Loci Controlling Resistance to High Plains Virus and Wheat Streak Mosaic Virus in a B73 × Mo17 Population of Maize

High Plains disease has the potential to cause significant yield loss in susceptible corn (Zea mays L.) and wheat (Triticum aestivum L.) genotypes, especially in the central and western USA. The primary causal agent, High Plains virus (HPV), is vectored by wheat curl mite (WCM; Aceria tossicheila Keifer), which is also the vector of wheat streak mosaic virus (WSMV). In general, the two diseases occur together as a mixed infection in the field. The objective of this research was to characterize the inheritance of HPV and WSMV resistance using B73 (resistant to HPV and WSMV) × Mo17 (moderately susceptible to HPV and WSMV) recombinant inbred lines. A population of 129 recombinant inbred lines scored for 167 molecular markers was used to evaluate resistance to WSMV and to a mixed infection of WSMV and HPV. Loci conferring resistance to systemic movement of WSMV in plants mapped to chromosomes 3, 6, and 10, consistent with the map position of wsm2, wsm1, and wsm3, respectively. Major genes for resistance to systemic spread of HPV in doubly infected plants mapped to chromosomes 3 and 6, coincident or tightly linked with the WSMV resistance loci. Analysis of doubly infected plants revealed that chromosome 6 had a major effect on HPV resistance, consistent with our previous analysis of B73 × W64A and B73 × Wf9 populations. Quantitative trait loci (QTL) affecting resistance to localized symptom development mapped to chromosomes 4 (umc66), 5 (bnl5.40), and 6 (umc85), and accounted for 24% of the phenotypic variation. Localized symptoms may reflect the amount of mite feeding or the extent of virus spread at the point of infection. Identification of cosegregating markers may facilitate selection for HPV and WSMV resistance in corn breeding programs

Identification of a Novel Aminopeptidase P-Like Gene (OnAPP) Possibly Involved in Bt Toxicity and Resistance in a Major Corn Pest (Ostrinia nubilalis)

Studies to understand the Bacillus thuringiensis (Bt) resistance mechanism in European corn borer (ECB, Ostrinia nubilalis) suggest that resistance may be due to changes in the midgut-specific Bt toxin receptor. In this study, we identified 10 aminopeptidase-like genes, which have previously been identified as putative Bt toxin receptors in other insects and examined their expression in relation to Cry1Ab toxicity and resistance. Expression analysis for the 10 aminopeptidase-like genes revealed that most of these genes were expressed predominantly in the larval midgut, but there was no difference in the expression of these genes in Cry1Ab resistant and susceptible strains. This suggested that altered expression of these genes was unlikely to be responsible for resistance in these ECB strains. However, we found that there were changes in two amino acid residues of the aminopeptidase-P like gene (OnAPP) involving Glu305 to Lys305 and Arg307 to Leu307 in the two Cry1Ab-resistant strains as compared with three Cry1Ab-susceptible strains. The mature OnAPP contains 682 amino acid residues and has a putative signal peptide at the N-terminus, a predicted glycosylphosphatidyl-inositol (GPI)-anchor signal at the C-terminal, three predicted N-glycosylation sites at residues N178, N278 and N417, and an O-glycosylation site at residue T653. We used a feeding based-RNA interference assay to examine the role of the OnAPP gene in Cry1Ab toxicity and resistance. Bioassays of Cry1Ab in larvae fed diet containing OnAPP dsRNA resulted in a 38% reduction in the transcript level of OnAPP and a 25% reduction in the susceptibility to Cry1Ab as compared with larvae fed GFP dsRNA or water. These results strongly suggest that the OnAPP gene could be involved in binding the Cry1Ab toxin in the ECB larval midgut and that mutations in this gene may be associated with Bt resistance in these two ECB strains

The Present and Future Role of Insect-Resistant Genetically Modified Maize in IPM

Commercial, genetically-modified (GM) maize was first planted in the United States (USA, 1996) and Canada (1997) but now is grown in 13 countries on a total of over 35 million hectares (\u3e24% of area worldwide). The first GM maize plants produced a Cry protein derived from the soil bacteriumBacillus thuringiensis (Bt), which made them resistant to European corn borer and other lepidopteran maize pests. New GM maize hybrids not only have resistance to lepidopteran pests but some have resistance to coleopteran pests and tolerance to specific herbicides. Growers are attracted to the Btmaize hybrids for their convenience and because of yield protection, reduced need for chemical insecticides, and improved grain quality. Yet, most growers worldwide still rely on traditional integrated pest management (IPM) methods to control maize pests. They must weigh the appeal of buying insect protection “in the bag” against questions regarding economics, environmental safety, and insect resistance management (IRM). Traditional management of maize insects and the opportunities and challenges presented by GM maize are considered as they relate to current and future insect-resistant products. Four countries, two that currently have commercialize Bt maize (USA and Spain) and two that do not (China and Kenya), are highlighted. As with other insect management tactics (e.g., insecticide use or tillage), GM maize should not be considered inherently compatible or incompatible with IPM. Rather, the effect of GM insect-resistance on maize IPM likely depends on how the technology is developed and used

