Skip to main content


This page provides an overview of past and current research projects. They are either focused on screening technology developments, or tackle questions of stem cell biology.  Technology projects include the development of a biobank for conditional mutagenesis in haploid mouse stem cells, as well as improvements in CRISPR/Cas9 technologies. Biology focused projects tackle lineage transitions such as reprogramming or induced generation of neurons, as well as mechanistic studies on novel epigenetic regulator complexes.



Sergei Zhuk

I’m interested in mechanisms of transcriptional gene silencing in ES cells. Precise and continuous maintenance of heterochromatin state is a prerequisite for cell type-specific silencing of gene expression, protection of genome stability and repression of mobile elements. Using gene trap screens in haploid ES cells and CRISPR-Cas9 technology, we identified several poorly described transcriptional repressors that are involved in epigenetic silencing of viral reporters and participate in establishing H3K9 methylation upon recruitment to target site.

Georg Michlits

I am motivated in my research by a translational angle and want to study disease pathology maybe to find new therapeutic targets and strategies that may one day improve or save lives. My PhD-project is focused on technology-development, I designed and cloned a CRISPR-Cas9 knockout library of 30.000 guide RNAs targeting 6000 genes. I determine enrichment or depletion of individual single cell derived clones using high throughput sequencing and write algorithms for data analysis and hit scoring. Currently I use mouse embryonic stem cells to uncover new genes and pathways that increase the efficacy of etoposide chemotherapy and identify weaknesses of Brca1 breast and ovarian cancer. I hope that my efforts will contribute to the ongoing improvements of genetic screening systems and lead to more exciting discoveries in our lab and others.

Gintautas Vainorius

Establishing and maintaining cell identity is one of the core fundamental questions in developmental biology. Transdifferentiation via ectopic expression of transcription factors gives a unique opportunity to address these questions. I am amazed how few expressed transcription factors are able to overcome the initial cell genetic program and reinstall the new transcriptional network besides the enormous epigenetic barriers imposed by the initial cell type. Furthermore, transdifferentiation allows derivation of patient specific cell types, which can be used for both, medical purposes as well as disease modeling. Thus, it is vital to understand these processes. To achieve this, I employ forward genetic screens to identify core components and transcriptional logic behind them by using neuronal transdifferentiation as my model system.

Maria Hubmann

I see myself as an integral member of this dynamic network of scientists called Elling lab. I help to interconnect the different characters and phenotypes in the team so that everyone can benefit from our different skills in this scientifically heterogenous research group. I am in a constant mode of transdifferentiation between acting as Ulis third and forth hands, helping our students with all kinds of tasks they could come up with, and working on my own collaborative scientific project on the improvement of the CRISPR-Cas9 technology.

Cecilia Raupach

Induced reprogramming of cells into pluripotency state allows to derive cells with the potential to differentiate into virtually any tissue. The understanding of factors and mechanisms underlying cell identity is closely linked to our ability to mimic these decisions to produce a certain cell type for disease modelling or even cell replacement in case of damage. The discovery of the four Yamanaka factors, being sufficient to reprogram differentiated cells back to pluripotency state opened a great field of research opportunities. However, this process remains inefficient as only a small proportion of cells dedifferentiate. A genetic screen, previously performed in the Elling lab, pointed out factors, that may be promising candidates to improve reprogramming. In my master thesis, I want to characterize their mechanism of action and their potential role in reprogramming.

Roadblocks of reprogramming

In collaboration with the labs of Konrad Hochedlinger (Harvard) and Johannes Zuber (IMP) we identified CAF-1 as well as SUMOylation as powerful roadblocks of reprogramming to induced pluripotency. We could show, that knockdown of the histone chaperone complex resulted in markedly improved reprogramming efficiency do to an increased accessibility of the genome for the transcription factors governing this transition.


To empower the genetic mapping of ES cell biology, we generated a biobank of 100 000 conditional mutant cell lines. These haploid ES cells clones can be readily reverted to wildtype sister clones and enable phenotyping side by side to the control cells with identical genetic and epigenetic background. We use these clones for rapid validation of screening outcomes.