Marie Curie postdoc fellowship

The European Commission recently announced the dates for the opening and submission of Marie-Curie Postdoctoral Fellowships. The goal of these fellowships is to support the career of researchers with a PhD interested in diversification and development of new skills through intersectoral and international mobility.

Please make sure that you contact the Postdoc Office / Career Center by July 15th with:

  • detailed CV
  • motivation letter
  • PhD certificate or a document that confirms the eligibility for the program
  • name of the hosting group at MDC

as a single pdf to

Note for MDC Postdocs: you are eligible to apply to the MSCA fellowship if you are less than 1 year at the MDC by October 12th, 2021.



Researchers do not need to be affiliated with the MDC beforehand, but need an MDC host Group Leader willing to support their applications. They also need to fulfill the eligibility criteria:

  • Mobility Rule: Researchers must not have resided or carried out their main activity in Germany for more than 12 months in the previous 3 years before the call deadline (12.10.2021)
  • Research experience: PhD (successfully defended doctoral thesis at the call deadline)
  • Scientific age: up to 8 years full time equivalent experience in research after PhD. Career breaks (e.g. due to parental leave), will not be taken into account.
  • Researchers are expected to be familiar with the call and the proposal template.

Help us support your application as best as possible. Please follow the timeline below for applications:

July 15th: Notification of Postdoc Office / Career Center that you want to apply for a MSCA fellowship including the following information and documents:

  • detailed CV
  • motivation letter
  • PhD certificate or a document that confirms the eligibility for the program
  • name of the hosting group at MDC

as a single pdf to

August 13th: Group Leaders notify Career Center/PDO of candidates of interest

September 5th: Deadline for proposal submission to Career Center/ Funding Office

August 17thThe MDC webinar presenting application support, postdoc opportunities and life at MDC

October 1st: Deadline for completion of administrative formalities

October 12th: Deadline for submission of MSCA fellowship


MDC Support for Applicants


The MDC funding office provides support material for applicants for preparations of outstanding proposals and an information webinar presenting application support, postdoc opportunities and life at MDC. The webinar will take place on August 17th. 

The MDC Career Center and funding office also provide detailed feedback for MSCA proposals.

*We provide feedback only for proposals submitted by the internal deadline (September 5th) and formatted according to the MSCA template and guidelines.

We cannot provide feedback on proposal that have already been rejected more than once and proposals which reach us after the deadline.


Potential MDC host Group Leaders


Some groups may offer various projects and have not described a specific project below; in this case explore the research group’ s webpage.

Michael Bader

Preclinical studies on the SARS-CoV2 receptor ACE2 as therapeutic target

We are looking for a postdoc (or recent PhD graduate) in pre-clinical research who considers applying for the MSCA Postdoctoral Fellowship 2021 call. Selected candidates will receive dedicated support from our group to write a strong proposal.

Angiotensin-converting enzyme 2 (ACE2) is a multifunctional protein, that was discovered as a carboxypeptidase, converting the vasoactive peptide Ang II to Ang-(1-7). However, later studies revealed other substrates of the enzyme, but also non-enzymatic functions of ACE2, such as aminoacid transport in the gut. Recently ACE2 was characterized as receptor for SARS-CoV2 causing COVID-19. Therefore, the interaction of the SARS-CoV2 spike protein with ACE2, which is essential for cell entry of the virus, became a valid antiviral drug target.

We have studied the physiological functions of ACE2 in transgenic and knockout animal models. In one of our projects we discovered that ACE2-deficient mice show an increased melanin production in the skin. The mechanism is not yet completely clarified and will be subject of the Postdoc project. Moreover, this effect could be exploited therapeutically using topically applied ACE2 inhibitors in the skin, which not only would induce melanin production and skin tanning but also anti-inflammatory actions to treat diseases such as psoriasis and acne.

In the planned Postdoc project, high-throughput screening approaches will be developed to find novel inhibitors of the (A) ACE2 enzymatic activity and (B) SARS-CoV2 spike protein binding to ACE2, using ACE2 activity assays as readouts. The compounds will be chemically optimized in collaboration with the Chemical Biology core facility at the MDC and characterized in suitable cell culture and animal models. In parallel the basic biology of ACE2, including its interaction with other proteins, trafficking, and shedding will be further studied using these tools. Eventually newly discovered active compounds will be further developed to be used in clinical trials.

Michela Di Virgilio

Expression of Interest for hosting a MSCA fellow at the Max Delbrück Center for Molecular Medicine in Berlin, Germany

We are looking for a postdoc who considers applying for the MSCA Postdoctoral Fellowship 2021 call on the topic Genome Integrity & Diversification during Immune Responses.

