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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.

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

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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