Welcome to the homepage of the Institute for Developmental Immunology (IDI) at the Biocenter of the Medical University of Innsbruck. The IDI is currently headed by Prof. Andreas Villunger, PhD, who was appointed as a head of this unit in 2007 as junior professor and is now full professor for Developmental Immunology at MUI.
The Institute is organized in four research groups, run by head Andreas Villunger and associate professors Jan Wiegers, Verena Labi and Sebastian Herzog. Please click the logo to learn more about the respective group!
With their coworkers, DDI investigators explore basic mechanisms of immune cell development and differentiation with a focus on microRNAs and steroid hormones. In addition, we are interested in studying general principles of cellular transformation, focusing on the role of BCL2-regulated cell death and the p53 signalling network as barrier against malignant disease.
All group leaders are involved in training undergraduate as well as graduate students of different life-science disciplines, including biochemistry, biology as well as molecular and human medicine. If you are interested in research training opportunities at different levels (summer students, BSc, MSc, or MD/PhD), or have any teaching related questions, please contact Claudia in administration to organize an appointment with your group leader of interest (Claudia.Ram@i-med.ac.at).
For her PhD work on the PIDDosome in hepatocyte development, regeneration and cancer (see below),
Valentina has received the prestigious Award of Excellence sponsored by the Austrian state. Each year, this award honors the best 40 dissertations in the country. On top of it, she also got an
EMBO fellowship for her Postdoc studies that she has recently started in the United States. Well done, Valentina!
Polyploidization is a hallmark of cancer cells but also occurs during normal development in several tissues, e.g. in the liver. Loss of the regulator of hepatocyte ploidy, the PIDDosome, drastically increases polyploidy, but it has been unclear to what extent this affects tumorigenesis. Here, Valentina showed that PIDDosome deficiency reduced tumor number and burden, despite the inability to activate p53 in polyploid cells. Thus, the PIDDosome may be a therapeutic target to manipulate hepatocyte polyploidization in order to prevent and/or treat hepatocellular carcinoma.
Who is your pick for the "Ugly Christmas Sweater" contest?
Lab retreat 2020, tyrolean style
MiRNAs are generated from long primary transcripts in which local stem-loop structures are recognized and
cut by the Microprocessor. However, it is still unclear how exactly the enzymatic machinery distinguishes an authentic miRNA hairpin from the thousands of similar folds found in RNA. Here,
Sebastian and his team describe a SAFB2- and ERH-dependent mechanism they refer to as "cluster assistance", in which a suboptimal primary miRNA fold is properly processed only when expressed
together with a standard miRNA on the same transcript. The features that define a primary miRNA are thus not only encoded in the stem-loop itself, but also by the larger sequence