The mechanisms underlying α-amanitin resistance in Drosophila melanogaster: a microarray analysis.
The rapid evolution of toxin resistance in animals has important consequences for the ecology of species and our economy. Pesticide resistance in insects has been a subject of intensive study; however, very little is known about how Drosophila species became resistant to natural toxins with ecological relevance, such as α-amanitin that is produced in deadly poisonous mushrooms. Here we performed a microarray study to elucidate the genes, chromosomal loci, molecular functions, biological processes, and cellular components that contribute to the α-amanitin resistance phenotype in Drosophila melanogaster. We suggest that toxin entry blockage through the cuticle, phase I and II detoxification, sequestration in lipid particles, and proteolytic cleavage of α-amanitin contribute in concert to this quantitative trait. We speculate that the resistance to mushroom toxins in D. melanogaster and perhaps in mycophagous Drosophila species has evolved as cross-resistance to pesticides, other xenobiotic substances, or environmental stress factors.
Department of Biological Sciences, Michigan Technological University, Houghton, Michigan, United States of America.
Chelsea L
CL
Mitchell
Department of Zoology, University of Wisconsin-Madison, Madison, Wisconsin, United States of America.
Michael C
MC
Saul
School of Forest Resources and Environmental Science, Michigan Technological University, Houghton, Michigan, United States of America.
Liang
L
Lei
School of Forest Resources and Environmental Science, Michigan Technological University, Houghton, Michigan, United States of America.
Hairong
H
Wei
Department of Biological Sciences, Michigan Technological University, Houghton, Michigan, United States of America.
Thomas
T
Werner
D053959:Alpha-Amanitin / Q000633:toxicity*; D000818:Animals; D001669:Biochemical Phenomena / Q000235:genetics; D005075:Biological Evolution; D004331:Drosophila melanogaster / Q000235:genetics*; D004351:Drug Resistance / Q000235:genetics*; D008055:Lipids / Q000235:genetics; D050216:Metabolic Detoxication, Phase I / Q000235:genetics; D050217:Metabolic Detoxication, Phase II / Q000235:genetics; D046228:Microarray Analysis / Q000379:methods; D010641:Phenotype
D053959:Alpha-Amanitin; D008055:Lipids