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Seroude, L.

Publications and source records attributed to Seroude, L..

2 recordsLinked to original sources

Regulating the UAS/GAL4 system in adult Drosophila with Tet-off GAL80 transgenes

The UAS/GAL4 system is the most used method In Drosophila melanogaster for directing the expression of a gene of interest to a specific tissue. However, the ability to control the temporal activity of GAL4 with this system is very limited. This study constructed and characterized Tet-off GAL80 transgenes designed to allow temporal control of GAL4 activity in aging adults. By placing GAL80 under the control of a Tet-off promoter, GAL4 activity is regulated by the presence or absence of tetracycline in the diet. Almost complete inhibition of the expression of UAS transgenes during the pre-adult stages of the life cycle is obtained by using four copies and two types of Tet-off GAL80 transgenes. Upon treatment of newly emerged adults with tetracycline, induction of GAL4 activity is observed but the level of induction is influenced by the concentration of the inducer, the age, the sex and the anatomical location of the expression. The inhibition of GAL4 activity and the maintenance of induced expression is altered in old animals. This study reveals that the repressive ability of GAL80 is affected by the age and sex of the animal which is a major limitation to regulate gene expression with GAL80 in aged Drosophila.

genetics

Tissue-specific downregulation of EDTP removes polyglutamine protein aggregates and extends lifespan in Drosophila

Drosophila egg-derived tyrosine phosphatase (EDTP, also called JUMPY) is a lipid phosphatase essential in oogenesis and muscle function in the adult stage. Although mammalian JUMPY negatively regulates autophagy, loss-of-JUMPY causes muscle dysfunction and is associated with a rare genetic disorder called centronuclear myopathy. Here we show that tissue-specific downregulation of EDTP in Drosophila non-muscle tissues, particularly glial cells, suppresses the expression of polyglutamine (polyQ) protein aggregates in the same cells and improves survival. Additionally, tissue-specific downregulation of EDTP in glial cells or motoneurons extends lifespan. We demonstrate an approach to fine-tune the expression of a disease-associated gene EDTP for the removal of polyQ protein aggregate and lifespan extension in Drosophila.

genetics