Genetic Variability Among Maize Inbred Lines for Resistance to the High Plains Virus–Wheat Streak Mosaic Virus Complex

High plains virus (HPV) is a pathogen that causes a severe disease, especially in susceptible corn genotypes. The virus is transmitted by the eriophyid mite Aceria tosichella, which also transmits wheat streak mosaic virus (WSMV). This often results in a mixed infection by these two viruses. Genetic variability for resistance to the HPV exists among maize inbred lines but has not been characterized. The disease reaction of 30 maize inbred lines to the mixed infection and to WSMV alone was characterized in this study. Evaluation was based on symptom expression and virus titer (HPV and WSMV), as measured by enzyme-linked immunosorbent assay. All lines showed some HPV symptoms, which ranged from a few visible spots to rapid plant death. HPV-resistant inbreds include B73 and B14. Susceptible inbreds include W64A, Wf9, H100, N213, N215, and N194. Five of the six inbreds most severely affected by HPV also had a high WSMV titer, although they displayed few symptoms when inoculated with WSMV alone. Inbred N194 was one of the genotypes most susceptible to HPV, but it showed no detectable WSMV titer. Seedlings of highly susceptible genotypes often died within 2 weeks of infection

Loci Controlling Resistance to High Plains Virus and Wheat Streak Mosaic Virus in a B73 × Mo17 Population of Maize

High Plains disease has the potential to cause significant yield loss in susceptible corn (Zea mays L.) and wheat (Triticum aestivum L.) genotypes, especially in the central and western USA. The primary causal agent, High Plains virus (HPV), is vectored by wheat curl mite (WCM; Aceria tossicheila Keifer), which is also the vector of wheat streak mosaic virus (WSMV). In general, the two diseases occur together as a mixed infection in the field. The objective of this research was to characterize the inheritance of HPV and WSMV resistance using B73 (resistant to HPV and WSMV) × Mo17 (moderately susceptible to HPV and WSMV) recombinant inbred lines. A population of 129 recombinant inbred lines scored for 167 molecular markers was used to evaluate resistance to WSMV and to a mixed infection of WSMV and HPV. Loci conferring resistance to systemic movement of WSMV in plants mapped to chromosomes 3, 6, and 10, consistent with the map position of wsm2, wsm1, and wsm3, respectively. Major genes for resistance to systemic spread of HPV in doubly infected plants mapped to chromosomes 3 and 6, coincident or tightly linked with the WSMV resistance loci. Analysis of doubly infected plants revealed that chromosome 6 had a major effect on HPV resistance, consistent with our previous analysis of B73 × W64A and B73 × Wf9 populations. Quantitative trait loci (QTL) affecting resistance to localized symptom development mapped to chromosomes 4 (umc66), 5 (bnl5.40), and 6 (umc85), and accounted for 24% of the phenotypic variation. Localized symptoms may reflect the amount of mite feeding or the extent of virus spread at the point of infection. Identification of cosegregating markers may facilitate selection for HPV and WSMV resistance in corn breeding programs

Impact of Transesophageal Electrophysiologic Study to Elucidate the Mechanism of Arrhythmia on Children With Supraventricular Tachycardia and No Preexcitation

International audienceAn electrophysiologic study (EPS) of children and teenagers with paroxysmal supraventricular tachycardia (SVT) and normal electrocardiography (ECG) in sinus rhythm was evaluated. Generally, EPS is performed only before paroxysmal SVT ablation in these patients. In this study, 140 patients (mean age, 15 ± 3 years) with normal ECG in sinus rhythm were studied for SVT by a transesophageal route in baseline state and after isoproterenol. Idiopathic left or right ventricular tachycardia was diagnosed in four patients (3 %). Anterograde conduction over an atrioventricular (AV) left lateral (n = 10) or septal (n = 9) accessory pathway (AP) was noted in 19 patients (13.5 %) at atrial pacing. Orthodromic AV reentrant tachycardia (AVRT) was induced in these children. Five of the patients had a high rate conducted over AP (>240 bpm in baseline state or >290 bpm after isoproterenol). Two of the patients (a 10-year-old girl with well-tolerated SVT and a 17-year-old with syncope-related SVT) had the criteria for a malignant form with the induction of atrial fibrillation conducted over AP at a rate exceeding 290 bpm in baseline state. Of the 140 patients, 74 (53 %) had typical AV node reentrant tachycardia (AVNRT), nine had atypical AVNRT (6 %), 1 had atrial tachycardia (0.7 %), and 33 (23.5 %) had AVRT related to a concealed AP with only retrograde conduction. Electrophysiologic study is recommended for children with paroxysmal SVT and normal ECG in sinus rhythm. The data are helpful for guiding the treatment. Ventricular tachycardia or atrial tachycardia can be misdiagnosed. Masked preexcitation syndrome with anterograde conduction through AP was present in 13.5 % of the patients, and 1.4 % had a malignant preexcitation syndrome