Jared Sterneckert
Professor Dr. at Technische Universität Dresden
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Positions (2)
Jared Sterneckert
Technische Universität Dresden
9 months ago
The Center for Regenerative Therapies Dresden (CRTD) at Technische Universität Dresden is offering a PhD student position focused on the study of ribonucleoprotein (RNP) granules in the pathogenesis of amyotrophic lateral sclerosis (ALS). This opportunity is part of the DFG-funded Research Training Group “Biomolecular Condensates: From Physics to Biological Functions” (RTG 3120), which provides a vibrant interdisciplinary research environment at the interface of physics and biology. The project aims to characterize the role of RNP granules in motor neuron (MN) axons, investigating how these condensates protect mRNA and regulate local translation, and how their dysfunction contributes to ALS. The research leverages advanced technologies, including induced pluripotent stem cell (iPSC)-derived MNs, FUS-eGFP reporter lines for live-cell imaging, and custom microfluidic devices to study axonal granules and neuromuscular junctions. Key questions include the maintenance of diverse RNP granules, protein exchange dynamics, and mechanisms preventing granule fusion. The project will utilize dCas13d-mediated proximity labeling and pulse-chase experiments to identify protein-mRNA interactions and assess the impact of ALS mutations using isogenic iPSC models. The team will also explore therapeutic strategies using oligonucleotide 'bait RNAs' to reverse ALS pathogenesis. The successful candidate will join a world-leading research community embedded in the CMCB, with access to state-of-the-art infrastructure and shared core facilities. The CRTD is closely linked to other major research centers in Dresden, fostering collaboration across cell biology, genomics, biophysics, tissue engineering, bioinformatics, and regenerative medicine. The position is remunerated according to salary group E 13 TV-L (65% of full-time weekly hours), funded by the DFG RTG 3120, and initially limited until March 31, 2030, with possible extension. Applicants should hold a Master’s degree (or equivalent) in Biology or a related field, with experience in cell culture highly desired. Candidates must demonstrate the ability to work in an international, interdisciplinary team, possess excellent communication and social skills, and be fluent in English. Applications from women and candidates with disabilities are strongly encouraged. The application deadline is January 15, 2026. To apply, submit a single PDF containing your CV, cover letter (describing research experience and interests), list of academic achievements/publications, degree certificates/transcripts, and contact information for at least two references via the TUD SecureMail Portal or by email to [email protected]. For more information about the research group, visit https://tud.link/vprn and https://dresdencondensates.org .
9 months ago
Jared Sterneckert
Technische Universität Dresden
9 months ago
Technische Universität Dresden, a University of Excellence, invites applications for a PhD position in the DFG-funded Research Training Group RTG 3120, "Biomolecular Condensates: From Physics to Biological Functions." The position is hosted at the Center for Regenerative Therapies Dresden (CRTD), within the Chair of iPS Cells and Neurodegenerative Diseases led by Prof. Dr. Jared Sterneckert. This interdisciplinary program offers a vibrant research environment at the interface of physics, biology, and biomedical engineering, focusing on the role of biomolecular condensates in cellular function and disease. The PhD project aims to characterize the role of ribonucleoprotein (RNP) granules in the pathogenesis of amyotrophic lateral sclerosis (ALS). Motor neurons (MNs) rely on RNP granules for local mRNA translation, and alterations in these granules are linked to ALS and MN degeneration. The research will utilize iPSC-derived MNs, FUS-eGFP reporter lines for live-cell imaging, and microfluidic devices to study axonal RNP granules and neuromuscular junctions. Key questions include how RNP granules maintain individualized mRNA cargo, regulate protein exchange, and prevent fusion to preserve mRNA separation. Advanced techniques such as dCas13d-mediated proximity labeling and pulse-chase experiments will be employed to identify protein-mRNA interactions and assess granule dynamics. The project also explores therapeutic strategies using oligonucleotide "bait RNAs" to reverse ALS pathogenesis. The successful candidate will join a world-leading research community embedded in the CMCB, which includes the B CUBE Center for Molecular Bioengineering, the Biotechnology Center (BIOTEC), and CRTD. The campus is highly interdisciplinary, with close links to the German Center for Neurodegenerative Diseases (DZNE), the Medical Theoretical Center (MTZ), the Carl Gustav Carus University Clinic, and the Max-Planck-Institute for Molecular Cell Biology and Genetics (MPI-CBG). Research topics span cell biology, genomics, biophysics, tissue engineering, bioinformatics, and regenerative medicine, bridging fundamental science and clinical applications. Applicants must hold a Master’s degree (or equivalent) in Biology or a related field, with experience in cell culture highly desired. Candidates should demonstrate strong motivation, multidisciplinary thinking, excellent communication and social skills, and fluency in English. The position is remunerated according to salary group E 13 TV-L (65% of full-time weekly hours), initially limited until March 31, 2030, with possible extension depending on funding. The program offers structured training, close mentoring, access to advanced infrastructure, and integration into an international scientific network. Applications from women and candidates with disabilities are strongly encouraged. Please submit your application (CV, cover letter, academic achievements/publications, degree certificates/transcripts, and contact information for at least two referees) by January 15, 2026, preferably via the TUD SecureMail Portal as a single PDF to [email protected]. For more information about the research group, visit https://tud.link/vprn and about the RTG program at https://dresdencondensates.org .
