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Morphological and molecular effects of 20‐hydroxyecdysone and its agonist tebufenozide on CF‐203, a midgut‐derived cell line from the spruce budworm, Choristoneura fumiferana
Author(s) -
Hu Wenqi,
Cook Barbara J.,
Ampasala Dinakara R.,
Zheng Sichun,
Caputo Guido,
Krell Peter J.,
Retnakaran Arthur,
Arif Basil M.,
Feng Qili
Publication year - 2004
Publication title -
archives of insect biochemistry and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.576
H-Index - 66
eISSN - 1520-6327
pISSN - 0739-4462
DOI - 10.1002/arch.10124
Subject(s) - ecdysone , 20 hydroxyecdysone , ecdysteroid , spruce budworm , biology , choristoneura fumiferana , agonist , ecdysterone , cell culture , midgut , ecdysone receptor , medicine , endocrinology , transcription factor , microbiology and biotechnology , receptor , biochemistry , botany , lepidoptera genitalia , hormone , tortricidae , nuclear receptor , genetics , gene , larva
The morphological and molecular responses of a midgut‐derived cell line of the spruce budworm, Choristoneura fumiferana , to 20‐hydroxyecdysone (20E) and the nonsteroidal ecdysone agonist, tebufenozide (RH‐5992), were investigated. The cells responded to these compounds by clumping, generating filamentous extensions, increased mortality and expression of the transcription factor, Choristoneura hormone receptor 3 (CHR3). This cell line can be used as a model system to study the mode of action of ecdysone and its agonists. With subsequent passaging in ecdysteroid‐containing medium, the degree of clumping increased and the clumping could not be reversed by subculturing in ecdysteroid‐free medium. Cell numbers of the adapted cell lines in 20E and RH‐5992 containing media were not significantly decreased, compared to the control, but both cell lines accumulated less 14 C‐labeled RH‐5992 and lost the capability of expressing CHR3 in response to these compounds. Taken together, the cell lines appeared to develop a mechanism to adapt to the toxic effects of these compounds. Arch. Insect Biochem. Physiol. 55:68–78, 2004. © 2004 Wiley‐Liss, Inc.