Overexpression of HmgD causes the failure of pupariation in Drosophila by affecting ecdysone receptor pathway.

HmgD encodes Drosophila homologue of high mobility group proteins (HMGD), which are thought to have an architectural function in chromatin organization. However, current opinions about the function of HMGD in Drosophila development are controversial. Our previous studies have shown that ubiquitous overexpression of HmgD caused the formation of melanotic tumors in the Drosophila larvae by prematurely activating the Ras-MAPK pathway. Here we report that under maternal control, the viability of flies links with overexpression of HmgD, while under ubiquitous control, ActGal4, overexpressing HmgD animals, which display prolonged larval stages around day 13, developmentally stagnate in the larva-white pupa transition. Ecdysone feeding did not rescue overexpressing HmgD animals. RT-PCR analyses show that overexpression of HmgD does not affect the temporal expression pattern of ecdysone receptor gene EcR, whereas transcriptional patterns of some key regulatory genes, such as E74A, E74B, E75A, E75B, betaFTZ-F1, are changed greatly. These results suggest that ubiquitous overexpression of HmgD results in the failure of pupariation neither by affecting the process of ecdysone synthesis and release nor by abnormal EcR transcription, but by causing expression of EcR regulatory nuclear receptors out of schedule. The results led us to postulate that overexpression of HMGD likely changes the signaling cascade of Drosophila metamorphosis by an interaction between HMGD and DNA strands, and subsequently by an error of DNA binding abilities and transcriptional activities of some nuclear receptor genes. Arch. Insect Biochem. Physiol. 2008.