tailieunhanh - Báo cáo y học: "The genomic response to 20-hydroxyecdysone at the onset of Drosophila metamorphosis"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Wertheim cung cấp cho các bạn kiến thức về ngành y đề tài: The genomic response to 20-hydroxyecdysone at the onset of Drosophila metamorphosis. | Open Access Research The genomic response to 20-hydroxyecdysone at the onset of Drosophila metamorphosis Robert B Beckstead Geanette Lam and Carl S Thummel Address Department of Human Genetics Howard Hughes Medical Institute University of Utah School of Medicine Salt Lake City UT 841125331 USA. Correspondence Carl S Thummel. E-mail Published 21 November 2005 Genome Biology 2005 6 R99 doi 186 gb-2005-6-12-r99 The electronic version of this article is the complete one and can be found online at http 2005 6 12 R99 Received 17 June 2005 Revised 5 August 2005 Accepted 20 October 2005 2005 Beckstead et al. licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Background The steroid hormone 20-hydroxyecdysone 20E triggers the major developmental transitions in Drosophila including molting and metamorphosis and provides a model system for defining the developmental and molecular mechanisms of steroid signaling. 20E acts via a heterodimer of two nuclear receptors the ecdysone receptor EcR and Ultraspiracle to directly regulate target gene transcription. Results Here we identify the genomic transcriptional response to 20E as well as those genes that are dependent on EcR for their proper regulation. We show that genes regulated by 20E and dependent on EcR account for many transcripts that are significantly up- or downregulated at puparium formation. We provide evidence that 20E and EcR participate in the regulation of genes involved in metabolism stress and immunity at the onset of metamorphosis. We also present an initial characterization of a 20E primary-response regulatory gene identified in this study brain tumor brat showing that brat mutations lead to defects during .