scholarly journals Genetic basis of resistance to the Vip3Aa Bt protein in Helicoverpa zea

2020 ◽  
Author(s):  
Fei Yang ◽  
José C Santiago González ◽  
Gregory A Sword ◽  
David L Kerns
Keyword(s):  
Helicoverpa Zea ◽  
Genetic Basis ◽  
Bt Protein

Extended evaluation of Bt protein cross‐pollination in seed blend plantings on survival, growth, and development of Helicoverpa zea feeding on refuge ears

2019 ◽  
Vol 76 (3) ◽  
pp. 1011-1019 ◽  
Author(s):  
Fei Yang ◽  
David L Kerns ◽  
Graham P Head ◽  
Paula A Price ◽  
Ronnie Levy ◽  
...  
Keyword(s):  
Growth And Development ◽  
Helicoverpa Zea ◽  
Cross Pollination ◽  
Bt Protein

scholarly journals Influence of Dual-Bt Protein Corn on Bollworm,Helicoverpa zea(Boddie), Survivorship on Bollgard II Cotton

2016 ◽  
Vol 109 (2) ◽  
pp. 860-864 ◽  
Author(s):  
M. B. Von Kanel ◽  
J. Gore ◽  
A. Catchot ◽  
D. Cook ◽  
F. Musser ◽  
...  
Keyword(s):  
Helicoverpa Zea ◽  
Bt Protein

scholarly journals Development, survival, and feeding behavior of Helicoverpa zea (Lepidoptera: Noctuidae) relative to Bt protein concentrations in corn ear tissues

PLoS ONE ◽  
2019 ◽  
Vol 14 (8) ◽  
pp. e0221343 ◽  
Author(s):  
Tom R. Bilbo ◽  
Francis P. F. Reay-Jones ◽  
Dominic D. Reisig ◽  
Jeremy K. Greene ◽  
Matthew W. Turnbull
Keyword(s):  
Feeding Behavior ◽  
Helicoverpa Zea ◽  
Bt Protein ◽  
Lepidoptera Noctuidae

Association of Insect-Derived Ear Injury With Yield and Aflatoxin of Maize Hybrids Varying in Bt Transgenes

2019 ◽  
Vol 48 (6) ◽  
pp. 1401-1411 ◽  
Author(s):  
Luke S Pruter ◽  
Michael J Brewer ◽  
Mark A Weaver ◽  
Seth C Murray ◽  
Thomas S Isakeit ◽  
...  
Keyword(s):  
Helicoverpa Zea ◽  
Fall Armyworm ◽  
Integrated Approach ◽  
Corn Earworm ◽  
Data Sets ◽  
Maize Production ◽  
Maize Hybrids ◽  
Corpus Christi ◽  
Bt Protein ◽  
Ear Injury

Abstract Environmental factors have been associated with the production of aflatoxin in maize, Zea mays L., and it is inconclusive whether transgenic, Bacillus thuringiensis (Bt), maize has an impact on aflatoxin accumulation. Maize hybrids differing in transgenes were planted in two locations from 2014 to 2017. Yield, aflatoxin, and ear injury caused by corn earworm, Helicoverpa zea (Boddie), and fall armyworm, Spodoptera frugiperda (J. E. Smith) (Lepidoptera: Noctuidae), were measured across three groups of hybrids differing in transgenes including near-isogenic hybrids, and water-stressed conditions. The hybrid groups consisted of non-Bt hybrids with no Bt transgenes, a second group with one or more Cry-Bt transgenes, and the third group with vegetative insecticidal Bt protein and Cry-Bt transgenes (Cry/Vip-Bt). Across the six data sets derived from 11 experiments, the Cry-Bt and Cry/Vip-Bt hybrids had less ear injury and aflatoxin on average than non-Bt hybrids. The effects of ear injury on yield and aflatoxin were more prominent and consistent in Corpus Christi, TX, where hybrids experienced more water-limited conditions than in College Station, TX. The trend of increased aflatoxin among hybrids with increased ear injury was further resolved when looking at Cry-Bt and Cry/Vip-Bt isogenic hybrids in Corpus Christi. The results supported that the maize hybrids with the inclusion of Cry-Bt and Cry/Vip-Bt transgenes warrant further investigation in an integrated approach to insect and aflatoxin management in sub-tropical rain-fed maize production regions. Research outcomes may be improved by focusing on areas prone to water-stress and by using hybrids with similar genetic backgrounds.

scholarly journals Novel genetic basis of resistance to Bt toxin Cry1Ac in Helicoverpa zea

2021 ◽  
Author(s):  
Kyle M Benowitz ◽  
Carson W Allan ◽  
Benjamin A Degain ◽  
Xianchun Li ◽  
Jeffrey A Fabrick ◽  
...  
Keyword(s):  
Helicoverpa Zea ◽  
Genetic Basis ◽  
Stop Codon ◽  
Premature Stop Codon ◽  
Pest Resistance ◽  
The United States ◽  
Chromosome 13 ◽  
Bt Toxin ◽  
Bt Toxins ◽  
A Genome

