- 2006- present: Senior Lecturer, University of Sheffield
- 1999 - 2005: Junior Group Leader Hubrecht Laboratory, Utrecht, The Netherlands
- 1997 - 1999: Post-doctoral worker, D. StJohnston Lab, Wellcome/CRC Inst. Cambridge UK
- 1992 - 1997: PhD, C. Nüsslein-Volhard Lab. Max Planck Inst. für Entwicklungsbiologie, Tübingen, Germany
- 1986 - 1992 MSc. Wageningen Agricultural University, The Netherlands
Using the zebrafish as a genetic tool to study development and disease. We are interested in understanding the role of the patched genes in Hedgehog signaling. In addition, we have created a knockout for the von Hippel Lindau disease (VHL) gene and are interested in modeling VHL deficient cancers in zebrafish.
- My research group is part of the Bateson Centre
Activities and distinctions
- Invited teacher at regular EMBO courses at the MPI in Tübingen (recently also Sheffield)
- Presenter at open science days and public lectures in Utrecht/Wageningen
- International collaboration on TILLING with Hubrecht Laboratory Utrecht/Sanger Inst. Cambridge
- Invited speaker at: ZDM8, Boston, Aug 2015; Zebrafish PI Meeting Ein gedi 2014; BSDB meeting 2013; European zebrafish meeting Barcelona 2013
- Reviewer for: BBSRC, Development, FNRS, Swiss research council, Singapore, Hong-Kong and many others
- Savage AM, Mayo C, Kim HR, Markham E, van Eeden FJM, Chico TJA & Wilkinson RN (2016)
GENERATION AND CHARACTERISATION OF NOVEL TRANSGENIC ZEBRAFISH ALLOWING IN VIVO IMAGING OF ENDOTHELIAL CELL BIOLOGY.
ATHEROSCLEROSIS, 244, E10-E10.
- Greenald D, Jeyakani J, Pelster B, Sealy I, Mathavan S & van Eeden FJ (2015)
Genome-wide mapping of Hif-1α binding sites in zebrafish.
BMC Genomics, 16(1).
- Novodvorsky P, Watson O, Gray C, Wilkinson RN, Reeve S, Smythe C, Beniston R, Plant K, Maguire R, M. K. Rothman A, Elworthy S, van Eeden FJM & Chico TJA (2015)
klf2ash317 Mutant Zebrafish Do Not Recapitulate Morpholino-Induced Vascular and Haematopoietic Phenotypes.
PLOS ONE, 10(10), e0141611-e0141611. View this article in White Rose Research Online
- Elks PM, Renshaw SA, Meijer AH, Walmsley SR & van Eeden FJ (2015)
Exploring the HIFs, buts and maybes of hypoxia signalling in disease: lessons from zebrafish models.
Disease Models & Mechanisms, 8(11), 1349-1360.
- Njegic AM, Chico TJA, van Eeden FJ & Watson OJ (2015)
The effect of macrophage depletion on hypoxia signalling induced angiogenesis in zebrafish.
Atherosclerosis, 244, E8-E9.
- Elks PM, van der Vaart M, Walmsley SR, van Eeden FJ, Spaink HP, Meijer AH & Renshaw SA (2014)
Hypoxic signalling modulates neutrophil nitric oxide in a zebrafish tuberculosis model.
EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, 44, 12-12.
- Wilkinson RN, Jopling C & van Eeden FJ (2014)
Zebrafish as a model of cardiac disease.
Prog Mol Biol Transl Sci, 124, 65-91.
- Wilkinson RN & van Eeden FJ (2014)
The zebrafish as a model of vascular development and disease.
Prog Mol Biol Transl Sci, 124, 93-122.
- Elks PM, Brizee S, van der Vaart M, Walmsley SR, van Eeden FJ, Renshaw SA & Meijer AH (2013)
Hypoxia inducible factor signaling modulates susceptibility to mycobacterial infection via a nitric oxide dependent mechanism.
PLoS Pathog, 9(12), e1003789. View this article in White Rose Research Online
Full publications list
The zebrafish provides a powerful organism to model human development and disease. We are exploiting and developing the zebrafish, e.g. by creating such disease models, by using knockout technology like CRISPR, or by looking for chemicals that can modify disease-relevant phenotypes.
One of our current projects, models the human Von Hippel Lindau disease, caused by mutation of the VHL gene. VHL is a negative regulator of the Hypoxia Inducible Factor (HIF) signalling pathway, which is vital for development and survival of many tumours. However, this is not the only function of VHL and over the years numerous others have been identified. We found that in zebrafish, the functions of human VHL have been split over two genes, which we named vhl and vhl-like (vll).
Interestingly, we found that the fish vhl gene has an important role in HIF regulation, as mutants we made by reverse genetics show all hallmarks of an inappropriate hypoxic response under normoxic conditions. The role of vll was initially enigmatic, null mutants that we created in this gene were viable and fertile. However, using a unique and novel in vivo reporter for genome stability that we created, we discovered that the vll gene is important for maintaining genome stability, which is a major driver for tumour initiation. This is what we are currently trying to understand better.
Current collaborations: Sherif El-Khamisy (genome stability), Albert Ong (pkd2 model), Jane McKeating (Birmingham), Francesco Argenton (Padua) (both glucocorticoid-HIF interaction).