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Genome Engineering Facility

The WIMM Genome Engineering Facility is a central service open to the Oxford research community.

We assist researchers in experimental planning and assembly of reagents for the generation of tailor-made experimental model systems. We are highly experienced in the generation of engineered immortalized cell lines, primary cells and stem cells of different origins, and provide a service platform for the generation of transgenic models.

Meet the team

We mainly apply the CRISPR/Cas9 technology for targeted in vivo mutagenesis. Our portfolio ranges from simple NHEJ-based knockout to defined exon excision, from modelling of simple SNPs to insertion of complex knock-in alleles, all in a variety of model systems. In addition, we assemble custom DNA-based targeting constructs in plasmid or BAC format, e.g. as donors in Cas9-mediated HDR experiments or as transgenic constructs for pronuclear injection. For mouse models requiring insertion of larger cassettes, we tend to suggest using Cas9-assisted homologous recombination in embryonic stem cells. The Cas9-assisted targeting is done in collaboration with the MRC WIMM Transgenic Core Facility and the WTCHG transgenics core.

We are not exclusive to MRC WIMM research groups and offer our services also to researchers in other departments of the University of Oxford. If you have a project in mind and would like to discuss the details, require advice on genome engineering issues and molecular cloning technology, or need a detailed quote for your specific project, please feel free to contact us at any time to find out how we can help.

Selected Publications

Unexpectedly high levels of inverted re-insertions using paired sgRNAs for genomic deletions. Blayney et al., (2020), Methods and Protocols, doi: 10.3390/mps3030053.

RIG-I plays a dominant role in the induction of transcriptional changes in Zika virus-infected cells and protects from virus-induced cell death. Schilling et al., (2020), Cells, doi: 10.3390/cells9061476.

SAMHD1 Limits the Efficacy of Forodesine in Leukemia by Protecting Cells against the Cytotoxicity of dGTP. Davenne et al., (2020), Cell Reports 31, doi: 10.1016/j.celrep.2020.107640

Mouse model of the human serotonin transporter-linked polymorphic region. Piszczek et al., (2019), Mamm Genome (11-12), p. 319-328.

Polyamines Control eIF5A Hypusination, TFEB Translation, and Autophagy to Reverse B Cell Senescence. Zhang et al., (2019), Molecular Cell, 76, 1-16.

Microhomologies are prevalent at Cas9-induced larger deletions. Owens et al., (2019), Nucleic Acids Research, doi: 10.1093/nar/gkz459.

Colonic epithelial cell diversity in health and inflammatory bowel disease. Parikh et al., (2019), Nature 567, pages 49-55 

SCL/TAL1 cooperates with Polycomb RYBP-PRC1 to suppress alternative lineages in blood-fated cells. Chagraoui et al., (2018), Nature Communications, 9, doi: 10.1038/s41467-018-07787-6. 

Infection with a Brazilian isolate of Zika virus generates RIG-I stimulatory RNA and the viral NS5 protein blocks type I IFN induction and signaling. Hertzog et al., (2018), European Journal of Immunology, doi: 10.1002/eji.201847483 

Genetic abrogation of immune checkpoints in antigen-specific cytotoxic T-lymphocyte as a potential alternative to blockade immunotherapy. Zhang C. et al, (2018), Scientific Reports, 8 (5549)

Lack of Truncated IFITM3 Transcripts in Cells Homozygous for the rs12252-C Variant That is Associated With Severe Influenza Infection. Makvandi-Nejad S. et al, (2018), Journal of Infectious Diseases, 217, 257-262

Autophagy-dependent generation of free fatty acids is critical for normal neutrophil differentiation. Riffelmacher T. et al, (2017), Immunity, 19, 466 - 480

Editing an α-globin enhancer in primary, long-term repopulating human hematopoietic stem cells: a new approach to therapy for β-thalassemia. Mettananda S. et al, (2017). Nature Communications, 8, doi: 10.1038/s41467-017-00479-7

Internal user?

Detailed information on services, technology platforms and advice on genome engineering procedures can be found in our intranet.

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