Potato mop-top virus and its protist vector, Spongospora subterranea, cause internal and external damage to potato tubers that make them unmarketable. Currently, there are no effective control methods to eliminate these soilborne and seedborne pathogens, so resistant germplasm is highly desired. A greenhouse assay was designed and validated to screen a large number of plants grown in both sandy soil and potting mix. High pathogen pressure was selected (20 sporosori/g of soil) to ensure successful inoculation, with an incubation time of 60 to 90 days. The successful use of conetainers was demonstrated to screen a large number of plants in limited greenhouse space. Thirteen susceptible commercial cultivars or breeding lines were screened in the greenhouse, with S. subterranea detected in 99.5% of the plants grown in both soil types. Potato mop-top virus was detected in 79.4% of the plants grown in 5-inch clay pots filled with sandy soil and 97.5% of the plants screened in conetainers filled with potting mix. The high pathogen levels detected in the 13 susceptible cultivars indicate that it is possible to assess potato germplasm resistance to S. subterranea and potato mop-top virus in the greenhouse. In the absence of a research field with consistently high pressure of S. subterranea and potato mop-top virus, this new greenhouse assay could rapidly identify germplasm with resistance to these two economically important pathogens year-round. Future identification of S. subterranea or potato mop-top virus-resistant germplasm will enable development of disease resistance markers that can help breeders rapidly identify resistant material. [Formula: see text] The author(s) have dedicated the work to the public domain under the Creative Commons CC0 “No Rights Reserved” license by waiving all of his or her rights to the work worldwide under copyright law, including all related and neighboring rights, to the extent allowed by law, 2025.
For many years, potato seed lots have been tested for economically important pathogens in order to restrict their spread. Despite this, some pathogens inevitably make it into commercial fields and require management. Although knowledge about pathogen prevalence in commercial seed lots has increased over the last decade, assessment of the tuber necrotic viruses, Tobacco rattle virus and Potato mop-top virus, has been lacking. For seven years, four tubers from each seed lot in the Washington State University Seed Lot Trial were assessed for these two viruses. Tobacco rattle virus levels were negligible, but 1.76 to 5.50% of seed lots were infected with Potato mop- top virus each year. Potato mop-top virus was found in seven seed growing regions and 23 cultivars. These results are concerning, as the rate of transmission from seed to daughter tubers is largely unknown, and fields across the region are infested with Spongospora subterranea, the vector of Potato mop-top virus.
Abstract Corky ringspot (CRS) is a widespread potato tuber necrotic disease caused by Tobacco rattle virus (TRV) infection. In the Pacific Northwest, this virus is transmitted by the stubby root nematode (SRN) within the genus Paratrichodorus. Remediating CRS affected fields is a major challenge that can be mitigated by growing plant varieties that are resistant to TRV infection. Growing alfalfa has been shown to reduce TRV levels in CRS infested fields over time but the development of a potato cultivar with these same capabilities would be of great economic benefit to potato growers. Castle Russet is a new potato clone that does not develop symptoms of CRS disease. To assess its ability to reduce soil virus load, Castle Russet, tobacco var. “Samsun NN”, alfalfa var. “Vernema”, and Russet Burbank potato were grown for a period of 1 to 3 months in soils containing viruliferous SRN populations at two different inoculation pressures (60 nematodes/pot and 1060 nematodes/pot) in greenhouse pot experiments. SRN population size and the presence of TRV were assessed over several months post inoculation. Results indicate that plant host and length of exposure significantly influence SRN population dynamics, whereas the TRV infection status of bait plants was significantly affected by both of these factors as well as inoculation pressure. These results suggest that both alfalfa var. “Vernema” and Castle Russet are resistant to TRV infection and may potentially be used to eliminate the virus from fields affected by CRS.
Tobacco rattle virus (TRV) causes the economically important corky ring spot disease in potato. Chemical control is difficult due to the soilborne nature of the TRV-transmitting nematode vector, and identifying natural host resistance against TRV is considered to be the optimal control measure. The present study investigated the sensitivity of 63 cultivars representing all market types (evaluated at North Dakota and Washington over 2 years) for the incidence of TRV-induced tuber necrosis and severity. This article also investigates the cultivar-location interaction (using a mixed-effects model) for TRV-induced necrosis. TRV-induced tuber necrosis (P < 0.0001) and severity (P < 0.0001) were significantly different among cultivars evaluated separately in North Dakota and Washington trials. Mixed-effects model results of pooled data (North Dakota and Washington) demonstrated that the interaction of cultivar and location had a significant effect (P = 0.03) on TRV-induced necrosis. Based on the virus-induced tuber necrosis data from both years and locations, cultivars were categorized into sensitive, moderately sensitive, insensitive, and moderately insensitive groups. Based on data from North Dakota, 10 cultivars, including Bintje, Centennial Russet, Ciklamen, Gala, Lelah, Oneida Gold, POR06V12-3, Rio Colorado, Russian Banana, and Superior, were rated as insensitive to TRV-induced tuber necrosis. Similar trials assessing TRV sensitivity among cultivars conducted in Washington resulted in a number of differences in sensitivity rankings compared with North Dakota trials. A substantial shift in sensitivity of some potato cultivars to TRV-induced tuber necrosis was observed between the two locations. Four cultivars (Centennial Russet, Oneida Gold, Russian Banana, and Superior) ranked as insensitive for North Dakota trials were ranked as sensitive for Washington trials. These results can assist the potato industry in making cultivar choices to reduce the economic impact of TRV-induced tuber necrosis.
