The Treeck Laboratory | The Cell Biology of Host - Pathogen Interactions
Lab Members
Moritz Treeck | Group Leader
Broadly speaking, I am really interested to understand how host- pathogen interaction works on multiple levels. The parasites we work with, Plasmodium falciparum and Toxoplasma gondii both evolved to excel at infecting and modifying host cells and a huge proportion of the proteins important for these processes are poorly characterized. I very much enjoy working with a team of talented and enthusiastic individuals in the lab to unravel the complexity of host pathogen interaction. Often this involves the development of new methods to overcome challenges. The scientific environment of the Gulbenkian Institute of Science (IGC) provides us with an outstanding intellectual environment and superbe technical support facilities.
Biography: I was born in the rainy city of Hamburg in northern Germany and I almost ended up as a lawyer. I prepared two applications, one for law and one for biology, and inserted one application blind-folded into the post-box. Law was still in my hands and I am thankful for this until the very day. Throughout my academic career I was interested in parasites and I have tried to attract as many as possible during my travels to Central America and South-East Asia. However, it was not until I met my future PhD advisor Tim Gilberger during a semester in Melbourne, Australia, where I got hooked working with malaria. I spent my PhD thesis at the Bernhard-Nocht Institute for Tropical Medicine in Hamburg, Germany, studying protein trafficking and invasion of red blood cells by the malaria parasite. After that I moved to John Boothroyd’s lab in Stanford, California to learn as much as I could about another really interesting parasite, Toxoplasma. After 4 years I returned to Europe to join the Francis Crick institute where I ran my lab for ~10 years before relocating to the Gulbenkian Institute of Science where outstanding science and sunshine meet (almost) every day!
Francesca Torelli | Post-doctoral Researcher
What are the common and specific tools different Toxoplasma strains use to succeed in infection? Toxoplasma secretes a large number of proteins that mediate adhesion and invasion, establishment and defence of the parasitophorous vacuole, and influence various host cell pathways. However, most of these secreted proteins have unknown functions. I will be using our arrayed CRISPR library with both in vitro and in vivo selection methods to identify which of those proteins is important for Toxoplasma's success to establish an infection. Furthermore, by performing the screen on strains that differ in virulence, I will identify which of these virulence factors are generic and which are strain-specific. My position as post-doctoral fellow is currently funded by German Research Foundation (DFG).
Francesca completed her PhD in the Seeber lab at the Robert Koch Institute in Berlin, working on the resistance mechanisms of wild rodents to Toxoplasma infection. In future work she aims to explore tolerance mechanisms of parasites to host immune responses.
Francesca Torelli
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Toxoplasma effectors across different strains
Stephanie Nofal | Wellcome Trust Early Career Fellow
How do P. falciparum gametocytes remodel their host cell?
Gametocytes are the only stage of the malaria lifecycle that can be transmitted from humans to mosquitos to sustain disease transmission. Prior to being taken up by mosquitos, immature gametocytes sequester to the bone marrow where they extensively remodel the host cell in which they reside. However, the parasite effectors responsible for these critical remodelling events remain to be identified. I am currently investigating how exported parasite effectors are responsible for subverting the host cell.
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Stephanie completed her PhD in David Baker’s lab at the London School of Hygiene & Tropical Medicine, where she worked on cyclic nucleotide signalling and molecular motor function in the malaria parasite.
Stephanie Nofal
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Gametocyte exported effectors required for host cell remodelling
Hugo Belda | Post-doctoral Researcher
What is the function of post-translational modification in host cell remodelling by Plasmodium falciparum?
P. falciparum exports a large number of proteins out into its host red blood cell. These proteins drive the transformation of red blood cells from oxygen-transporting cells with no nucleus and little of a typical cell’s internal machinery into a parasite-production facility that causes all of malaria’s most severe symptoms. We and others have found that many of these exported proteins are phosphorylated, but the kinases responsible are not currently known and - most importantly - the functional consequences are a mystery. I am using quantitative phoshoproteomic methods and am developing new genetic tools to try and figure out how P. falciparum uses post-translational modification to take over red blood cells and cause disease.
Hugo Belda​
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Function of post-translational modifications in host cell remodelling
Franziska Hildebrandt | Post- doctoral Researcher
How do Toxoplasma effector proteins reprogram the host cell?
Toxoplasma secretes a large number of effector proteins into its host cell which inhibit immune responses to the parasite and reprogram host transcription, but how these effectors work in the context of the different parasite strain and host species pairings is not understood. I am using our recently developed Dual-PerTurbSeq to identify and characterise effector proteins that influence host reprogramming across the tree of life.
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Franziska obtained her PhD in the Ankarklev lab at the University of Stockholm studying transcriptonal responses in the liver to Plasmodium infection using spatial transcriptomics.
Franziska Hildebrandt
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Reprogramming of the host cell by Toxoplasma gondii
David Anaguano | Postdoc
How does P. falciparum sense its environment? Plasmodium falciparum parasites export a great number of proteins to remodel their host red blood cells (RBC’s). Among these modifications, RBC rigidification and cytoadhesion to endothelial cells are important to avoid parasite clearance. Some of the modifications are regulated by a family of exported atypical FIKK kinases, but how the kinases are regulated is not known. My work will focus on understanding the mechanisms some of these FIKK kinases use to sense changes in the environment, as well as investigating the role of some of the non-exported FIKK kinases.
