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Developmental effects of a chimeric ultraspiracle gene derived from Drosophila and Chironomus
Author(s) -
Henrich Vincent C.,
Vogtli Martin E.,
Antoniewski Christophe,
SpindlerBarth Margarethe,
Przibilla Sabina,
Noureddine Maher,
Lezzi Markus
Publication year - 2000
Publication title -
genesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.093
H-Index - 110
eISSN - 1526-968X
pISSN - 1526-954X
DOI - 10.1002/1526-968x(200011/12)28:3/4<125::aid-gene50>3.0.co;2-s
Subject(s) - biology , ecdysone receptor , metamorphosis , ecdysone , nuclear receptor , microbiology and biotechnology , moulting , drosophila melanogaster , transgene , ecdysteroid , transcription factor , mutant , gene , genetics , receptor , larva , hormone , endocrinology , botany
Summary: The ultraspiracle ( usp ) gene encodes a nuclear receptor that forms a heterodimer with the ecdysone receptor (EcR) to mediate transcriptional responses to the insect steroid hormone, 20‐hydroxyecdysone (20HE). The responses ultimately elicit changes associated with molting and metamorphosis. Although Ultraspiracle (USP) is required at several developmental times, it is unclear whether USP plays stage‐specific roles in Drosophila . A chimeric transgene ( d / cusp ), produced by replacing the ligand‐binding domain (LBD) of Drosophila USP with the equivalent domain from another Diptera, Chironomus tentans , was tested for its ability to rescue Drosophila usp mutants from early larval lethality. A single copy of the d / cusp was sufficient to rescue transformants from several lines through larval development but they died suddenly during the late third instar. Additional doses of d / cusp were required to allow survival through the adult stage, but they did not restore a normal prepupal contraction. Thus, the arrest at the onset of metamorphosis apparently is caused by the impaired ability of the chimeric USP to mediate a stage‐specific function associated with the LBD. genesis 28:125–133, 2000. © 2000 Wiley‐Liss, Inc.