• Alumni

Daniel Swan

Head of Platforms and Pipelines


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I’ve been embroiled in genomics for over twenty years in academia and the private sector, and have managed bioinformatics groups and core facilities, although at the very start of my scientific career I started off at the lab bench. In that time I‘ve seen DNA sequencing evolve from hand-poured, acrylamide radioactive gels to high-throughput NGS technologies. Because of my background my interests extend everywhere from synthetic biology to genomics, bioinformatics to lab automation, from clinical to crop genetics and microbes to metagenomes. I’ll always have a soft spot for developmental biology from my PhD and early post-doc days.

My role at EI was to oversee our largest group - ‘Platforms and Pipelines’. They enabled all of EI’s high-throughput genomics projects across a huge breadth of organisms and our expertise in the lab is matched by that of our dedicated bioinformaticians and project managers. Together with our colleagues in Scientific Computing we delivered the BBSRC National Capability in Genomics providing access to techniques, platforms and expertise to the BBSRC community and beyond. Extensive, well-resourced labs allowed us to apply multiple sequencing platforms, whole genome optical mapping and single cell technologies to deliver rapid, high-quality genomics data and analysis. The lab works closely with the Technical Development Group at EI, and also administers the DNA Foundry Facility at the Norwich Research Park, a high-throughput lab for generating synthetic biology constructs.


The supposed tumor suppressor gene WWOX is mutated in an early lethal microcephaly syndrome with epilepsy, growth retardation and retinal degeneration.

G Abdel-Salam, M Thoenes, H H Afifi, F Körber, D Swan and H Jörn BolzEmail author. Orphanet Journal of Rare Diseases 20149:12. DOI: 10.1186/1750-1172-9-12©  Abdel-Salam et al.; licensee BioMed Central Ltd. 2014. Published: 23 January 2014.

A mutation in the 5'-UTR of IFITM5 creates an in-frame start codon and causes autosomal-dominant osteogenesis imperfecta type V with hyperplastic callus.

O Semler, L Garbes, K Keupp, D Swan, K Zimmermann, J Becker, S Iden, B Wirth, P Eyse, F Koerber, E Schoenau, S K. Bohlander, B Wollnik, C Netzer. The American Journal of Human Genetics. Volume 91, Issue 2.

A CD4 T cell gene signature for early rheumatoid arthritis implicates interleukin 6-mediated STAT3 signalling, particularly in anti-citrullinated peptide antibody-negative disease.

A G Pratt, D C Swan, S Richardson, G Wilson, C M U Hilkens, D A Young, J D Isaacs. Annals of the Rheumatic Diseases 2012;71:1374-1381 doi:10.1136/annrheumdis-2011-200968

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