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Oral toxicity of Photorhabdus culture media on gene expression of the adult sweetpotato whitefly, Bemisia tabaci

Shrestha, Yam Kumar, Lee, Kyeong-Yeoll
Journal of invertebrate pathology 2012 v.109 no.1 pp. 91-96
Bemisia tabaci, Heterorhabditis bacteriophora, Heterorhabditis megidis, Photorhabdus luminescens subsp. laumondii, acetylcholinesterase, adults, bacteria, carboxylesterase, cholinergic receptors, culture media, diet, ecdysone, entomopathogenic nematodes, gene expression, gene expression regulation, genes, immunity, ingestion, metabolism, microsymbionts, mortality, nervous system, reproduction, reverse transcriptase polymerase chain reaction, sodium channels, sucrose, toxicity, vitellogenin
The oral toxicity of culture media of the symbiotic bacteria, Photorhabdus temperata, mutually associated with entomopathogenic nematode Heterorhabditis megidis and Photorhabdus luminescens ssp. laumondii (TT01) mutually associated with Heterorhabditis bacteriophora, were investigated in the adults of Bemisia tabaci. The oral ingestion of sucrose diet solutions (20%) containing bacteria-free supernatant of the culture media from symbiotic bacteria gradually increased mortalities and was completely lethal at 60h after the treatments, whereas the mortalities of the controls, sucrose solutions with or without media that uncultured with bacteria, were less than 17% up to 84h of incubation. The effects of oral ingestion of symbiont culture media were demonstrated on the expression rates of several genes of B. tabaci using quantitative real-time RT-PCR analysis. Genes associated with immunity (knottin) and nervous system (acetylcholine receptor, acetylcholine esterase and sodium channel) were up-regulated while genes involved in metabolism (cytochromep450 and carboxylesterase) were down-regulated, but genes involved in development (ecdysone receptor), reproduction (vitellogenin) and stress (hsp70, hsp90 and shsp) did not change transcription rates. Our results provide information for the understanding of the mechanism of symbiont pathogenic factors for the manipulation of host physiology at the transcription level.