Crops genetically engineered to produce insecticidal proteins from the bacterium Bacillus thuringiensis (Bt) have advanced pest management, but their benefits are diminished when pests evolve resistance. Elucidating the genetic basis of pest resistance to Bt toxins can improve resistance monitoring, resistance management, and design of new insecticides. Here, we investigated the genetic basis of resistance to Bt toxin Cry1Ac in the lepidopteran Helicoverpa zea, one of the most damaging crop pests in the United States. To facilitate this research, we built the first chromosome-level genome assembly for this species. Using a genome-wide association study, fine-scale mapping, and RNA-seq, we identified a 250kb QTL on chromosome 13 that was strongly associated with resistance in a strain of H. zea that had been selected for resistance in the field and lab. This QTL contains no genes with a previously reported role in resistance or susceptibility to Bt toxins. However, within this QTL, we discovered a premature stop codon in a kinesin gene. We hypothesize that this mutation contributes to resistance. The results indicate the mutation on chromosome 13 was necessary but not sufficient for resistance, and therefore conclude that mutations in more than one gene contributed to resistance. Moreover, we found no changes in gene sequence or expression consistently associated with resistance for 11 genes previously implicated in lepidopteran resistance to Cry1Ac. Thus, the results reveal a novel and polygenic basis of resistance and extend the list of genes contributing to pest resistance to Bt toxins.

Molecular Basis and Clinical Aspects of Hereditary Megakaryocyte and Platelet Membrane Glycoprotein Disorders

1996 ◽  
Vol 16 (02) ◽  
pp. 114-138 ◽  
Author(s):  
R. E. Scharf
Keyword(s):  
Genetic Basis ◽  
Molecular Mechanisms ◽  
Molecular Genetic ◽  
Platelet Membrane ◽  
Clinical Aspects ◽  
Membrane Glycoprotein ◽  
Membrane Glycoproteins ◽  
Membrane Expression ◽  
Receptor Complexes ◽  
Platelet Membrane Glycoprotein

SummarySpecific membrane glycoproteins (GP) expressed by the megakaryocyte-platelet system, including GPIa-lla, GPIb-V-IX, GPIIb-llla, and GPIV are involved in mediat-ing platelet adhesion to the subendothelial matrix. Among these glycoproteins, GPIIb-llla plays a pivotal role since platelet aggregation is exclusively mediated by this receptor and its interaction with soluble macromolecular proteins. Inherited defects of the GPIIb-llla or GPIb-V-IX receptor complexes are associated with bleeding disorders, known as Glanzmann's thrombasthenia, Bernard-Soulier syndrome, or platelet-type von Willebrand's disease, respectively. Using immuno-chemical and molecular biology techniques, rapid advances in our understanding of the molecular genetic basis of these disorders have been made during the last few years. Moreover, analyses of patients with congenital platelet membrane glycoprotein abnormalities have provided valuable insights into molecular mechanisms that are required for structural and functional integrity, normal biosynthesis of the glycoprotein complexes and coordinated membrane expression of their constituents. The present article reviews the current state of knowledge of the major membrane glycoproteins in health and disease. The spectrum of clinical bleeding manifestations and established diagnostic criteria for each of these dis-orders are summarized. In particular, the variety of molecular defects that have been identified so far and their genetic basis will be discussed.

Anti-Myelin Oligodendrocyte Glycoprotein Encephalomyelitis and Extensive Longitudinal Transverse Myelitis Associated with Compound Heterozygous NLRP3 Missense Mutations in a Young Child

2020 ◽  
Author(s):  
Deirdre O'Sullivan ◽  
Michael Moore ◽  
Susan Byrne ◽  
Andreas O. Reiff ◽  
Susanna Felsenstein
Keyword(s):  
Young Child ◽  
Genetic Basis ◽  
Transverse Myelitis ◽  
Acute Disseminated Encephalomyelitis ◽  
Myelin Oligodendrocyte Glycoprotein ◽  
Compound Heterozygous ◽  
Missense Mutations ◽  
Childhood Onset

AbstractAcute disseminated encephalomyelitis in association with extensive longitudinal transverse myelitis is reported in a young child with positive anti-myelin oligodendrocyte glycoprotein (MOG) antibody with heterozygous NLRP3 missense mutations; p.(Arg488Lys) and p.(Ser159Ile). This case may well present an exceptional coincidence, but may describe a yet unrecognized feature of the spectrum of childhood onset cryopyrinopathies that contribute to the understanding of the genetic basis for anti-MOG antibody positive encephalomyelitis. Based on this observation, a larger scale study investigating the role of NLRP3 and other inflammasomes in this entity would provide important pathophysiological insights and potentially novel avenues for treatment.

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