الفهرس | Only 14 pages are availabe for public view |
Abstract Juvenile hormone (JH) is responsible for controlling many biological processes. In several insect species JH has been implicated as a key regulator of developmental timing and preventing the premature onset of metamorphosis during larval growth periods. However, the molecular basis of JH action is not well studied. Here, we highlight recent advances which demonstrate the importance of transcription factors from the bHLH-PAS and nuclear receptors (NRs) families in mediating the response to JH. In this current study, we utilized yeast two hybrid system to study nuclear receptors isolated from Drosophila melanogaster and tested the extent of increase or decrease in the intensity of NRs interactions when adding Juvenile hormone analogue (pyriproxyfen). Fushi tarazu factor 1 (Ftz-F1) nuclear receptor was found to be highly interacting with ultraspiracle (USP) nuclear receptors especially when pyriproxyfen was added to this interaction. Accordingly, two transgenic flies carrying mutation in either Ftz-F1 or gce were produced in order to further studies of these two candidate receptors. Our data revealed that mutation in either Ftz-F1 or gce cause precautious metamorphosis which are monitored by the early br gene expression in the young larvae. The mutation in any of these two genes caused resistance in the genetically engineered insects to pyriproxyfen, insect growth regulators (IGRs). It was indicated that JH mediates its antimetamorphic function at the transcriptional level through FtzF1 and Gce. Other experiment was conducted to study Met gene that causes resistance in insects to IGRs through the study of changes in the resulting DNA using specific primers to isolate the change in that gene using the PCR and sequencing techniques. |