Shared Genetic Basis of Resistance to Bt Toxin Cry1Ac in Independent Strains of Pink Bollworm

2004 ◽  
Vol 97 (3) ◽  
pp. 721-726 ◽  
Author(s):  
Bruce E. Tabashnik ◽  
Yong-Biao Liu ◽  
Devika C. Unnithan ◽  
Yves Carrière ◽  
Timothy J. Dennehy ◽  
...  
2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jeffrey A. Fabrick ◽  
Dannialle M. LeRoy ◽  
Lolita G. Mathew ◽  
Yidong Wu ◽  
Gopalan C. Unnithan ◽  
...  

AbstractCrops genetically engineered to produce insecticidal proteins from Bacillus thuringiensis (Bt) have many benefits and are important globally for managing insect pests. However, the evolution of pest resistance to Bt crops reduces their benefits. Understanding the genetic basis of such resistance is needed to better monitor, manage, and counter pest resistance to Bt crops. Previous work shows that resistance to Bt toxin Cry2Ab is associated with mutations in the gene encoding the ATP-binding cassette protein ABCA2 in lab- and field-selected populations of the pink bollworm (Pectinophora gossypiella), one of the world’s most destructive pests of cotton. Here we used CRISPR/Cas9 gene editing to test the hypothesis that mutations in the pink bollworm gene encoding ABCA2 (PgABCA2) can cause resistance to Cry2Ab. Consistent with this hypothesis, introduction of disruptive mutations in PgABCA2 in a susceptible strain of pink bollworm increased the frequency of resistance to Cry2Ab and facilitated creation of a Cry2Ab-resistant strain. All Cry2Ab-resistant individuals tested in this study had disruptive mutations in PgABCA2. Overall, we found 17 different disruptive mutations in PgABCA2 gDNA and 26 in PgABCA2 cDNA, including novel mutations corresponding precisely to single-guide (sgRNA) sites used for CRISPR/Cas9. Together with previous results, these findings provide the first case of practical resistance to Cry2Ab where evidence identifies a specific gene in which disruptive mutations can cause resistance and are associated with resistance in field-selected populations.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Jeffrey A. Fabrick ◽  
Dannialle M. LeRoy ◽  
Gopalan C. Unnithan ◽  
Alex J. Yelich ◽  
Yves Carrière ◽  
...  
Keyword(s):  

Epilepsia ◽  
2021 ◽  
Author(s):  
Remi Stevelink ◽  
Jurjen J. Luykx ◽  
Bochao D. Lin ◽  
Costin Leu ◽  
Dennis Lal ◽  
...  

2015 ◽  
Vol 22 (2) ◽  
pp. 119-131 ◽  
Author(s):  
Haoran George Wang ◽  
Joseph Joel Jeffries ◽  
Tianren Frank Wang

Language and communication through it are two of the defining features of normally developed human beings. However, both these functions are often impaired in autism and schizophrenia. In the former disorder, the problem usually emerges in early childhood (~2 years old) and typically includes a lack of communication. In the latter condition, the language problems usually occur in adolescence and adulthood and presents as disorganized speech. What are the fundamental mechanisms underlying these two disorders? Is there a shared genetic basis? Are the traditional beliefs about them true? Are there any common strategies for their prevention and management? To answer these questions, we searched PubMed by using autism, schizophrenia, gene, and language abnormality as keywords, and we reconsidered the basic concepts about these two diseases or syndromes. We found many functional genes, for example, FOXP2, COMT, GABRB3, and DISC1, are actually implicated in both of them. After observing the symptoms, genetic correlates, and temporal progression of these two disorders as well as their relationships more carefully, we now infer that the occurrence of these two diseases is likely developmentally regulated via interaction between the genome and the environment. Furthermore, we propose a unified view of autism and schizophrenia: a single age-dependently occurred disease that is newly named as Systemic Integral Disorder: if occurring in children before age 2, it is called autism; if in adolescence or a later age, it is called schizophrenia.


2020 ◽  
Vol 40 (6) ◽  
pp. 586-599 ◽  
Author(s):  
Megan P. Leask ◽  
Nicholas A. Sumpter ◽  
Alexa S. Lupi ◽  
Ana I. Vazquez ◽  
Richard J. Reynolds ◽  
...  

SLEEP ◽  
2018 ◽  
Vol 41 (11) ◽  
Author(s):  
Maryam El Gewely ◽  
Mélanie Welman ◽  
Lan Xiong ◽  
Sophie Yin ◽  
Hélène Catoire ◽  
...  

2018 ◽  
Author(s):  
Devon E. Pearse ◽  
Nicola J. Barson ◽  
Torfinn Nome ◽  
Guangtu Gao ◽  
Matthew A. Campbell ◽  
...  

AbstractTraits with different fitness optima in males and females cause sexual conflict when they have a shared genetic basis. Heteromorphic sex chromosomes can resolve this conflict and protect sexually antagonistic polymorphisms but accumulate deleterious mutations. However, many taxa lack differentiated sex chromosomes, and how sexual conflict is resolved in these species is largely unknown. Here we present a chromosome-anchored genome assembly for rainbow trout (Oncorhynchus mykiss) and characterize a 56 Mb double-inversion supergene that mediates sex-specific migration through sex-dependent dominance, a mechanism that reduces sexual conflict. The double-inversion contains key photosensory, circadian rhythm, adiposity, and sexual differentiation genes and displays frequency clines associated with latitude and temperature, revealing environmental dependence. Our results constitute the first example of sex-dependent dominance across a large autosomal supergene, a novel mechanism for sexual conflict resolution capable of protecting polygenic sexually antagonistic variation while avoiding the homozygous lethality and deleterious mutation load of heteromorphic sex chromosomes.


2020 ◽  
Vol 116 (9) ◽  
pp. 1600-1619 ◽  
Author(s):  
Ali J Marian ◽  
Babken Asatryan ◽  
Xander H T Wehrens

Abstract Cardiac arrhythmias are common, often the first, and sometimes the life-threatening manifestations of hereditary cardiomyopathies. Pathogenic variants in several genes known to cause hereditary cardiac arrhythmias have also been identified in the sporadic cases and small families with cardiomyopathies. These findings suggest a shared genetic aetiology of a subset of hereditary cardiomyopathies and cardiac arrhythmias. The concept of a shared genetic aetiology is in accord with the complex and exquisite interplays that exist between the ion currents and cardiac mechanical function. However, neither the causal role of cardiac arrhythmias genes in cardiomyopathies is well established nor the causal role of cardiomyopathy genes in arrhythmias. On the contrary, secondary changes in ion currents, such as post-translational modifications, are common and contributors to the pathogenesis of arrhythmias in cardiomyopathies through altering biophysical and functional properties of the ion channels. Moreover, structural changes, such as cardiac hypertrophy, dilatation, and fibrosis provide a pro-arrhythmic substrate in hereditary cardiomyopathies. Genetic basis and molecular biology of cardiac arrhythmias in hereditary cardiomyopathies are discussed.


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