Assessing Potato Cultivar Sensitivity to Tuber Necrosis Caused by Tobacco rattle virus.

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.

Calcium is involved in the R Mc1 (blb)-mediated hypersensitive response against Meloidogyne chitwoodi in potato.

KEY MESSAGE: Functional characterization of the Columbia root-knot nematode resistance gene R Mc1 ( blb ) in potato revealed the R gene-mediated resistance is dependent on a hypersensitive response and involves calcium. The resistance (R) gene R Mc1(blb) confers resistance against the plant-parasitic nematode, Meloidogyne chitwoodi. Avirulent and virulent nematodes were used to functionally characterize the R Mc1(blb)-mediated resistance mechanism in potato (Solanum tuberosum). Histological observations indicated a hypersensitive response (HR) occurred during avirulent nematode infection. This was confirmed by quantifying reactive oxygen species activity in response to avirulent and virulent M. chitwoodi. To gain an insight into the signal transduction pathways mediating the R Mc1(blb)-induced HR, chemical inhibitors were utilized. Inhibiting Ca(2+) channels caused a significant reduction in electrolyte leakage, an indicator of cell death. Labeling with a Ca(2+)-sensitive dye revealed high Ca(2+) levels in the root cells surrounding avirulent nematodes. Furthermore, the calcium-dependent protein kinase (CDPK), StCDPK4 had a higher transcript level in R Mc1(blb) potato roots infected with avirulent nematodes in comparison to roots infected with virulent M. chitwoodi. The results of this study indicate Ca(2+) plays a role in the R Mc1(blb)-mediated resistance against M. chitwoodi in potato.

RNA Interference of Effector Gene Mc16D10L Confers Resistance Against Meloidogyne chitwoodi in Arabidopsis and Potato.

Meloidogyne chitwoodi, a quarantine pathogen, is a significant problem in potato-producing areas worldwide. In spite of considerable genetic diversity in wild potato species, no commercial potato cultivars with resistance to M. chitwoodi are available. Nematode effector genes are essential for the molecular interactions between root-knot nematodes and their hosts. Stable transgenic lines of Arabidopsis and potato (Solanum tuberosum) with resistance against M. chitwoodi were developed. RNA interference (RNAi) construct pART27(16D10i-2) was introduced into Arabidopsis thaliana and potato to express double-stranded RNA complementary to the putative M. chitwoodi effector gene Mc16D10L. Plant-mediated RNAi led to a significant level of resistance against M. chitwoodi in Arabidopsis and potato. In transgenic Arabidopsis lines, the number of M. chitwoodi egg masses and eggs was reduced by up to 57 and 67% compared with empty vector controls, respectively. Similarly, in stable transgenic lines of potato, the number of M. chitwoodi egg masses and eggs was reduced by up to 71 and 63% compared with empty vector controls, respectively. The relative transcript level of Mc16D10L was reduced by up to 76% in M. chitwoodi eggs and infective second-stage juveniles that developed on transgenic pART27(16D10i-2) potato, suggesting that the RNAi effect is systemic and heritable in M. chitwoodi.

5-Lipoxygenase-deficient mice infected with Borrelia burgdorferi develop persistent arthritis.

The enzyme 5-lipoxygenase (5-LO) catalyzes the conversion of arachidonic acid into the leukotrienes, which are critical regulators of inflammation and inflammatory diseases, such as asthma and arthritis. Although leukotrienes are present in the synovial fluid of Lyme disease patients, their role in the development of Lyme arthritis has not been determined. In the current study, we used a murine model of Lyme arthritis to investigate the role 5-LO products might have in the development of this inflammatory disease. After infection of Lyme arthritis-susceptible C3H/HeJ mice with Borrelia burgdorferi, mRNA expression of 5-LO and 5-LO-activating protein was induced in the joints, and the 5-LO product leukotriene B(4) was produced. Using C3H 5-LO-deficient mice, we demonstrated that 5-LO activity was not necessary for the induction of Lyme arthritis, but that its deficiency resulted in earlier joint swelling and an inability to resolve arthritis as demonstrated by sustained arthritis pathology through day 60 postinfection. Although production of anti-Borrelia IgG was decreased in 5-LO-deficient mice, bacterial clearance from the joints was unaffected. Phagocytosis of B. burgdorferi and efferocytosis of apoptotic neutrophils was defective in macrophages from 5-LO-deficient mice, and uptake of opsonized spirochetes by neutrophils was reduced. These results demonstrate that products of the 5-LO metabolic pathway are not required for the development of disease in all models of arthritis and that caution should be used when targeting 5-LO as therapy for inflammatory diseases.

Pigmented potato consumption alters oxidative stress and inflammatory damage in men.