The research in the Di Virgilio laboratory aims at addressing a fundamental question in Life Sciences: What are the molecular mechanisms that ensure both the integrity and diversity of our genome by modulating the formation of DNA damage (specifically DNA double-strand breaks) and by steering their repair towards the appropriate physiological outcome? We employ mature B lymphocytes as ideal model system since in addition to experiencing programmed DNA breaks during CSR, these cells are highly proliferative and therefore susceptible to stochastic replication-associated damage, thus allowing us to comprehensively investigate the mechanisms ensuring genome diversity and stability, and their relationship.

For the MSCA project, we plan on dissecting the molecular composition and regulation of DNA end processing in the context of B lymphocytes undergoing antibody gene diversification.

Sofia Forslund

High-throughput host-microbiome systems medicine approaches

Jan Philipp Junker

The Junker lab studies cell fate decisions in health and disease, using the zebrafish as their primary model organism, and combining experimental and computational work. A particular focus of the group is to study principles of organ regeneration – many organs of the zebrafish, such as the heart, brain and pancreas, regenerate fully after injuries that lead to permanent damage in humans. To address their questions, the lab develops and uses methods in single-cell genomics, including novel experimental and computational strategies for massively parallel lineage analysis, single cell RNA labelling, and single cell open chromatin profiling. The Junker lab is currently particularly interested in recruiting a computational biologist with an interest in multi-modal single cell analysis of organ regeneration.

Gaetano Gargiulo

The scientific projects proposed by the applicant can be entirely conceived by the applicant and make use of our technological strengths and model systems or could be tailored to open questions pursued in the lab. The lab routinely uses mouse and rat xenografts, has a large collection of publicly available and custom genome-wide CRISPR interference and activation libraries for human and mouse targets, is equipped to perform in vivo chemo and radiotherapy, and has well-established workflows for all the major bulk and single-cell molecular assays, including computational tools for analysis. We generally apply these tools to transformed neural stem cells and patient-derived glioblastoma stem cells. Among other questions, we are open to clarify the cellular and molecular mechanisms regulating the crosstalk between innate immune cells and glioblastoma in vitro and in vivo, we are interested in understanding the developmental and pathophysiological routes of brain tumor identities and win more unbiased manner - we are pursuing adult and pediatric brain tumors' vulnerabilities through large-scale genetic screens in vivo and drug screens in vitro.

Enno Klußmann

Elucidating molecular mechanisms underlying PDE3A-mediated cardioprotection

Hypertension with brachydactyly (HTNB) is caused by mutations in different exons of the gene encoding phosphodiesterase (PDE)3A. Surprisingly, despite the decade-long hypertension the patients do not develop hypertension-induced cardiac damage such as hypertrophy or heart failure. We have shown that the hypertension resides in smooth muscle, and that mutant PDE3A enzymes are hyperactive, aberrantly phosphorylated and their interaction with the adaptor protein, 14-3-3θ, is enhanced. The aim of the project is to elucidate the underlying cardioprotective mechanisms and eventually turn them into novel approaches for the treatment of heart failure. Methodologically, the project involves high-resolution microscopy, FRET and single cell sequencing approaches.

The project will be carried out in the Anchored Signalling group of E. Klussmann at the Max-Delbrück-Center for Molecular Medicine in the Helmholtz Association (MDC) on the campus Berlin Buch.

We are an international group and look for a highly motivated postdoc with an interest in cardiac myocyte biology, imaging, single cell techniques.

Validation of AKAP18 protein-protein interactions as target for the treatment of heart failure

A-kinase anchoring proteins (AKAPs) comprise a family of scaffolding proteins which engage in direct protein-protein interactions and thereby tether protein complexes as signal transduction units to defined cellular compartments. AKAPs confer specificity to cellular signalling processes. We have discovered AKAP18δ, and shown that it participates in the control of Ca2+ reuptake into the sarcoplasmic reticulum (SR) of cardiac myocytes, and thereby cardiac myocyte relaxation and diastole. We have recently discovered new interactions of AKAP18δ and found that it is also involved in Ca2+ release from the SR of cardiac myocytes and thus in systole. The aim of the proposed project is to validate the new interactions as drug targets for the treatment of heart failure. The project involves development of pharmacological agents and small molecule screening and characterising their effects on cardiac myocytes, e.g. on Ca2+ transients and cAMP signalling.

The project is a joint endeavour with Cathrine Carlson, University of Oslo, Norway. It will be carried out mainly in the Anchored Signalling group of E. Klussmann at the Max-Delbrück-Center for Molecular Medicine in the Helmholtz Association (MDC) on the campus Berlin Buch. Secondments to the Oslo lab are planned.

We are looking for a highly motivated postdoc with an interest in pharmacology and translational science.

Michael Sigal

The impact of colibactin of colonic stem cell integrity and colorectal carcinogenesis.

