The general theme of the laboratory is the use of Drosophila to understand the molecular mechanisms of human inherited neurodegenerative diseases and the functions of the corresponding Drosophila ortologue genes.
Although a number of approaches have been taken in this direction, most of the generated models for human disease have often taken questionable shortcuts (expression of human genes considerably different from the fly ones, or of synthetic genetic constructs) that limited the analysis of the molecular machinery underlying the pathologies modelled allowing only very simple questions about protein aggregation and cell survival to be answered convincingly.
In our approaches disease modelling is guided by the knowledge of the endogenous fly background and is always paralleled by the study of the normal processes in which the corresponding fly genes are involved.
The main research line in the lab is concerned with Atrophins, a family of transcriptional co-repressors with several additional roles and implicated in many cellular and developmental processes. Atrophin-1 in humans is responsible for the polyglutammine disease Dentatorubropallydoluisian atrophy (DRPLA). atro is the only fly atrophin and the only gene of those involved in polyQ diseases that has been mutated and studied in Drosophila.
We are developing research projects that address:

1. The normal function of Atro, in particular in signalling and transcription
2. The ability of Atro and its interactor Fat, an atypical cadherin to induce neurodegeneration independent of polyQ
3. The generation of a fly model for DRPLA by expansion of the endogenous stretches of polyQ in Atro.