A Model for Predicting Onset of Stagonospora nodorum Blotch in Winter Wheat Based on Preplanting and Weather Factors.

Stagonospora nodorum blotch (SNB) caused by Parastagonospora nodorum is a serious disease of wheat worldwide. In the United States, the disease is prevalent on winter wheat in many eastern states, and its management relies mainly on fungicide application after flag leaf emergence. Although SNB can occur prior to flag leaf emergence, the relationship between the time of disease onset and yield has not been determined. Such a relationship is useful in identifying a threshold to facilitate prediction of disease onset in the field. Disease occurred in 390 of 435 disease cases that were recorded across 11 counties in North Carolina from 2012 to 2014. Using cases with disease occurrence, the effect of disease onset on yield was analyzed to identify a disease onset threshold that related time of disease onset to yield. Regression analysis showed that disease onset explained 32% of the variation in yield (P < 0.0001) and from this relationship, day of year (DOY) 102 was identified as the disease onset threshold. Below-average yield occurred in 87% of the disease cases when disease onset occurred before DOY 102 but in only 28% of those cases when onset occurred on or after DOY 102. Subsequently, binary logistic regression models were developed to predict the occurrence and onset of SNB using preplanting factors and cumulative daily infection values (cDIV) starting 1 to 3 weeks prior to DOY 102. Logistic regression showed that previous crop, latitude, and cDIV accumulated 2 weeks prior to DOY 102 (cDIV.2) were significant (P < 0.0001) predictors of disease occurrence, and wheat residue, latitude, longitude, and cDIV.2 were significant (P < 0.0001) predictors of disease onset. The disease onset model had a correct classification rate of 0.94 and specificity and sensitivity rates >0.90. Performance of the disease onset model based on the area under the receiver operating characteristic curve (AUC), κ, and the true skill statistic (TSS) was excellent, with prediction accuracy values >0.88. Similarly, internal validation of the disease onset model based on AUC, κ, and TSS indicated good performance, with accuracy values >0.88. This disease onset prediction model could serve as a useful decision support tool to guide fungicide applications to manage SNB in wheat.

Quantifying the Effects of Wheat Residue on Severity of Stagonospora nodorum Blotch and Yield in Winter Wheat.

Stagonospora nodorum blotch (SNB), caused by the fungus Parastagonospora nodorum, is a major disease of wheat (Triticum aestivum). Residue from a previously infected wheat crop can be an important source of initial inoculum, but the effects of infected residue on disease severity and yield have not previously been quantified. Experiments were conducted in Raleigh and Salisbury, North Carolina, in 2012, 2013, and 2014 using the moderately susceptible winter wheat cultivar DG Shirley. In 2014, the highly susceptible cultivar DG 9012 was added to the experiment and the study was conducted at an additional site in Tyner, North Carolina. Four (2012) or six (2013 and 2014) wheat residue treatments were applied in the field in a randomized complete block design with five replicates. Treatments in 2012 were 0, 30, 60, and 90% residue coverage of the soil surface, while 10 and 20% residue treatments were added in 2013 and 2014. Across site-years, disease severity ranged from 0 to 50% and increased nonlinearly (P < 0.05) as residue level increased, with a rapid rise to an upper limit and showing little change in severity above 20 to 30% soil surface coverage. Residue coverage had a significant (P < 0.05) effect on disease severity in all site-years. The effect of residue coverage on yield was only significant (P < 0.05) for DG Shirley at Raleigh and Salisbury in 2012 and for DG 9012 at Salisbury in 2014. Similarly, residue coverage significantly (P < 0.05) affected thousand-kernel weight only of DG 9012 in 2014 at Raleigh and Salisbury. Our results showed that when wheat residue was sparse, small additions to residue density produced greater increases in SNB than when residue was abundant. SNB only led to effects on yield and test weight in the most disease-conducive environments, suggesting that the economic threshold for the disease may be higher than previously assumed and warrants review.

Novel necrotrophic effectors from Stagonospora nodorum and corresponding host sensitivities in winter wheat germplasm in the southeastern United States.

Stagonospora nodorum blotch (SNB), caused by the necrotrophic fungus Stagonospora nodorum (teleomorph: Phaeosphaeria nodorum), is among the most common diseases of winter wheat in the United States. New opportunities in resistance breeding have arisen from the recent discovery of several necrotrophic effectors (NEs, also known as host-selective toxins) produced by S. nodorum, along with their corresponding host sensitivity (Snn) genes. Thirty-nine isolates of S. nodorum collected from wheat debris or grain from seven states in the southeastern United States were used to investigate the production of NEs in the region. Twenty-nine cultivars with varying levels of resistance to SNB, representing 10 eastern-U.S. breeding programs, were infiltrated with culture filtrates from the S. nodorum isolates in a randomized complete block design. Three single-NE Pichia pastoris controls, two S. nodorum isolate controls, and six Snn-differential wheat controls were also used. Cultivar-isolate interactions were visually evaluated for sensitivity at 7 days after infiltration. Production of NEs was detected in isolates originating in each sampled state except Maryland. Of the 39 isolates, 17 produced NEs different from those previously characterized in the upper Great Plains region. These novel NEs likely correspond to unidentified Snn genes in Southeastern wheat cultivars, because NEs are thought to arise under selection pressure from genes for resistance to biotrophic pathogens of wheat cultivars that differ by geographic region. Only 3, 0, and 23% of the 39 isolates produced SnToxA, SnTox1, and SnTox3, respectively, by the culture-filtrate test. A Southern dot-blot test showed that 15, 74, and 39% of the isolates carried the genes for those NEs, respectively; those percentages were lower than those found previously in larger international samples. Only two cultivars appeared to contain known Snn genes, although half of the cultivars displayed sensitivity to culture filtrates containing unknown NEs. Effector sensitivity was more frequent in SNB-susceptible cultivars than in moderately resistant (MR) cultivars (P = 0.008), although some susceptible cultivars did not exhibit sensitivity to NEs produced by isolates in this study and some MR cultivars were sensitive to NEs of multiple isolates. Our results suggest that NE sensitivities influence but may not be the only determinant of cultivar resistance to S. nodorum. Specific knowledge of NE and Snn gene frequencies in this region can be used by wheat breeding programs to improve SNB resistance.

