Effects of juvenile hormone on the ecdysone response of Drosophila Kc cells

Abstract

Drosophila Kc cells are ecdysone-responsive: hormone treatment leads rapidly to increased synthesis of several ecdysone-inducible polypeptides (EIPs) and to commitment to eventual proliferative arrest. Later, the treated cells undergo morphological transformation, cease to proliferate, and develop new enzymatic activities, notably, acetylcholinesterase (AChE) activity. These responses have proven useful as models for studying ecdysone action. Here we report the sensitivity of Kc cells to another important insect developmental regulator--juvenile hormone (JH). We find that JH inhibits some, but not all, aspects of the ecdysone response. When Kc cells are treated with ecdysone in the presence of either natural JHs or synthetic analogues, the morphological and proliferative responses are inhibited and AChE induction is blocked. Most striking is that JHs protect the cells from the rapid proliferative commitment induced by ecdysone alone. The JH effects exhibit reasonable dose-response curves with half-maximal responses occurring at very low JH concentrations. Nonetheless, even at high JH concentrations the inhibitory effects are incomplete. It is interesting that EIP induction appears to be refractory to JH. It seems clear that JH is not simply a generalized inhibitor of ecdysone-induced responses.

Insect cell culture and applications to research and pest management

“…Earlier studies (Lezzi and Wyss 1976;Cherbas et al 1989) showed the modulation of ecdysteroid-induced effects by JH and JHAs in Drosophila, Chironomus, and Plodia cells. More recently, Soin et al (2008) tested the three best known JHAs, methoprene, fenoxycarb, and pyriproxyfen, with transformed lepidopteran Bm5 and dipteran S2 cells.…”

Farnesoid secretions of dipteran ring glands: What we do know and what we can know

“…There has been considerable contemplation over to what extent the methoprene receptor (MET protein) is the same or a different cellular target than is the target of the endogenous, ring gland-produced farnesoate methyl esters (Cherbas et al, 1989;Wilson et al, 2003). A number of lines of evidence indicate that an endogenous signaling pathway during larval development and metamorphosis exists other than, or in addition to, the MET protein pathway:…”

A juvenile hormone agonist reveals distinct developmental pathways mediated by Ecdysone-inducible broad complex transcription factors

“…(The term juvenoids includes endogenous compounds and chemical analogs with JH-like activity.) Studies in several insect species indicate that juvenoids can modulate cellular responses to 20E [Chihara and Fristrom, 1973;Wyss, 1976;Mitsui and Riddiford, 1978;Levine et al, 1986;Booker and Truman, 1987;Truman and Reiss, 1988;Cherbas et al, 1989;Jacobs and Weeks, 1990;Prugh et al, 1992]. We tested the hypothesis that juvenoid-induced lethality results from interfering with the function of the Broad Complex (BRC), a gene essential for transducing 20E signals into the metamorphic development of larval and imaginal tissues, including the epidermis, salivary glands, central nervous system (CNS), gut, and musculature [Kiss et al, 1988;White, 1991, 1992].…”