9 months ago
Articles (14)
The degeneration of axon terminals before the soma, referred to as “dying back”, is a feature of Parkinson’s disease (PD). Axonal assays are needed to model early PD pathogenesis as well as identify protective therapeutics. We hypothesized that defects in axon lysosomal trafficking as well as injury repair might be important contributing factors to “dying back” pathology in PD. Since primary human PD neurons are inaccessible, we developed assays to quantify axonal trafficking and injury repair using induced pluripotent stem cell (iPSC)-derived neurons with LRRK2 G2019S, which is one of the most common known PD mutations, and isogenic controls. We observed a subtle axonal trafficking phenotype that was partially rescued by a LRRK2 inhibitor. Mutant LRRK2 neurons showed increased phosphorylated Rab10-positive lysosomes, and lysosomal membrane damage increased LRRK2-dependent Rab10 phosphorylation. Neurons with mutant LRRK2 showed a transient increase in lysosomes at axotomy injury sites. This was a pilot study that used two patient-derived lines to develop its methodology; we observed subtle phenotypes that might correlate with heterogeneity in LRRK2-PD patients. Further analysis using additional iPSC lines is needed. Therefore, our axonal lysosomal assays can potentially be used to characterize early PD pathogenesis and test possible therapeutics.
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2024
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2024
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2024
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2023
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2023
Mutations in the Fused in Sarcoma (FUS) gene cause the familial and progressive form of amyotrophic lateral sclerosis (ALS). FUS is a nuclear RNA-binding protein involved in RNA processing and the biogenesis of a specific set of microRNAs. Here we report that Drosha and two previously uncharacterized Drosha-dependent miRNAs are strong modulators of FUS expression and prevent the cytoplasmic segregation of insoluble mutant FUS in vivo. We demonstrate that depletion of Drosha mitigates FUS-mediated degeneration, survival and motor defects in Drosophila. Mutant FUS strongly interacts with Drosha and causes its cytoplasmic mis-localization into the insoluble FUS inclusions. Reduction in Drosha levels increases the solubility of mutant FUS. Interestingly, we found two Drosha dependent microRNAs, miR-378i and miR-6832–5p, which differentially regulate the expression, solubility and cytoplasmic aggregation of mutant FUS in iPSC neurons and mammalian cells. More importantly, we report different modes of action of these miRNAs against mutant FUS. Whereas miR-378i may regulate mutant FUS inclusions by preventing G3BP-mediated stress granule formation, miR-6832–5p may affect FUS expression via other proteins or pathways. Overall, our research reveals a possible association between ALS-linked FUS mutations and the Drosha-dependent miRNA regulatory circuit, as well as a useful perspective on potential ALS treatment via microRNAs.
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2023
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2023
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2023
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2023
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2022
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2021
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2021
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2021
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2021
Collaborators (10)
Bettina Seeger
Junior Professor for Alternative/Complementary Methods to Animal Experiments
University of Veterinary Medicine Hannover, Foundation
Maximina H. Yun
Technische Universität Dresden
Bhuvaneish Thangaraj Selvaraj
University of Edinburgh
Cläre von Neubeck
Universität Duisburg-Essen
Jonathan Gilthorpe
Senior Lecturer
Umea University
Jerome Mertens
Associate Professor, Riford Chair for Neurodegenerative Disease and Dementia
University of California, San Diego
SILVIA PELUCCHI
University of Milan
Udai Bhan Pandey
University of Pittsburgh Medical Center
Doris Steinemann
Prof. Dr. rer. nat.
Medizinische Hochschule Hannover
Andreas Hermann
PI/Prof. Dr. Dr.
University of Rostock
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