A Degree-Day Model for the Latent Period of Stagonospora nodorum Blotch in Winter Wheat.

Stagonospora nodorum blotch (SNB), which is caused by Stagonospora nodorum, occurs frequently in the southeastern United States, and severe epidemics can lead to substantial yield losses. To develop a model for the progress of SNB based on the effects of temperature on the latent period of the pathogen, batches of two winter wheat cultivars, AGS 2000 and USG 3209, were inoculated with S. nodorum at weekly intervals for 16 weeks. After 72 h of incubation, inoculated plants were exposed to outdoor conditions where temperatures ranged from -6.6 to 35.8°C, with a mean batch temperature ranging from 9.7 to 24.7°C. Latent period, expressed as time from inoculation until the first visible lesions with pycnidia, ranged from 13 to 34 days. The relationship between the inverse of the latent period and mean temperature was best described by a linear model, and the estimated thermal time required for the completion of the latent period was 384.6 degree-days. A shifted cumulative gamma distribution model with a base temperature of 0.5°C significantly (P < 0.0001) described the relationship between increasing number of lesions with pycnidia and accumulated thermal time. When latent period was defined as time to 50% of the maximum number of lesions with pycnidia (L50), the model estimated L50 as 336 and 326 degree-days above 0.5°C for AGS 2000 and USG 3209, respectively. The relationship between 1/L50 and mean temperature was also best described using a linear model (r2 = 0.93, P < 0.001). This study provides data that link disease progress with wheat growth, which facilitates accurate identification of thresholds for timing of fungicide applications.

Appearance of Powdery Mildew of Wheat Caused by Blumeria graminis f. sp. tritici on Pm17-Bearing Cultivars in North Carolina.

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.

Frequency of sexual recombination by Mycosphaerella graminicola in mild and severe epidemics.

The importance of sexual recombination in determining fungal population structure cannot be inferred solely from the relative abundance of sexual and asexual spores and reproductive structures. To complement a previously reported study of proportions of Mycosphaerella graminicola ascocarps and pycnidia, we investigated the share of sexual recombinants among isolates randomly derived from the same field at the same time. Early in three successive growing seasons (those ending in 1998, 1999, and 2000), field plots of the susceptible winter wheat cultivar Stephens were inoculated with suspensions of two M. graminicola isolates that each had rare alleles at restriction fragment length polymorphism (RFLP) loci. Near harvest time, leaves were randomly sampled from the same plots, and a population of over 100 monopycnidial isolates was created for each year of the experiment. Natural populations were also sampled from noninoculated plots in the 1999 and 2000 seasons, in order to compare allele frequencies. Based on RFLP haplotypes and DNA fingerprints, isolates from the inoculated plots were categorized by both inspection and Bayesian methods as inoculant clones, recombinants, or immigrants. Inoculation in the 2000 season was delayed, and the recovery rate of inoculant types was just 1 to 2%. In 1998, a high-disease year, and 1999, a low-disease year, inoculants comprised 36 and 22 to 23% of end-of-season samples, respectively. In those 2 years, recombinants as a percentage of inoculant descendants (both sexual and asexual) were 35 and 32%, respectively. By comparison, the study of fruiting bodies had found 93 and 32% of M. graminicola fruiting bodies were ascocarps in 1998 and 1999, respectively. These findings support the hypothesis that sexual recombination makes a relatively consistent contribution to M. graminicola population structure, despite differences in epidemic severity and ascocarp proportions.

Chromosomal location of Pm35, a novel Aegilops tauschii derived powdery mildew resistance gene introgressed into common wheat (Triticum aestivum L.).

A single gene controlling powdery mildew resistance was identified in the North Carolina germplasm line NC96BGTD3 (NCD3) using genetic analysis of F(2) derived lines from a NCD3 X Saluda cross. Microsatellite markers linked to this Pm gene were identified and their most likely order was Xcfd7, 10.3 cM, Xgdm43, 8.6 cM, Xcfd26, 11.9 cM, Pm gene. These markers and the Pm gene were assigned to chromosome 5DL by means of Chinese Spring Nullitetrasomic (Nulli5D-tetra5A) and ditelosomic (Dt5DL) lines. A detached leaf test showed a distinctive disease reaction to six pathogen isolates among the NCD3 Pm gene, Pm2 (5DS) and Pm34 (5DL). An allelism test showed independence between Pm34 and the NCD3 Pm gene. Together, the tests provided strong evidence for the presence of a novel Pm gene in NCD3, and this gene was designated Pm35.

Assessing client strengths: clinical assessment for client empowerment.

The proposition that client strengths are central to the helping relationship is simple enough and seems uncontroversial as an important component of practice. Yet deficit, disease, and dysfunction metaphors are deeply rooted in clinical social work, and the emphasis of assessment has continued to be diagnosing abnormal and pathological conditions. This article argues that assessment in clinical practice, among other things, is a political activity. Assessment that focuses on deficits provides obstacles to client exercise of personal and social power and reinforces those social structures that generate and regulate unequal power relationships that victimize clients. Clinical practice based on metaphors of client strengths is also political in that it is congruent with the potential for client empowerment. This article discusses the importance of a client strengths perspective for assessment and proposes 12 practice guidelines that foster a strengths perspective.