Meloidogyne chitwoodi (Columbia root-knot nematode, CRKN) can cause serious damage in potato production systems, decreasing tuber value in the fresh market and processing industries. Genetic resistance to CRKN was first identified from the wild diploid potato species Solanum bulbocastanum accession SB22 and was successfully introgressed into tetraploid potato breeding material. To expand the base of genetic resistance, 40 plant accessions representing nine wild potato species were screened for their resistance to M. chitwoodi. Greenhouse screening identified fifteen clones from S. hougasii, one clone from S. bulbocastanum, and one clone from S. stenophyllidium with moderate to high levels of resistance against three isolates of M. chitwoodi. Geographical mapping showed that the resistance sources identified in this and previous studies primarily originated in the states of Jalisco and Michoacán in west-central Mexico. These new sources of resistance will be introgressed into elite potato populations to facilitate the development of potato cultivars with durable resistance to M. chitwoodi.
The diversity of traits in varieties of potato outside of its South American birthplace is a small subset of that available in the Andean center of origin. Among the traits that evoke most interest are skin and flesh pigments. Recent studies have pointed to the high antioxidant activity and potential healthful benefits from these pigments or other antioxidant compounds. The market for potatoes with unusual color patterns has been supplied largely by heirloom varieties of uncertain origin and the highly successful Yukon Gold. Interest has intensified and been transformed into a focused effort in the breeding of specialty varieties, remarkable for their unusual colors. The purpose of this paper is to describe a new potato variety in the Fingerling Class with red skin and red flesh.
Black dot is caused by the fungus Colletotrichum coccodes (Wallr.) S.J. Hughes. The disease is prevalent in potato fields and can be of economic concern by itself, or as a part of the potato early dying syndrome. Little is known about resistance to this disease. In the present study resistance to potato black dot was tested in Solanum tuberosum Group Andigena. Forty accessions were chosen randomly from the core collection and screened. The accessions originated from Peru, Mexico, Bolivia, Columbia, Ecuador, Argentina and Costa Rica. Five accessions had less (P ≤ 0.05) disease on roots and stems than a set of commercial standards. These accessions were: PIs 189473, 230475, 161683, 243367 and 230470. They were retested to validate their partial resistance. Fifteen plants, each a unique genotype, were selected from each accession and were propagated into multiple clones that were inoculated with the pathogen. Three genotypes were identified with less (P < 0.05) disease on roots and stems than the industry standard. These genotypes originated from the accessions PI-243367 and PI-230475. Clones of the resistant genotypes were added to the potato germplasm collection located at the Potato Improvement Laboratory of the USDA-ARS near Prosser, WA, to be used in the development of black dot resistant commercial varieties.
Black dot is caused by the fungus (Wallr.) S.J. Hughes. The disease is prevalent in potato fields and can be of economic concern by itself, or as a part of the potato early dying syndrome. Little is known about resistance to this disease. In the present study resistance to potato black dot was tested in Group . Forty accessions were chosen randomly from the core collection and screened. The accessions originated from Peru, Mexico, Bolivia, Columbia, Ecuador, Argentina and Costa Rica. Five accessions had less ( ≤ 0.05) disease on roots and stems than a set of commercial standards. These accessions were: PIs 189473, 230475, 161683, 243367 and 230470. They were retested to validate their partial resistance. Fifteen plants, each a unique genotype, were selected from each accession and were propagated into multiple clones that were inoculated with the pathogen. Three genotypes were identified with less ( < 0.05) disease on roots and stems than the industry standard. These genotypes originated from the accessions PI-243367 and PI-230475. Clones of the resistant genotypes were added to the potato germplasm collection located at the Potato Improvement Laboratory of the USDA-ARS near Prosser, WA, to be used in the development of black dot resistant commercial varieties. La mancha negra es producida por el hongo (Wallr.) S.J. Hughes. La enfermedad es prevalente en los campos de papa y puede ser de importancia económica de por sí, o es parte del síndrome de muerte temprana de la papa. Se sabe poco respecto de la resistencia a esta enfermedad. En el presente estudio se probó la resistencia a la mancha negra de la papa en grupo . Se seleccionaron y evaluaron cuarenta accesiones al azar de la colección principal. Las accesiones fueron originarias de Perú, México, Bolivia, Colombia, Ecuador, Argentina y Costa Rica. Cinco accesiones tuvieron menos enfermedad (P ≤ 0.05) en raíces y tallos que un juego de estándares comerciales. Estas accesiones fueron: PIs 189473, 230475, 161683, 243367 y 230470. Se volvieron a probar para validar su resistencia parcial. Quince plantas, cada una de un genotipo único, se seleccionaron de cada accesión y se propagaron en múltiples clones que se inocularon con el patógeno. Se identificaron tres genotipos con menos enfermedad (P ≤ 0.05) en raíces y tallos que los estándares de la industria. Estos genotipos se originaron de las accesiones Pl-243367 y Pl230475. Los clones de los genotipos resistentes se agregaron a la colección de germoplasma de papa ubicada en el Laboratorio de Mejoramiento de Papa del USDA-ARS cerca de Prosser, WA, para usarse en el desarrollo de variedades comerciales resistentes a la mancha negra.
