates were grown on a plant with or without R6. Thus, it is possible that the fitness cost of R6 virulence occurs regardless of host genotype. In field studies, powdery mildew was suppressed by at least 50% on plants possessing R6 as compared with those without R6 when coinoculated with R6-virulent and avirulent isolates. R6 virulence in P. macularis appears to be race specific and, at this time, imposes a measurable fitness penalty on the fungus. Resistance genes R1 and R2 appear to remain effective against R6-virulent isolates of P. macularis in the U.S. Pacific Northwest.


Plant Disease ◽  
2008 ◽  
Vol 92 (7) ◽  
pp. 1074-1082 ◽  
Author(s):  
Ryan Parks ◽  
Ignazio Carbone ◽  
J. Paul Murphy ◽  
David Marshall ◽  
Christina Cowger

Little is known about the population structure of wheat powdery mildew in the eastern United States, and the most recent report on virulence in this population involved isolates collected in 1993–94. In the present study, wheat leaves naturally infected with powdery mildew were collected from 10 locations in the southeastern United States in 2003 and 2005 and a collection of 207 isolates was derived from single ascospores. Frequencies of virulence to 16 mildew resistance (Pm) genes were determined by inoculating the isolates individually on replicated plates of detached leaves of differential wheat lines. These virulence frequencies were used to infer local effectiveness of Pm genes, estimate virulence complexity, detect significant associations between pairs of pathogen avirulence loci, and assess whether phenotypic differences between pathogen subpopulations increased with geographic distance. In both years, virulence to Pm3a, Pm3c, Pm5a, and Pm7 was present in more than 90% of sampled isolates and virulence to Pm1a, Pm16, Pm17, and Pm25 was present in fewer than 10% of isolates. In each year, 71 to 88% of all sampled isolates possessed one of a few multilocus virulence phenotypes, although there were significant differences among locations in frequencies of virulence to individual Pm genes. Several significant associations were detected between alleles for avirulence to pairs of Pm genes. Genetic (phenotypic) distance between isolate subpopulations increased significantly (R2 = 0.40, P < 0.001) with increasing geographic separation; possible explanations include different commercial deployment of Pm genes and restricted gene flow in the pathogen population.


1996 ◽  
Vol 89 (5) ◽  
pp. 1309-1317 ◽  
Author(s):  
Roger H. Ratcliffe ◽  
Herbert W. Ohm ◽  
Fred L. Patterson ◽  
Sue E. Cambron ◽  
Gregory G. Safranski

Phytotaxa ◽  
2017 ◽  
Vol 290 (1) ◽  
pp. 1 ◽  
Author(s):  
LUCAS C. MAJURE ◽  
WALTER S. JUDD ◽  
PAMELA S. SOLTIS ◽  
DOUGLAS E. SOLTIS

The Humifusa clade represents a recent radiation that originated in the late Pliocene or early Pleistocene and consists of about 10 species widely distributed in North America from northern Mexico north to Ontario, Canada, and south to the Florida Keys. This clade likely originated in the edaphically subxeric regions of northern Mexico and the southwestern United States, and from there it later spread to the southeastern United States and ultimately produced a small radiation in the eastern United States. Hybridization among evolutionarily divergent diploid species of the southeastern (SE) and southwestern (SW) United States subclades led to the origin of many polyploid taxa, which today occupy about 75% of the distribution of the clade. Here we present a taxonomic revision of the SE subclade of the Humifusa clade and polyploid derivatives that commonly occur in the eastern United States (i.e., the O. humifusa complex). We recognize eight taxa: Opuntia abjecta, O. austrina, O. cespitosa, O. drummondii, O. humifusa, O. mesacantha subsp. mesacantha, O. mesacantha subsp. lata, and O. nemoralis, as well as the interclade allopolyploid, Opuntia ochrocentra, derived, in part, from a member of the O. humifusa complex. Diagnostic keys, descriptions, original photos, and distribution maps are provided for each taxon. Neotypes are designated for the names O. austrina (NY) and O. youngii (USF), and O. drummondii and O. tracyi are lectotypified from an illustration in Maund & Henslow and a specimen at NY, respectively.


2012 ◽  
Vol 104 (5) ◽  
pp. 1321-1335 ◽  
Author(s):  
Maheteme T. Gebremedhin ◽  
Henry W. Loescher ◽  
Teferi D. Tsegaye

2010 ◽  
Vol 103 (6) ◽  
pp. 2229-2235 ◽  
Author(s):  
Sue E. Cambron ◽  
G. David Buntin ◽  
Randy Weisz ◽  
Jeffery D. Holland ◽  
Kathy L. Flanders ◽  
...  

Crop Science ◽  
2012 ◽  
Vol 52 (5) ◽  
pp. 2097-2108 ◽  
Author(s):  
Andrew J. Green ◽  
G. Berger ◽  
C. A. Griffey ◽  
R. Pitman ◽  
W. Thomason ◽  
...  

Plant Disease ◽  
2012 ◽  
Vol 96 (8) ◽  
pp. 1216-1221 ◽  
Author(s):  
J. A. Kolmer ◽  
D. L. Long ◽  
M. E. Hughes

Collections of Puccinia triticina were obtained from rust-infected leaves provided by cooperators throughout the United States and from wheat fields and breeding plots by United States Department of Agriculture–Agricultural Research Service personnel and cooperators in the Great Plains, Ohio River Valley, southeastern states, Oregon, and Washington State in order to determine the virulence of the wheat leaf rust population in 2010. Single uredinial isolates (537 total) were derived from the collections and tested for virulence phenotype on 19 lines of ‘Thatcher’ wheat and a winter wheat line that are near-isogenic for 20 leaf rust resistance genes. In 2010, 38 virulence phenotypes were described in the United States. Virulence phenotypes MLDSD, TDBJG, and TCRKG were the three most common phenotypes. Phenotype MLDSD is virulent to Lr17 and Lr39/Lr41 and was widely distributed throughout the United States. Phenotype TDBJG is virulent to Lr24 and was found in both the soft red winter wheat and hard red winter wheat regions. Phenotype TCRKG is virulent to Lr11, Lr18, and Lr26 and was found mostly in the soft red winter wheat region in the eastern United States. Virulence to Lr21 was found for the first time in North America in isolates collected from spring wheat cultivars in North Dakota and Minnesota.


Sign in / Sign up

Export Citation Format

Share Document