We study the origin and evolution of cell type programs and associated genome regulation mechanisms: transcription factors, 3D chromatin architecture, histone modifications, and more. To this end, we combine single-cell genomics, chromatin profiling, and phylogenetic comparative methods in diverse animals and unicellular eukaryotes.

We offer 2 PhD positions.

PhD1: Single-cell lineage tracing at the scale of human populations. During ageing, some blood stem cell clones expand, increasing the risk of blood cancer and cardiovascular disease. You will use a novel, ultra-scalable single-cell lineage-tracing technology to test whether the functional properties of these clones predict disease risk better than somatic mutations.
or 
PhD2: Causes of clonal expansions of blood stem cells. During ageing, blood stem cell clones expand, increasing the risk of blood cancer and cardiovascular disease, yet most expansions lack known driver mutations. You will develop new single-cell multi-omic and functional-genomic technologies to discover why these clones expand.

The Gebauer lab studies how RNA-binding proteins (RBPs) control mRNA translation and impact cancer progression. We are interested in RBP regulatory networks, which mechanisms RBPs use to regulate translation, and how they can be harnessed for cancer treatment.

Who are we looking for?

We are looking for a highly motivated, creative and collaborative student with a degree in molecular biology, biochemistry, biotechnology or related disciplines willing to pursue ambitious projects. Prior experience in RNA-related research is desirable.

Our lab investigates, at the scale of the population, how the genes of the individual, the genes of social partners and the genes of the gut microbiota influence complex traits and diseases. We use advanced statistical analyses of genomes, metagenomes and phenotypes to understand the complex biological and evolutionary interplay between the individual, the social partners and the microbiota.

Our research is centered around cell type-specific transcriptomes. Using computational and experimental approaches, we investigate how these transcriptomes are generated (e.g. through microexon alternative splicing or fine transcriptional regulation) and how they contribute to human health, disease and evolution.

How do the two meters of DNA in our genome fold inside a micron-sized nucleus? How does improper folding contribute to disease?

The “Dynamics of Protein Synthesis & RNA Decay” group, led by Markus Höpfler, investigates fundamental mechanisms of cellular protein and RNA homeostasis. A particular focus of the lab is the emerging phenomenon of peptide-mediated RNA decay, in which RNA degradation is triggered during translation by the ribosome.

We investigate how chromatin and epigenetic mechanisms control cell identity and how their dysregulation drives cancer, particularly leukemia and pediatric brain tumors.

The Surrey lab studies the design principles of biological self-organization, focusing on the cytoskeleton. Their interdisciplinary research merges synthetic biology, biophysics, biochemistry, cell biology and mathematical modelling.

Our laboratories try to understand the molecular mechanisms that control alternative pre-mRNA splicing and their alterations in cancer. We aim to use this information to design novel therapeutic approaches, particularly in oncology. The project will be a collaboration between the groups of Ben Lehner and Juan Valcárcel.

Our lab focuses on the understanding of normal B-cell differentiation and lymphoma formation from the perspective of 3D chromatin organization, DNA methylation and single-cell heterogeneity in healthy and pre-malignant lymphocyte cell populations.

Our lab decodes and engineers human cell fates using single-cell omics, perturbation screening, and human stem cell models.

Our group studies how isolated mountain lakes record environmental pressure in the DNA they shed, and how such biodiversity signals can be used to predict ecosystem states. Working across Pyrenean high-mountain lakes, thermal springs and airborne samples, we combine 1.) large-scale environmental DNA sampling and biobanking, 2.) long-read sequencing of metagenomes, and 3.) comparative genomic analyses, from community composition to codon usage.

Our group aims to 'decode' the molecular rules by which sensor proteins can monitor highly diverse and specific environmental chemicals. To this end, we combine 1.) large-scale mutagenesis and functional data generation, 2.) AI-enhanced evolutionary modeling and 3.) engineering of chemically inducible protein folds.

Our group is centered on understanding the neurobiology of learning and memory and how these processes are disrupted in brain disorders and neurodegenerative diseases. By integrating multi-omic approaches, gene editing, and in vivo causal testing, we aim to uncover the molecular cascades underlying the initiation and progression of neurodegeneration, with a particular focus on the role of retrotransposons.