Potato (Solanum tuberosum) selections (clones and commercial cultivars) were examined for resistance to root galling, caused by the powdery scab pathogen Spongospora subterranea f. sp. subterranea in seven field trials conducted between 2003 and 2007 in the states of Washington and Idaho. Four industry reference cultivars—Shepody, Russet Burbank, Russet Ranger, and Umatilla Russet—were used as susceptible standards. Every year, selections less susceptible than the standards were considered resistant and progressed to the next season. Selections that did not demonstrate resistance in at least two consecutive trials were discarded. Eight potato selections were more resistant to root galling than the susceptible standards in two or more trials: PA98NM38-1 was more resistant than the susceptible standards in 5 of 5 trials, PO94A009-10 in 4 of 5 trials, PA95B2-4 and PA98N5-2 in 3 of 5 trials, POR00HG5-1 in 2 of 5 trials, PO94A009-7 in 3 of 4 trials, PO94A012-2 in 2 of 3 trials, and Summit Russet in 2 of 2 trials. POR00HG5-1 has Solanum hougasii in its ancestry, while the other selections have the Mexican wild species Solanum bulbocastanum and the commercial cultivar Summit Russet appearing in their ancestry. Summit Russet is the most plausible source of resistance.
A variety of transcriptional and post-transcriptional mechanisms regulate the expression of the inducible nitric-oxide synthase (iNOS, or NOS2). Although neurons and endothelial cells express proteins that interact with and inhibit neuronal NOS and endothelial NOS, macrophage proteins that inhibit NOS2 have not been identified. We show that murine macrophages express a 110-kDa protein that interacts with NOS2, which we call NOS-associated protein-110 kDa (NAP110). NAP110 directly interacts with the amino terminus of NOS2, and inhibits NOS catalytic activity by preventing formation of NOS2 homodimers. Expression of NAP110 may be a mechanism by which macrophages expressing NOS2 protect themselves from cytotoxic levels of nitric oxide.
Although nitric oxide (NO) kills or inhibits the replication of a variety of intracellular pathogens, the antimicrobial mechanisms of NO are unknown. Here, we identify a viral protease as a target of NO. The life cycle of many viruses depends upon viral proteases that cleave viral polyproteins into individual polypeptides. NO inactivates the Coxsackievirus protease 3C, an enzyme necessary for the replication of Coxsackievirus. NO S-nitrosylates the cysteine residue in the active site of protease 3C, inhibiting protease activity and interrupting the viral life cycle. Substituting a serine residue for the active site cysteine renders protease 3C resistant to NO inhibition. Since cysteine proteases are critical for virulence or replication of many viruses, bacteria, and parasites, S-nitrosylation of pathogen cysteine proteases may be a general mechanism of antimicrobial host defenses.
Nitric oxide (NO) acts as a neurotransmitter. However, excess NO produced from neuronal NO synthase (nNOS) or inducible NOS (iNOS) during inflammation of the central nervous system can be neurotoxic, disrupting neurotransmitter and hormone production and killing neurons. A screen of a hippocampal cDNA library showed that a unique region of the iNOS protein interacts with Kalirin, previously identified as an interactor with a secretory granule peptide biosynthetic enzyme. Kalirin associates with iNOS in vitroand in vivo and inhibits iNOS activity by preventing the formation of iNOS homodimers. Expression of exogenous Kalirin in pituitary cells dramatically reduces iNOS inhibition of ACTH secretion. Thus Kalirin may play a neuroprotective role during inflammation of the central nervous system by inhibiting iNOS activity.