Transcriptomic and Proteomic Responses of Sweetpotato Whitefly, Bemisia tabaci, to Thiamethoxam

Abstract

BackgroundThe sweetpotato whitefly, Bemisia tabaci (Hemiptera: Aleyrodidae), is one of the most widely distributed agricultural pests. Although it has developed resistance to many registered insecticides including the neonicotinoid insecticide thiamethoxam, the mechanisms that regulate the resistance are poorly understood. To understand the molecular basis of thiamethoxam resistance, “omics” analyses were carried out to examine differences between resistant and susceptible B. tabaci at both transcriptional and translational levels.ResultsA total of 1,338 mRNAs and 52 proteins were differentially expressed between resistant and susceptible B. tabaci. Among them, 11 transcripts had concurrent transcription and translation profiles. KEGG analysis mapped 318 and 35 differentially expressed genes and proteins, respectively, to 160 and 59 pathways (p<0.05). Thiamethoxam treatment activated metabolic pathways (e.g., drug metabolism), in which 118 transcripts were putatively linked to insecticide resistance, including up-regulated glutathione-S-transferase, UDP glucuronosyltransferase, glucosyl/glucuronosyl transferase, and cytochrome P450. Gene Ontology analysis placed these genes and proteins into protein complex, metabolic process, cellular process, signaling, and response to stimulus categories. Quantitative real-time PCR analysis validated “omics” response, and suggested a highly overexpressed P450, CYP6CX1, as a candidate molecular basis for the mechanistic study of thiamethoxam resistance in whiteflies. Finally, enzymatic activity assays showed elevated detoxification activities in the resistant B. tabaci.ConclusionsThis study demonstrates the applicability of high-throughput omics tools for identifying molecular candidates related to thiamethoxam resistance in an agricultural important insect pest. In addition, transcriptomic and proteomic analyses provide a solid foundation for future functional investigations into the complex molecular mechanisms governing the neonicotinoid resistance in whiteflies.

Characterization of UDP‐glucuronosyltransferase genes and their possible roles in multi‐insecticide resistance in Plutella xylostella (L.)

“…Previous studies had proved the contribution of UGTs to organophosphate insecticide resistance in H. virescens and M. domestica based on their enhanced catalysis , . Recent research revealed the upregulation of some UGT mRNAs by transcriptome sequencing and therefore speculated on the involvement of UGTs in resistance to other classes of insecticides such as DDT, pyrethroids, carbamates and neonicotinoids . However, the specific role of a single UGT gene in insecticide resistance had not been investigated until our previous study .…”

Resistance to neonicotinoid insecticides and expression changes of eighteen cytochrome P450 genes in field populations of Bemisia tabaci from Xinjiang, China

“…2012; Yang et al . 2013a, b, 2014, 2016a). In addition, it was found that CYP6DZ4 , CYP6CX5 , CYP6DZ7 , CYP6DW3 , CYP6DW2 and CYP301B1 were expressed significantly more in laboratory MED than in laboratory MEAM1 (Guo et al .…”

Comparative susceptibility of Bemisia tabaci to imidacloprid in field‐ and laboratory‐based bioassays

“…Oxidative metabolism of neonicotinoid compounds through enhanced expression of various cytochrome P450 genes, CYP6CM1 in particular, has been implicated as a primary mechanism of imidacloprid resistance in several instances . Additional P450s have been identified in resistant strains from China, including overexpression of CYP6CX1 in a thiamethoxam‐resistant strain compared with a susceptible strain …”

“…14 -16 Additional P450s have been identified in resistant strains from China, including overexpression of CYP6CX1 in a thiamethoxamresistant strain compared with a susceptible strain. 17,18 Biochemical or molecular assays that test for increased titers of detoxification enzymes or enhanced expression of detoxification genes are useful in identifying and characterizing resistance that is due to a specific metabolic enzyme 19 or target site such as insensitive AchE-R. 20 -22 However, such capability arises only after thorough research to establish a causal relationship between the biochemical or molecular process and the phenotypic expression of resistance. Even then, monitoring data obtained by using a biochemical procedure must be understood to represent only the specific mechanism for which it is designed and not an overall appraisal of other potential resistance mechanisms in an organism.…”