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GENEtic DiSsection of Innate Immune Sensing and Signalling

Total Cost €


EC-Contrib. €






 GENESIS project word cloud

Explore the words cloud of the GENESIS project. It provides you a very rough idea of what is the project "GENESIS" about.

precision    mechanisms    viral    genes    platform    signalling    screens    format    imminent    invested    throughput    antiviral    downstream    intracellular    dissect    members    employing    hypotheses    receptor    detecting    obtain    molecules    arrayed    immune    roles    machinery    powerful    grown    cooperativity    epistatic    efforts    microbederived    perturbation    mainly    elucidate    self    engineering    cells    sensed    perform    questions    explore    relationships    host    systematically    generate    function    murine    validate    gene    pertinent    acids    effector    microbial    initiate    opportunity    genesis    individual    vertebrates    unprecedented    broad    validation    eliminate    kinome    render    nucleic    detect    receptors    innate    breadth    orchestrating    tackle    redundancy    models    considerable    context    genetic    genome    human    functional    dna    threat    polyclonal    expression    exploring    knockout    rna    infection    considerably    causes    activation    acid    sensing    events    applicable    altogether    combine   

Project "GENESIS" data sheet

The following table provides information about the project.


Organization address
postcode: 80539

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country Germany [DE]
 Project website
 Total cost 1˙970˙000 €
 EC max contribution 1˙970˙000 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2014-CoG
 Funding Scheme ERC-COG
 Starting year 2015
 Duration (year-month-day) from 2015-10-01   to  2020-09-30


Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 


 Project objective

In vertebrates, a receptor-based, innate sensing machinery is used to detect the presence of microbederived molecules or the perturbation microbial infection causes within the host. In the context of viral infection, non-self nucleic acids are sensed by a set of intracellular receptors that upon activation initiate broad antiviral effector responses to eliminate the imminent threat. Over the past years our understanding of these processes has considerably grown, mainly by employing murine knockout models. Recent advances in genome engineering now provide the opportunity to knockout genes or even to perform functional genetic screens in human cells, providing a powerful means to validate and generate hypotheses. We have developed a high-throughput genome targeting and validation platform that allows us to tackle large-scale loss-of-function studies both at a polyclonal as well as an arrayed format. In addition, we have invested considerable efforts to render this technology applicable to study innate immune sensing and signalling pathways in the human system. GENESIS will combine these efforts to tackle pertinent questions in this field that could not have been addressed before: We will systematically dissect known nucleic acid sensing pathways in the human system to explore their unique roles, cooperativity or redundancy in detecting non-self nucleic acids. We will perform polyclonal, genome-wide loss-of-function screens to elucidate signalling events downstream of intracellular DNA and RNA sensing pathways and their roles in orchestrating antiviral effector mechanisms. Moreover, in a large-scale perturbation study, we will specifically address the role of the kinome in antiviral innate immune signalling pathways, exploring the role of its individual members and their epistatic relationships in orchestrating gene expression. Altogether, these studies will allow us to obtain insight into innate immune signalling pathways at unprecedented precision, depth and breadth.


year authors and title journal last update
List of publications.
2017 Moritz M Gaidt, Veit Hornung
Alternative inflammasome activation enables IL-1β release from living cells
published pages: 7-13, ISSN: 0952-7915, DOI: 10.1016/j.coi.2016.10.007
Current Opinion in Immunology 44 2019-06-06
2017 Sarah Kim-Hellmuth, Matthias Bechheim, Benno Pütz, Pejman Mohammadi, Yohann Nédélec, Nicholas Giangreco, Jessica Becker, Vera Kaiser, Nadine Fricker, Esther Beier, Peter Boor, Stephane E. Castel, Markus M. Nöthen, Luis B. Barreiro, Joseph K. Pickrell, Bertram Müller-Myhsok, Tuuli Lappalainen, Johannes Schumacher, Veit Hornung
Genetic regulatory effects modified by immune activation contribute to autoimmune disease associations
published pages: , ISSN: 2041-1723, DOI: 10.1038/s41467-017-00366-1
Nature Communications 8/1 2019-06-06
2017 Moritz M. Gaidt, Thomas S. Ebert, Dhruv Chauhan, Katharina Ramshorn, Francesca Pinci, Sarah Zuber, Fionan O’Duill, Jonathan L. Schmid-Burgk, Florian Hoss, Raymund Buhmann, Georg Wittmann, Eicke Latz, Marion Subklewe, Veit Hornung
The DNA Inflammasome in Human Myeloid Cells Is Initiated by a STING-Cell Death Program Upstream of NLRP3
published pages: 1110-1124.e18, ISSN: 0092-8674, DOI: 10.1016/j.cell.2017.09.039
Cell 171/5 2019-06-06
2016 Jonathan L. Schmid-Burgk, Klara Höning, Thomas S. Ebert, Veit Hornung
CRISPaint allows modular base-specific gene tagging using a ligase-4-dependent mechanism
published pages: 12338, ISSN: 2041-1723, DOI: 10.1038/ncomms12338
Nature Communications 7 2019-06-06
2016 Jonathan L. Schmid-Burgk, Dhruv Chauhan, Tobias Schmidt, Thomas S. Ebert, Julia Reinhardt, Elmar Endl, Veit Hornung
A Genome-wide CRISPR (Clustered Regularly Interspaced Short Palindromic Repeats) Screen Identifies NEK7 as an Essential Component of NLRP3 Inflammasome Activation
published pages: 103-109, ISSN: 0021-9258, DOI: 10.1074/jbc.C115.700492
Journal of Biological Chemistry 291/1 2019-06-06

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