Colibactin is a genotoxin produced by commensal E. coli. We found that even a short-term interaction between colibactin-producing E.coli and colonic primary organoid cells promotes severe genomic alterations and triggers cellular transformation (Iftekhar et al., Nature communications 2021). Now we would like to use sophisticated mouse models developed in our lab, organoids and human patient data to elucidate the role of colibactin for colorectal carcinogenesis.

Leif Ludwig

We are looking for a postdoc who is planning to apply for the MSCA Postdoctoral Fellowship 2021 call. We are encouraging applicants to be creative in designing and formulating a project proposal that they foresee to accomplish in our laboratory. The selected candidate will receive guidance and professional support from our group to conceive a project and to write a competitive proposal.

Scientifically, the major goal of our group is to use clonal & lineage tracing approaches to unravel fundamental principles of in vivo stem cell dynamics with a focus on the hematopoietic and immune systems, its underlying genomic (dys-)regulation and the role of mitochondrial genotypes in shaping human phenotypes. To achieve this, we utilize and develop state-of-the-art single cell genomic technologies enabling multimodal omics readouts, including chromatin accessibility, gene & protein expression, and/or mutational profiles. We apply these approaches to clinical samples and cellular models of human disease, thereby aiming to bridge genomics and cell biology while being motivated by observations from genetics and the clinic.

Moreover, an interrelated key objective of the group is to better understand how mitochondrial genotypes contribute to metabolic and cellular phenotypes in the context of congenital disorders, an aging immune system and more generally human biology.

Thomas Sommer

Erich Wanker

Targeting huntingtin seeds from biosamples with therapeutic molecules

Inhibiting protein-protein interactions as a therapeutic concept

Zsuzsanna Izsvak

Endogenous retrovirus activated of Tol-like receptor (TLR) signalling in glioma and glioblastoma

Studying endogenous retroviral elements (HERVs) is not only relevant to evolutionary biology, it may also shed light on the nature of various pathologies as or cancer (1) or autoimmune disease. Besides germ and pluripotent stem cells (2), the human endogenous retrovirus HERV-K is transcribed in the human brain. Under pathological conditions, the transcription levels of specific HERV-K can change significantly during disease development. Our central hypothesis is that HERV-K-derived, GUUGUGU carrying single stranded RNA molecules (ssRNA), similarly to an external viral infection activates the Tol-like receptor (TLR7/8) signalling (3). TLR signalling has been associated with cancer, including glioblastoma (GBM), the most frequent highly malignant brain tumour disease in adults. There are currently no curative therapeutic options for GBM. Recent studies on the molecular mechanisms and gene mutations in GBM combined with clinical trials led to the development of more tailored therapeutic approaches such as immunotherapy. In principle, the induced TLR7/8 signalling activates the innate immune system and provokes an anti-tumour activity (viral mimicry), a concept used in immunotherapy. However, the success of these therapeutic approaches is sometimes rather contradicting, and the cells, instead of dying become even more invasive. The difficulties herein lie in the frequently contradictory outcome of the treatment. The project aims at identifying factors contribute to the two opposite cell fate. Our hypothesis is that TLR signaling may either inhibit or favor glioma growth. The effects of TLR agonists on tumor cells may depend on the tumor cell type. Determining whether TLR signaling activates pro- or anti-tumorigenic processes in an individual patient may be crucial for choosing the proper tumor immunotherapy strategy.

(1) Singh M, Cai H, Bunse M, Feschotte C, Izsvák Z. Viruses. 2020 Nov 13;12(11):1303. Human Endogenous Retrovirus K Rec forms a Regulatory Loop with MITF that Opposes the Progression of Melanoma to an Invasive Stage. doi: 10.3390/v12111303. PMID: 33202765 Free PMC article.

(2) Fuchs NV, Loewer S, Daley GQ, Izsvák Z, Löwer J, Löwer R. Retrovirology. 2013 Oct 24;10:115. Human endogenous retrovirus K (HML-2) RNA and protein expression is a marker for human embryonic and induced pluripotent stem cells. doi: 10.1186/1742-4690-10-115. PMID: 24156636 Free PMC article.

(3) Dembny P, Newman AG, Singh M, Hinz M, Szczepek M, Krüger C, Adalbert R, Dzaye O, Trimbuch T, Wallach T, Kleinau G, Derkow K, Richard BC, Schipke C, Scheidereit C, Stachelscheid H, Golenbock D, Peters O, Coleman M, Heppner FL, Scheerer P, Tarabykin V, Ruprecht K, Izsvák Z, Mayer J, Lehnardt S. JCI Insight. 2020 Apr 9;5(7):e131093. Human endogenous retrovirus HERV-K(HML-2) RNA causes neurodegeneration through Toll-like receptors. doi: 10.1172/jci.insight.131093. PMID: 32271161 Free PMC article.

