High expression of Cyp6g1, a cytochrome P450 gene, does not necessarily confer DDT resistance in Drosophila melanogaster

Kuruganti, Srilalitha; Lam, Vita; Zhou, Xuguo; Bennett, Gary W.; Pittendrigh, Barry R.; Ganguly, Ranjan

doi:10.1016/j.gene.2006.09.019

Cited by 33 publications

(37 citation statements)

References 28 publications

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“…Similarly, two laboratory strains of D. melanogaster, Canton-SH and Hikone-RH, were found to be DDT-susceptible although they carry the Accord insertion allele of CYP6G1 and exhibit high CYP6G1 expression (Festucci-Buselli et al, 2005;Kuruganti et al, 2007). The susceptible phenotype of Canton-SH and Hikone-RH strains is not due to mutation that may inactivate the CYP6G1 protein (Kuruganti et al, 2007).…”

Section: Introductionmentioning

confidence: 98%

“…Examination of natural populations of D. melanogaster or D. simulans collected from California and Africa revealed that some populations showing Accord-or Doc-mediated overexpression of CYP6G1 were DDTsusceptible (Schlenke and Begun, 2004). Similarly, two laboratory strains of D. melanogaster, Canton-SH and Hikone-RH, were found to be DDT-susceptible although they carry the Accord insertion allele of CYP6G1 and exhibit high CYP6G1 expression (Festucci-Buselli et al, 2005;Kuruganti et al, 2007). The susceptible phenotype of Canton-SH and Hikone-RH strains is not due to mutation that may inactivate the CYP6G1 protein (Kuruganti et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

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Accord insertion in the 5′ flanking region of CYP6G1 confers nicotine resistance in Drosophila melanogaster

Li¹,

Bai²,

Cass³

2012

Gene

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Section: Introductionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

Accord insertion in the 5′ flanking region of CYP6G1 confers nicotine resistance in Drosophila melanogaster

Li¹,

Bai²,

Cass³

2012

Gene

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“…This technique showed that DDT-R was associated with a region containing two cytochrome P450-encoding genes (Cyp6g1 and Cyp6g2), one of which (Cyp6g1) was overtranscribed in resistant flies (Daborn et al 2002). However, despite the broad cross-resistance associated with the DDT-R locus in a number of strains from a range of sources (Daborn et al 2001(Daborn et al , 2002, many investigators have pressured different fly lines in the laboratory, producing strains showing a range of different polygenic resistance mechanisms (Crow 1954;Maitra et al 1996;Brandt et al 2002;Festucci-Buselli et al 2005;Kuruganti et al 2007). This difference between the results of selection in the field vs. selection in the laboratory was clarified by further selection experiments in the laboratory and their analysis with a micro-array containing all of the known P450 genes from Drosophila; this showed that different laboratory selection regimes could indeed select for different P450s (LeGoff et al 2003).…”

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confidence: 99%

The Molecular Genetics of Insecticide Resistance

2013

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The past 60 years have seen a revolution in our understanding of the molecular genetics of insecticide resistance. While at first the field was split by arguments about the relative importance of mono-vs. polygenic resistance and field-vs. laboratory-based selection, the application of molecular cloning to insecticide targets and to the metabolic enzymes that degrade insecticides before they reach those targets has brought out an exponential growth in our understanding of the mutations involved. Molecular analysis has confirmed the relative importance of single major genes in target-site resistance and has also revealed some interesting surprises about the multi-gene families, such as cytochrome P450s, involved in metabolic resistance. Identification of the mutations involved in resistance has also led to parallel advances in our understanding of the enzymes and receptors involved, often with implications for the role of these receptors in humans. This Review seeks to provide an historical perspective on the impact of molecular biology on our understanding of resistance and to begin to look forward to the likely impact of rapid advances in both sequencing and genome-wide association analysis."Curiouser and curiouser!" cried Alice.Lewis Carroll L ewis Carroll sent Alice down a rabbit hole without the least idea of what was to happen next, but as Alice ventured deeper into Wonderland things became "Curiouser and curiouser!" So indeed have studies on the molecular basis of insecticide resistance. While starting with rather simplistic expectations about the role of single mutations in single genes, resistance has been shown to involve a panoply of multiple mutations in multiple genes, often with independent and complex origins. This review will attempt to place these current findings into context and to examine the extent to which the field has often been historically blindsided by dogma. My arguments will encompass key controversies debated in the field such as the relative importance of mono-vs. polygenic resistance and the implications of resistance-associated mutations for whole-organism fitness in the absence of pesticide. Importantly, we will also examine the role of dogma in shaping the way that resistance research has been pursued over the past 50 years. Key questions addressed are therefore: How many mutations per gene cause resistance? How many mechanisms are there per species (genome)? How many independent genetic origins (mutations) give rise to each mechanism? What new mechanisms are still undiscovered and how might they arise? Monogenic vs. Polygenic ResistanceCrow, DDT, and DrosophilaThe humble fruit fly Drosophila melanogaster has been a key tool in unlocking the molecular basis of insecticide resistance, and early studies by James Crow and others have helped to establish Drosophila as a genetic model for resistance studies. Studies of DDT resistance in Drosophila have also typified arguments surrounding mono-vs. polygenic inheritance of insecticide resistance. In his pioneering review of in...

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“…Which if any of these systems represent pathways or mechanisms by which grafts acquire resistance to injury in accommodation is unknown. For example, treatment of drosophila with DDT induces production of cytochrome P450 and possibly other genes that confer resistance to further exposure to this toxic substance [67], although other genes must be involved [68]. Exposure of organs to ischemia "preconditions" organs to resist injury by subsequent episodes of ischemia.…”

Section: Toward a Broader Concept Of Accommodationmentioning

confidence: 99%

Accommodation of grafts: Implications for health and disease

Tang

Platt

2007

Human Immunology

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Accommodation refers to the acquired resistance of a graft to immune-mediated injury. It is typically observed after antibodies that would cause rejection of a graft are removed from a recipient and then return. Besides being a condition so induced, accommodation can occur spontaneously, without the depleting of antibodies. Indeed, we postulate that spontaneous accommodation may be the most common outcome of clinical organ transplantation. This communication will review the current understanding of accommodation, emphasizing recent advances and important questions. Among the recent advances are the discoveries of potentially broader relevance of accommodation for biology and immunology and pathways by which accommodation may be achieved. To investigate these pathways and to understand how accommodation begins and how it evolves, clinical organ transplants might offer a useful and incisive model.

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High expression of Cyp6g1, a cytochrome P450 gene, does not necessarily confer DDT resistance in Drosophila melanogaster

Cited by 33 publications

References 28 publications

Accord insertion in the 5′ flanking region of CYP6G1 confers nicotine resistance in Drosophila melanogaster

Accord insertion in the 5′ flanking region of CYP6G1 confers nicotine resistance in Drosophila melanogaster

The Molecular Genetics of Insecticide Resistance

Accommodation of grafts: Implications for health and disease

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