Variation in mitochondria-derived transcript levels associated with DDT resistance in the 91-R strain of Drosophila melanogaster (Diptera: Drosophilidae)

Authors: STEELE, LAURA - Michigan State University; Coates, Brad; SEONG, KEON MOOK - University Of Illinois; VALERO, CARMEN - University Of Illinois; MITTAPALLI, OMPRAKASH - Omics Services Inc; CLARK, JOHN - University Of Massachusetts; PITTENDRIGH, BARRY - Michigan State University

Submitted to: Insect Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 9/25/2018
Publication Date: 11/1/2018
Citation: Steele, L.D., Coates, B.S., Seong, K., Valero, C.M., Mittapalli, O., Clark, J.M., Pittendrigh, B.R. 2018. Variation in mitochondria-derived transcript levels associated with DDT resistance in the 91-R strain of Drosophila melanogaster (Diptera: Drosophilidae). Insect Science. 18(6). https://doi.org/10.1093/jisesa/iey101.
DOI: https://doi.org/10.1093/jisesa/iey101

Interpretive Summary: Adaptations by insect populations that allow survival when exposed to chemical insecticides is a major threat to sustainable agriculture practices worldwide. Regardless of this threat, the mechanisms by which insects adapt to agricultural practices remain poorly understood. An ARS researcher in conjunction with university collaborators used a genomics approach to investigate the changes in genes within mitochondrial pathways associated with Dichlorodiphenyltrichloroethane (DDT) resistance in the fruit fly. This model system provides advantages for studying the evolution of insecticide resistance on a genome-wide scale, which can be transferred to analogous resistance traits among crop pest species. Fixed changes in the level of gene expression were shown for those involved in energy production, detoxification within the mitochondrion, and that regulate cell viability (programmed cell death). These results show that exposure to insecticides can result in the selection of genes encoding proteins destined for or impacting the function of the mitochondria. These findings are pertinent university, government, and private sector scientists interested in understanding the mechanisms by which chemical insecticide resistance can develop within insect populations.

Technical Abstract: The organochloride insecticide dichlorodiphenyltrichloroethane (DDT) and its metabolites can increase cellular levels of reactive oxygen species (ROS), cause mitochondrial dysfunction, and induce apoptosis. The highly DDT-resistant Drosophila melanogaster strain, 91-R, and its susceptible control, 91-C, were used to investigate functional and structural changes among mitochondrial-derived pathways. Re-sequencing of mitochondrial genomes (mitogenomes) detected no structural differences between the 91-R and 91-C, whereas RNA-seq suggested the differential expression of 220 mitochondrial genes. RT-qPCR validation of 33 candidates confirmed that transcripts for 6 (Cyp12d1-p, Cyp12a4, cyt-c-d, COX5BL, COX7AL, CG17140) and 2 (Dif, Rel) were respectively significantly up- and down-regulated in 91-R. Among the up-regulated genes, 4 are duplicated within the reference genome (Cyt-c-d, CG17140, COX5BL, and COX7AL). The predicted functions of the differentially expressed genes, or known functions of closely related genes, suggests that 91-R utilizes existing ROS regulation pathways of the mitochondria to combat increased ROS levels from exposure to DDT. This study represents, to our knowledge, the initial investigation of mitochondrial structural and functional adaptations in responses to intense DDT selection, and provides insights into ROS management mechanisms triggered by DDT exposure in Drosophila.