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David obtained his PhD in the lab of Vasant Muralidharan, at the University of Georgia
Eloise Lockyer​
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Human-specific Toxoplasma effectors
David Jones | PhD Student
How does P. falciparum respond to fever? David is interested in how the parasite Plasmodium falciparum responds and reacts to conditions met in a human host. While we can culture P. falciparum efficiently in human red blood cells, we miss the host environment and predict that the important function of many genes cannot be uncovered under standard cell culture conditions. Dave has identified a controlled response to physiological fever temperatures on the post-translational level that is linked to increased cytoadhesion, the major cause for pathology of this parasite. He is using cell culture models to mimic fever and identify the key regulators of this response. In collaboration with researchers in Africa we want to link cell culture studies to observations in patients.
David Jones​
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Plasmodium falciparum response to fever
Gwendolin Fuchs | PhD Student
How are P. falciparum surface antigens trafficked in the host cytosol compartment? Upon invasion of the red blood cell, P. falciparum exports numerous proteins to the host cell surface to interact with its surroundings. This, for example, includes the key virulence factor PfEMP1 which mediates cytoadhesion to endothelial cells preventing splenic clearance of the infected cell. Key structures of protein export like Maurer’s Clefts and the translocon PTEX are well characterised, however, it remains unclear how surface antigens are trafficked in the host cytosol compartment. I am using a proximity labelling approach to identify cytosolic proteins involved in the trafficking of different surface antigens.
Gwendolin Fuchs
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Trafficking of antigens to the surface of Plasmodium falciparum-infected cells
Ana Matias | PhD Student
How can Toxoplasma subvert the host cytoskeleton?
After invasion of a host cell, Toxoplasma’s vacuole is surrounded by host microtubules. This phenotype seems to be driven by the parasite. However, how and why the parasites surrounds itself with host microtubules is not clear. My goals are to find the Toxoplasma effector(s) responsible for this ability to subvert the host microtubule cytoskeleton, and to explore how Toxoplasma benefits from it.
Ana Matias​
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Subversion of host cell cytoskeleton by Toxoplasma gondii
Diogo Fonseca | Post-doctoral Researcher
How does Toxoplasma modulate host immune responses to favour parasite dissemination?
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Immune cells release key soluble mediators that initiate inflammation and orchestrate the immune response upon infection. These chemical messengers trigger a series of events including the recruitment of specialised immune cell types into infected sites, and the activation of molecular antimicrobial mechanisms, to ultimately restrict pathogens and curtail infection. Toxoplasma-infected immune cells alter their behaviour at a cellular and secretory level as a consequence of infection. How these changes affect local and systemic immune responses, and how this benefits the parasite is poorly understood. I leverage on several newly identified Toxoplasma effector proteins that alter host cell transcription to investigate this, using in vivo and ex vivo models of toxoplasmosis.
Diogo completed his PhD in Immunology at Selinda Orr’s and Phillip Taylor’s Lab at Cardiff University, where he assessed how clinically relevant fungal pathogens affect the host immune response during infection.
Diogo Fonseca​
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Changes in immune cell function following infection by Toxoplasma parasites
Nuno Carmo | Lab Manager
How do we provide the best working environment in the lab?
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The complexity of host-pathogen interactions requires a multidisciplinary approach, advanced techniques and relevant models. In our team, we explore Plasmodium falciparum and Toxoplasma gondii, making our work doubly fascinating.
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As a Lab Manager, Nuno supports and is committed to facilitating scientific excellence, safety, and efficiency through our shared passion for discovery and innovation.
Nuno completed his PhD at the University of Lisbon working on Mycobacterium tuberculosis host-pathogen interaction.
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Nuno completed his PhD at the University of Lisbon working on Mycobacterium tuberculosis host-pathogen interaction.
Nuno Carmo
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Making the lab run smoothly!
Carolina Albino | Lab research scientist
How does Toxoplasma alter host cells?
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Carolina is interested in how Toxoplasma alters host cells by secreted proteins. Specifically, she is interested in the essential aspects of host-cell remodling.
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Carolina completed her Master's degree at the LHSTM in London
Nuno Carmo
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Making the lab run smoothly!
Catarina Rosa | Post-doctoral Researcher
How does Toxoplasma manipulate the host cell across its life cycle?
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A large body of evidence has highlighted the ability of Toxoplasma acute stages – the tachyzoites - to export effector proteins which modulate various host signaling pathways to favor intracellular survival. Recently, our lab developed a method that couples a pooled CRISPR-Cas9 knockout screening with dual host–parasite single-cell RNA-sequencing, termed Dual-perturb-seq. It allowed to identify, in a high throughput fashion, novel tachyzoite effectors and their role in host cell reprogramming. However, interactions between other stages of Toxoplasma complex life cycle and its host cell remain largely understudied. I aim to expand the application of the Dual-Perturb-seq to other parasite stages and uncover less explored host-parasite interactions!
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Catarina completed her PhD at the in Jessica Bryant's lab at the Pasteur Institute in Paris.
Catarina Rosa
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Host cell subversion during the chronic stages of toxoplasmosis
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Christian Gnann | Post-doctoral Researcher
How does heteregeneity of host cells affect infection outcome?
Single-cell heterogeneity is an evolutionary conserved mechanism in cell biology. Cells exist in a variety of cellular states defined by differences in for example their cell cycle position, microenvironment, morphology as well as their metabolic and signalling potential. Interestingly, toxoplasma infection and potential clearance vary between individual host cells. The reasons for this remain unknown but we suggest a role of the cellular state at the time of infection on the outcome of infection. Therefore, we aim to characterize the interplay between the parasite and the host cell in heterogenous single-cell populations using high throughput imaging screens.
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Chris complete his PhD in Emma Lundberg's lab at the KTH Royal Institute of Technology.
You! | Postdoctoral position
Do you want to study how parasites remake their host cells?
We are frequently looking for postdoc candidates with an interest in host-parasite interactions. To join the lab outside open calls it is important to get in touch well in advance before you would like to join.
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Send me a CV and short letter describing the research you would like to perform in our team to start a conversation.