Contribution of endogenous transposable element derived sequences to the human specific features of placentation and pregnancy disorders

Transposable elements (TEs), including endogenous retroviruses, are discrete segments of DNA that had the distinctive ability to move and replicate within genomes across the tree of life. The evolutionary success of TEs is powerfully underscored by the finding that about 60% of the human genome is TE-derived. TEs accumulate inactivating mutations over evolutionary time and give rise to a genomic fraction, often referred as ’junk DNA’. Indeed, the vast majority of these sequences is not essential to the host. Nevertheless, the impact of TEs is underestimated. First, TEs have been markedly contributed to evolutionary processes. 

Placentation is an evolutionary young process with several human specific features. of trophoblast differentiation and invasion by providing regulatory sequences long non-long RNAs or even novel genes. The hypothesis is that the dysfunction of these processes might contribute to certain human specific pregnancy disorders, including preeclampsia. Preeclampsia (PE) is a complex and common human-specific pregnancy syndrome associated with placental pathology. The human-specificity provides both intellectual and methodological challenges, lacking a robust model system. Given the role of imprinted genes in human placentation and the vulnerability of imprinted genes to loss of imprinting changes, there has been extensive speculation that imprinted genes are involved in PE. We have shown the evidence that disturbed imprinting contributes to PE {}. Importantly, the suppression of transposable elements and the regulation of genomic imprinting share several features.

My laboratory is engaged in deciphering the biological function of human endogenous retrovirus H (HERVH)-derived long noncoding (lnc)RNAs (doi: 10.1038/nature13804; doi: 10.1002/bies.201500096; doi: 10.1038/nprot.2016.016). We also have a long-term interest in understanding the human pathology of preeclampsia (PE) (doi: 10.1161/CIRCULATIONAHA.117.028110).

HERVH-derived lncRNAs are expressed in pluripotent stem cells during early embryogenesis and, are involved in regulating pluripotency. The HERVH-derived (> 70 %) lncRNA, UCA1, by contrast, is expressed in the progenitor cells of the trophoectoderm (pre-TE) (unpublished) in the developing embryo. Currently, its biological function is unknown. In addition to physiological conditions, pathologic UCA1 upregulation has been observed in urothelial cancer (hence the name-urothelial cancer associated 1, UCA1) and in the placenta of PE patients. In this project, we aim at deciphering the cellular function of the (lnc)UCA1 in healthy pregnancy and its role in PE. In addition, while, UCA1 is not detectable in normal pregnancy, it is secreted into the blood of PE patients, indicating that UCA1 might be established as a valuable biomarker of PE pregnancy. This, project applies a system biological approach. The project is also in collaboration with clinicians.

Deciphering the molecular function of the HARBI1 and NAIF1 transposon-derived genes

Previously, we have reconstructed components of the Harbinger3_DR transposon in zebrafish (1), including a transposase and a second, transposon-encoded protein that has a Myb-like trihelix domain. The reconstructed Harbinger transposon shows efficient cut-and-paste transposition in human cells and preferentially inserts into a 15-bp consensus target sequence (1).

Harbi1 and Naif1 are evolutionary conserved genes in vertebrates. They have been co-opted of an ancient PIF/Harbinger transposon in a common ancestor of jawed vertebrates ~500 MY ago. Evolutionary conservation of Harbi1 and Naif1 implies that they have been under selection for important cellular functions. Curiously, their phylogenetic relationship as well as protein-protein interaction suggests a special co-evolution resulted in a dual co-option of PIF/Harbinger transposons in the in the same molecular pathway.

The human HARBI1 (Harbinger Transposase Derived 1) transposase-derived protein has a potential nuclease activity, whereas the Nuclear Apoptosis Inducing Factor 1 (NAIF1) contains a Myb-like trihelix domain, and has been implicated in apoptotic functions. Our preliminary data suggest that NAIF1 via protein-protein interaction promotes nuclear import of HARBI1 that binds certain genomic sites. Currently, the role(s) of these two genes remains enigmatic.

Diseases associated with HARBI1 include Hereditary Breast Ovarian Cancer Syndrome. Gene Ontology (GO) annotations related to this gene include hydrolase activity, acting on ester bonds and nuclease activity. SNPs in HARBI1 are detected in Schizofrenia, autism.

In this project we leverage various in vitro assays, genome engineering, genome-wide ChIP, transcriptional profiling and proteome analyses to understand and functionally annotate these genes and the genetic networks they regulate. The project will greatly contribute to our understanding of the mechanisms and roles of TEs as an important force in the creation of genetic novelty.

(1) Ludivine Sinzelle  1 Vladimir V KapitonovDawid P GrzelaTobias JurschJerzy JurkaZsuzsanna IzsvákZoltán Ivics PMID: 18339812;PMCID: PMC2290759



Previous MDC MSCA fellows


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