PhD Student Position: molecular biology : Adam Mickiewicz University, Poland
One position for PhD student is available in Institute of Molecular Biology and Biotechnology of Adam Mickiewicz University which is the largest institution of higher education in Poznan and one of the largest and best institutions of higher education in Poland. A highly motivated researcher is sought to join the human molecular genetics research team under the supervision of Dr. Krzysztof Sobczak. We focus on studying the molecular pathomechanism and experimental therapy of myotonic dystrophy which is the hereditary neuro-muscular disease.
Description : Myotonic dystrophy type 1 (DM1) is an RNA dominant disorder caused by expansion of a CTG repeat in the 3’-UTR of the DMPK gene. The DMPK transcripts containing highly expanded CUG repeats (CUGexp) are retained in the nucleus in discrete foci. Their nuclear retention is partly a function of the interaction of CUGexp RNA with poly(CUG) binding proteins, such as, splicing factors in the Muscleblind-like (MBNL) family. The pathogenic effects of CUGexp RNA are due in part to sequestration of MBNL proteins, which results in misregulated alternative splicing that these proteins normally regulate. In our research we focus on deeper understanding of some aspects of molecular pathomechanism of DM, especially associated with miRNA metabolism and MBNL1 function, as well as application of antisense oligomers to disrupt pathogenic interaction of CUGexp with protein. Positions and research will be covered from TEAM project entitled “Molecular Pathomechanism and RNA Interference-Based Therapy of Myotonic Dystrophy”. The TEAM program is implemented by Foundation for Polish Science through EU Structural Funds in Poland within the framework of Operational Programme Innovative Economy.
There are three main aims of our project (three areas of post-doc projects):
Aim 1 : High Throughput Analysis of RNA Target Sequences and Structural Motifs for MBNL1 Splicing Factor (RNA deep sequencing).
Aim 2 : Mechanism of miRNA Expression Changes in Muscle Development and in DM1 and functional implications.
Aim 3 : The miRNA-like Molecules as Therapeutic Tools in Experimental Therapy in models of DM1.