Call Autumn 2020 - Proposed PhD Projects
- Call closed -
Thank you for your interest in our graduate school. Here, you can find all proposed PhD projects for the autumn 2020 IMPRS-IDI call. The application platform will open on April 22nd and close on May 24th, 2020.
We are recruiting up to 7 PhD students for the International Max Planck Research School for Infectious Diseases, Immunology and Pathogenomics in this call. Our graduate school offers:
- outstanding research and training opportunities with access to state-of-the-art facilities
- an excellent scientific network - our faculty members are internationally recognized scientists affiliated with renowned research institutes and universities in Berlin and around the world
- a graduate school program with flexible curriculum structure and training courses and lectures on scientific topics as well as technical and complementary skills
- a stimulating international and multi-disciplinary research environment on a thriving campus in the heart of Berlin
We are looking for highly motivated candidates of all nationalities who are truly committed to research from the following disciplines:
- Infection biology
- Molecular and cell biology
- Evolutionary Biology
- Computer Science
Applicants must hold an excellent M.Sc. degree or similar. For more details, please see the individual project descriptions below.
Interested in joining us? For further information on the process and to apply, please visit our application page.
The following PhD projects are available and will start from December 2020 on, through 2021:
In vivo Imaging and Manipulation of the Tuberculous Granuloma
Tuberculosis kills more people than any other infectious disease worldwide. The goal of this project is to visualize, understand, and perturb the signaling events that drive formation of the granuloma, the central structure of tuberculosis infection. Using a unique zebrafish model of tuberculosis, the project will leverage genetic reporters, high-resolution in vivo imaging, and new genetic tools to understand the signaling events and immune cell populations that mediate this critical structure in mycobacterial infection. Through collaborations we will validate and extend these studies to samples from tuberculosis patients and mammalian tuberculosis models.
Proposed PhD project: Deciphering pathogen factors involved in and host immune responses to co-infections using Drosophila melanogaster as a model
There is a growing appreciation that many infections involve two or more microbes and therefore are polymicrobial either in origin or in manifestation. Importantly, an immune response to one pathogen can affect the response to another pathogen that happened to infect the same host. However, the mechanisms of how the host detects, responds, and eliminates multiple pathogens that infect the same host at the same time are poorly characterized. Also, microbes within polymicrobial infections often display synergy, characterized by prolonged pathogen persistence in the infection site and/or increased disease severity. Currently, little is known about the microbial factors that promote synergistic interactions and increased disease severity. The goals of this project are to examine in detail the cellular and molecular mechanisms of the host immune response to co-infections and to identify microbial factors that promote co-infection synergy, using Drosophila as a model.
Project 1 - Deep evolutionary history of microbial pathogens using ancient DNA
Uncovering the deep evolutionary history of infectious microbes intertwined with human prehistory is critical for our understanding about disease emergence and the development of successful strategies for prevention and intervention. Ancient DNA provides a unique resource that allows to trace the evolution of microbial pathogens directly back in time. Using ancient DNA and big data repositories combined with evolutionary inference methods, the project aims to reconstruct genomes from infectious pathogens thousands of years old, which we leverage to understand the timing and genetic changes associated with disease emergence and spread.
We are looking for a motivated student who has a background in bioinformatics, genetics, computer science, microbiology, evolutionary biology or neighboring disciplines. Knowledge in programming (python, bash, R etc.) as well as high-throughput sequencing is strongly desired. The interdisciplinary nature of the project requires a keen interest in archaeology, anthropology and human history.
The human microbiome comprises trillions of bacteria that generate billions of mutations every day – an enormous adaptive potential. While poorly understood, commensal bacteria might exploit this adaptive potential to translocate into new niches of the human microbiome where they contribute to disease. Using whole-genome sequencing cultured bacterial isolates from clinical samples combined with computational inference methods the project aims to reconstruct the within person evolution of commensal bacterial species during the initiation and progression of infection, which can provide new strategies for intervention or treatment.
We are looking for a motivated student to work at the interface of microbiology (incl. robotic automation) and computational genetics in our new lab. The ideal candidate has a background in microbiology, genetics, bioinformatics, evolutionary biology or neighboring disciplines. Knowledge/interest in wet lab microbiology, robotic automation, and programming (python, bash, R etc.) is strongly desired.
The role of endosome positioning on Toll-like receptor signaling
Our immune system utilizes a variety of pattern recognition receptors to detect pathogenic features and respond to infection. In my lab, we seek to understand how nucleic acid-sensing Toll-like receptors manage to successfully discriminate between foreign and self-derived DNA/RNA, in order to avoid self-recognition and autoimmunity. A major mechanism to limit self-recognition is their intracellular localization in late endosomes, which are poorly accessed by host-derived nucleic acids from the extracellular space. Endosomes are very motile organelles, and their correct positioning within the cell is relevant for many biological processes and vital to health. In this project you will explore how altered endosome positioning will affect immune sensing and signaling of nucleic acid-sensing TLRs and how this relates to autoimmunity. You will learn how to work with primary cell culture systems and mouse models, and use Crispr/Cas9-genome editing, advanced imaging and biochemical techniques.
The molecular mechanisms driving adaptive properties of innate lymphocytes (NK cells)
Natural Killer (NK) cells are a subset of innate lymphoid cells, playing a crucial role in the early defense against intracellular pathogens, especially herpesvirus. It has been shown that during mouse and human cytomegalovirus (CMV) infection, defined NK cell subsets undergo antigen-driven expansion and persist over time, partially resembling anti-viral adaptive responses. We have demonstrated that human adaptive NKG2C+ NK cells differentially recognize distinct HCMV strains in a peptide-dependent manner, thus identifying the long sought „antigen“ inducing these expansions. Building on these findings, we now aim to combine flow cytometry, single-cell RNA-, single-cell ATAC-sequencing, as well as in vitro and in vivo functional assays already established in the lab in order to decipher the imprints CMV infection has on the NK cell repertoire and differentiation and to understand how these characteristic expansions of adaptive NK cells are induced and maintained. Moreover, we aim to optimize our newly patented peptide-based vaccine in order to expand NKG2C+ NK cells and boost their anti-viral and anti-tumor activity in vitro and in vivo. This project will enable us to gain insights on the molecular mechanisms driving adaptive properties of innate lymphocytes and to exploit their specificity to potentiate anti-viral and anti-tumor immunity.
Mechanisms of Neutrophil Extracellular Trap formation
Neutrophils are the first line of defense of the cellular innate immune system. Upon stimulation, these cells undergo a reactive oxygen dependent form of cell death that results in the release of NETs. NETs, or Neutrophil Extracellular Traps, are made of modified chromatin and specific neutrophil proteins. NETs probably evolved to combat microbes and also stimulate other cells of the immune system and initiate coagulation. The project will investigate the mechanism of NET formation and the function of NETs in diseases.