Pigmented potatoes contain high concentrations of antioxidants, including phenolic acids, anthocyanins, and carotenoids. These bioactive compounds have been implicated in the inhibition or prevention of cellular oxidative damage and chronic disease susceptibility. We assessed the effects of pigmented potato consumption on oxidative stress and inflammation biomarkers in adult males. Free-living healthy men (18-40 y; n = 12/group) consumed 150 g of cooked white- (WP), yellow- (YP), or purple-flesh potatoes (PP) once per day for 6 wk in a randomized study. Blood was collected at baseline and wk 6 to analyze total antioxidant capacity (TAC), DNA damage as assessed by plasma 8-hydroxydeoxyguanosine (8-OHdG), protein oxidation, lipid peroxidation, C-reactive protein (CRP), inflammatory cytokines, lymphoproliferation, NK cytotoxicity, and phenotypes. Potatoes were analyzed for TAC, phenolic acids, anthocyanins, and carotenoids. Compared with the WP group, the YP group had higher concentrations of phenolic acids (P < 0.002) and carotenoids (P < 0.001), whereas the PP group had higher concentrations of phenolic acids (P < 0.002) and anthocyanins (P < 0.001). Men who consumed YP and PP tended to have lower (P < 0.08) plasma IL-6 compared with those consuming WP. The PP group tended to have a lower plasma CRP concentration than the WP group (P = 0.07). The 8-OHdG concentration was lower in men who consumed either YP or PP compared with WP. Pigmented potato consumption reduced inflammation and DNA damage in healthy adult males. This offers consumers an improved nutritional choice in potato consumption.

Resistance of potato germplasm to the potato tuberworm (Lepidoptera: Gelechiidae).

The evaluation of potato germplasm for resistance to potato tuberworm, Phthorimaea operculella (Zeller) (Lepidoptera: Gelechiidae), is a valuable component of integrated pest management; however, few attempts have been made to identify natural genetic tuber resistance to tuberworm on potato germplasm. The objective of this study was to screen potato germplasm with potential tuberworm resistance for tuber resistance under field and laboratory conditions. Experiments were conducted over a 2-yr period at the Hermiston Agricultural Research and Extension Center, Hermiston, OR. Of 125 germplasm that were tested in 2006, q13 were selected for further screening in 2007. These germplasm were: A0008-1TE, A97066LB, NY123, PA00N10-5, PA99N2, PA99N82, Paciencia, Q174-2, Russet Burbank, Rubi, Ranger Russet, Spunta G2, and T88-4. Tuber resistance of potato germplasm was determined based on the number of mines per tuber and the number of live larvae. Tubers of transgenic clone Spunta G2 were resistant to tuberworm damage. All other germplasm tested in this study, including Russet Burbank and Ranger Russet, were susceptible to tuberworm in the field and laboratory experiments. Incorporation of host plant resistance to tuber penetration by larvae together with appropriate cultural practices including limiting exposure time of tubers in the field may provide the best management option in the future.

Adenoviral delivery of interleukin-10 fails to attenuate experimental Lyme disease.

Production of interleukin-10 (IL-10) by C57BL/6 mice following infection with Borrelia burgdorferi has been proposed as a mechanism whereby resistance to the development of experimental Lyme arthritis is maintained. In the current study, we sought to determine the role of IL-10 during infection of arthritis- and carditis-susceptible C3H mice. Infection of C3H IL-10(-/-) mice led to increased joint swelling and arthritis severity scores over those of wild-type C3H mice. Measurement of B. burgdorferi numbers in joints or disseminated tissues indicated a more efficient clearance of spirochetes in the absence of IL-10, similar to that reported in C57BL/6 IL-10(-/-) mice. However, in contrast to previous in vitro work, infection of C3H IL-10(-/-) mice led to decreased in vivo expression of the cytokines KC, IL-1beta, IL-4, and IL-12p70 in the infected joints. Finally, adenoviral expression of IL-10 in the infected joints of C3H mice was unable to modulate the development of severe Lyme arthritis and had no effect on spirochete clearance or Borrelia-specific antibody production. Development of Lyme carditis appeared to be independent of modulation by IL-10. These results suggest that IL-10 limits the development of joint inflammation in both arthritis-resistant and -susceptible mouse strains infected with B. burgdorferi and that increased IL-10 production cannot rescue genetic susceptibility to development of pathology in this model.

Serum amyloid A-activating factor-1 (SAF-1) transgenic mice are prone to develop a severe form of inflammation-induced arthritis.

The transcription factor serum amyloid A-activating factor-1 (SAF-1) has been identified as a regulator of a number of cellular genes. To assess the pleiotropic role of SAF-1 in vivo, we generated SAF-1 transgenic mice, in which CMV immediate-early promoter was used to direct expression of the SAF-1 transgene in multiple organs. Our study shows that overexpression of SAF-1 predisposes animals to arthritis. Although SAF-1 transgenic mice do not spontaneously develop arthritis, they develop a severe form of arthritis when challenged with the Lyme disease agent Borrelia burgdorferi, which is known to promote arthritis development in both humans and mice. CMV-SAF-1 transgenic mice, upon B. burgdorferi infection, showed increased joint swelling and synovial inflammation compared with nontransgenic littermates. Immunohistochemical analysis of joint tissues collected 21 days after B. burgdorferi infection revealed colocalization of matrix metalloproteinase-1, a degradative enzyme that destroys type II collagen, a major architectural component of articular cartilage, and SAF-1 in both SAF-1 transgenic and nontransgenic mice. Further analysis by RNase protection assay and Western immunoblot demonstrated the presence of higher levels of matrix metalloproteinase-1 and SAF-1 in the inflamed joints of SAF-1 transgenic mice compared with their levels in nontransgenic mice. Consistent with these findings, reduced levels of proteoglycans were detected in the inflamed joint cartilage of transgenic mice, indicating damage to the cartilage structure. Together these results suggest a role of SAF-1 in the pathogenesis of inflammation-induced arthritis.