Technische Assistentin/technischer Assistent (IIIa), Sektion für Biologische Chemie [Chiffre: MEDI-16892]

Voraussetzungen: einschlägige Ausbildung oder Berufserfahrung.

Erwünscht: Erfahrung in der Protein-Präparation und -Analytik, Kultivierung von Bakterien, Insekten- und Säugerzellen, Klonierungstechniken (PCR etc.), Englischkenntnisse.

Aufgabenbereich: Herstellung, Reinigung und Analytik von Proteinen und Proteinkomplexen (Expression, chromatographische Techniken inkl. FPLC, SDS-PAGE etc.), biochemische Charakterisierung, Kristallisation, Herstellung von DNA-Konstrukten zur Proteinexpression, Generierung stabiler Zelllinien, Labororganisation und Bestellwesen, Unterstützung des biochemischen Praktikums.

Start: ab sofort

Gehalt: Das monatliche Mindestentgelt für diese Verwendung beträgt derzeit € 2.061,60 brutto (14 x jährlich) und kann sich eventuell auf Basis der kollektivvertraglichen Vorschriften durch die Anrechnung tätigkeitsspezifischer Vorerfahrungen sowie durch sonstige mit den Besonderheiten des Arbeitsplatzes verbundene Entgeltbestandteile erhöhen.

Informelle Anfragen: bitte an

Bewerbung bitte bis 23.05.2019 an (Betr: MEDI-16892)

PhD position, Medical University of Innsbruck, CCB-Biocenter/Division of Cell Biology, PI: David Teis

A PhD Position is available immediately in the ‘Membrane Traffic and Signaling’ research group, Division of Cell Biology (http://www.i- at the BIOCENTER @ Innsbruck Medical University, Innsbruck, Austria (

Background: The uptake of glucose, amino acids and nucleobases via nutrient transporters is essential for controlled cell growth and survival. How these processes are regulated in response to changes in the extracellular environment is poorly characterized.

The goal of the thesis is to identify the ‘Molecular mechanism of nutrient dependent plasma membrane remodeling’. We have recently shown that nutrient limitation induces global but selective remodeling of the plasma membrane proteome in yeast, including the lysosomal degradation of many different nutrient transporters. This process cooperates with autophagy in a catabolic cascade that mediates entry into quiescence and is required to survive nutrient limitation (Mueller et al., eLife 2015).

Methods used: Now we aim to characterize how cellular homeostasis and signaling networks regulate the ubiquitin dependent degradation of nutrient transporters. Therefore we will combine yeast genetics with quantitative proteomics and imaging approaches. Our results will help to understand how cells adjust their nutrient transporter repertoire on the cell surface in response to nutrient availability and thus have important general biological implications for the regulation of cellular growth.

Requirements: Applicants should be highly motivated, with a strong background in cell- and molecular biology and/or biochemistry.

Please send your application (CV and two contacts for reference) per email to David Teis (


  1. Huber, L.A., and Teis, D. (2016). Lysosomal signaling in control of degradation pathways. Curr Opin Cell Biol 39, 8-14.
  2. Muller, M.*, Schmidt, O.*, Angelova, M., Faserl, K., Weys, S., Kremser, L., Pfaffenwimmer, T., Dalik, T., Kraft, C., Trajanoski, Z., Lindner H.H. and Teis, D. (2015). The coordinated action of the MVB pathway and autophagy ensures cell survival during starvation. eLife 4.
  3. Adell, M.A.*, Vogel, G.F.*, Pakdel, M., Muller, M., Lindner, H., Hess, M.W., and Teis, D. (2014). Coordinated binding of Vps4 to ESCRT-III drives membrane neck constriction during MVB vesicle formation. J Cell Biol 205, 33-49.

Master thesis project in the Division of Cell Biology, Teis-Lab, Biocenter, Medical University of Innsbruck.

Molecular Mechanism of starvation induced endocytosis
Growth factor receptors and nutrient transporters in the plasma membrane (PM) of eukaryotic cells play a critical role in cell growth, differentiation, and survival. Their selective ubiquitin dependent removal from the PM helps cells to properly adapt to changes in the extracellular environment. The molecular mechanisms underlying the endocytosis of activated growth factor receptors are well understood. In contrast, little is know how cells control and regulate the abundance of nutrient transporters. Our recent results shown, that nutrient limitation induces selective endocytosis and degradation of many different nutrient transporters. This starvation-induced endocytosis of nutrient transporters together with autophagy is required for cell survival during nutrient limitation (Müller, Schmidt et al. eLife 2015). Our finding implicate new regulatory mechanisms for endocytosis and we have identified the first key molecules that are required for this process.

In this Master-thesis project, you will work in a team that aims to understand the molecular mechanism driving starvation-induced endocytosis.

To do so, you will learn how to use live cell imaging imaging and biochemical approaches in combination with genetic approaches in yeast. The goal of this master-thesis project is to define the mechanistic concept in which cellular starvation program communication with the endocytic machinery and thereby survive nutrient limitation. The results obtained could have general implications on our understanding of how cells cope with nutrient stresses, and will unravel mechanisms likely to be of prime importance in many pathologies, including metabolic diseases and cancer.

Requirements: high level of motivation to solve basic cell biological problems
Start: the sooner the better
If you are interested please contact: