Molecular cloning of sodium channel and identification of point mutations putatively associated with fenpropathrin resistance in Tetranychus urticae

AGRO 30

Deok Ho Kwon, jota486@hanmail.net1, Byung Ryul Choi, brchoi@rda.go.kr2, Si Woo Lee2, Hyoung Man Park2, John Marshall Clark, jclark@ent.umass.edu3, and Sihyeock Lee, shlee@snu.ac.kr1. (1) College of Agricultural Biotechnology, Seoul National University, San 56-1, Sillim-dong, Gwanak-gu, Seoul, South Korea, (2) Agricultural Biology, Rural Development Administration, 249 Seodun-dong Kweonseon-gu, Suwon, 441-857, South Korea, (3) Department of Veterinary and Animal Science, University of Massachusetts, Amherst, MA 01003
Tetranychus urticae Koch is a serious mite pest to various orchard trees and garden plants. A fenpropathrin-resistant mite strain (FenR) showed ca. 50-fold resistance. No significant differences were found in the activities of detoxification enzymes including carboxylesterase, glutathione-S-transferase, and cytochrome P450 between the susceptible (UDCM) and FenR strains. The FenR strain, however, showed ca. 10 fold slower knockdown response than UDCM as determined by knockdown bioassay, suggestive of the sodium channel insensitivity mechanism. We cloned cDNA fragments of para-homologous sodium channel α-subunit (TSSMscg) and determined its full length nucleotide sequences. The complete open reading frame of TSSMscg was 6618 nucleotides, encoding 2206 amino acids. The amino acid sequences of TSSMscg were 47% and 48% similar to the fruit fly and varroa mite, respectively. Amino acid comparison between the two strains revealed two mutations (L1031V and A1382D) found only in FenR mites, implying their possible role in knockdown resistance to fenpropathrin.