Master project "The basis for developmental robustness against disease in a mouse model for Fib[...]

vor 3 Wochen


Basel, Schweiz University of Basel Vollzeit

Organisation/Company: University of Basel

Department: Department of Biomedicine

Research Field: Biological sciences » Biology

Researcher Profile: Leading Researcher (R4) Positions

Country: Switzerland

Application Deadline: 31 Mar 2025 - 12:00 (Europe/Zurich)

Type of Contract: Not Applicable

Job Status: Not Applicable

Offer Starting Date: 1 Feb 2025

Is the job funded through the EU Research Framework Programme? Not funded by a EU programme

Is the Job related to staff position within a Research Infrastructure? No

Offer Description

The basis for developmental robustness against disease in a mouse model for Fibrodysplasia Ossificans Progressiva.

Developmental Genetics

Department Biomedicine, University of Basel

Embryonic development is a marvel of biological complexity as gene expression, cellular development and differentiation are seamlessly integrated across tissue, organ and the organism as a whole. Despite the susceptibility to molecular and cellular disturbances, an intrinsic robustness within embryos often prevails, shielding developmental processes from genetic perturbations. Our research has unveiled fascinating insights into the molecular basis of developmental robustness and we are now applying this knowledge to explore the underlying mechanisms of developmental robustness in congenital diseases, an emerging field of significant biomedical interest. Fibrodysplasia Ossificans Progressiva (FOP) is a rare human condition characterized by abnormal bone formation triggered by the R206H mutation in the ACVR1 receptor which leads to excessive BMP signaling. Intriguingly, the manifestation of FOP occurs postnatally despite embryonic activity of the receptor and the goal of this project is to uncover why embryos seem unaffected by the condition.

Project Aims:

  1. Aim 1: By investigating cellular and molecular changes in FOP mutant limb buds from the earliest stages, we aim to identify the compensatory mechanisms that protect the embryo from disease manifestation.
  2. Aim 2: The effects of excessive BMP signaling on FOP disease progression in the absence of BMP antagonism will be investigated genetically. Cellular, molecular, and phenotypic alterations will be analysed in embryos. Elucidating the mechanisms that enable embryos to evade or delay the onset of disease symptoms will be relevant for identifying potential therapeutic strategies for FOP.

This project encourages student interaction with several group members.

Methodologies:

Over approximately 9 months, the research project will immerse the student in a diverse array of molecular and cellular techniques. These include mouse genetics to investigate gene interplay affecting disease onset, phenotypic studies on cartilage and bone formation and the isolation and 3D culturing of limb mesenchymal progenitors from both wild type and FOP model for comparative analysis of molecular and cellular differentiation. Advanced techniques such as fluorescent RNA in situ hybridization (HCR) and immunofluorescence will enable detailed cellular studies.

This project provides the student with a valuable combination of scientific methodology, analytical thinking, and innovative research skills. Participation in research seminars, journal clubs, and the master thesis writing process will strengthen their ability to effectively communicate scientific findings in English, offering an enriching educational and research experience.

This project can be started as agreed with the master student.

Interested? Then drop us an email with your CV to arrange for an interview and project discussion.

We look forward to hearing from you

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