Edinburgh Research Explorer

Nick Hastie

(Former employee or visitor)

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Willingness to take PhD students: Yes

Education/Academic qualification

Doctor of Philosophy (PhD), University of Cambridge
The roel of the nucleus in influenza virus replication
Bachelor of Science, University of Liverpool

Professional Qualifications

Honorary Doctor of Science


Professor Nick Hastie is Director of the MRC Human Genetics Unit and the Institute of Genetics and Molecular Medicine in Edinburgh.  Nick Hastie was born in North Wales, where he attended Colwyn Bay Grammar School.  He went on to receive an honours degree in Medical Microbiology at Liverpool University.  Following that, he carried out his PhD work on Influenza Replication at Cambridge University.  Since then, he has worked in many areas including gene expression, genome organisation (including telomeres) and protein evolution.  He has had a long-term interest in human developmental genetics, concentrating on the childhood kidney cancer, Wilms’ tumour.  Over the past few years Professor Hastie has also become heavily engaged in a major population genetics project to identify genetic risk factors for common disease.  Nick Hastie was an International Scholar of the Howard Hughes Medical Institute; he chaired the General Motors Cancer MOT Awards


Committee and sat on the General Motors Assembly.  He is Chairperson of a number of Scientific Advisory Boards, including (until 2010) that for the Sanger Institute and the Wellcome Trust Centre for Human Genetics.   He was European Editor of Genes & Development for a decade and currently sits on the Advisory Boards of Genes & Development and PLoS Biology.  Professor Hastie is a Fellow of the Royal Society, a Fellow of the Royal Society of Edinburgh, a Member of EMBO and was awarded a CBE for Services to Science in 2006.  He was awarded the Medal of the Genetics Society of the UK in 2008.  In his spare time Nick likes to do body combat, sing, listen to music, read, garden and watch movies and rubbish on television.

My research in a nutshell

My laboratory focusses on the mechanisms underlying major diseases and pathologies arising from loss of function of the Wilms tumour gene Wt1. In humans mutation of this gene may lead to paediatric kidney cancer, major kidney disease, gonadal dysgenesis and heart disease. We have shown Wt1 is a key regulator of the balance between mesenchymal and epithelial states during development.

From a mechanistic perspective we have shown that in the developing kidney Wt1 is required for the mesenchyme to epithelial transition(MET) that leads to the formation of nephrons whereas in the developing heart it is essential for the reverse process, the EMT required for generating coronary vascular progenitors from the epicardium. Wt1 achieves this dichotomous role by activating genes required for epithelialisation in the kidney while repressing mesenchymal genes. Conversely in the epicardium it represses the same epithelial genes while activating the mesenchymal ones. We have shown the mechanism of action or repression involves chromatin domain switching which we call flip-flop.

Our recent studies also show that Wt1 is also a major regulator of adult tissue homeostasis and repair. Deletion of the gene in adult mice leads to rapid failure of kidney function, atrophy of the spleen and pancreas and widespread fat and bone loss. We hypothesise that Wt1 may be exerting many of its functions through controlling mesenchymal stem/progenitor populations. In submitted work we have shown for the first time that the bad, visceral fat and good subcutaneous fat have different origins in development and the adult and that Wt1 uniquely identifies visceral fat progenitors and their source.

In addition to acting as a transcription factor Wt1 binds to RNA and interacts with RNA processing complexes. We have unpublished evidence that Wt1 associates with the miRNA processing machinery and binds directly to mRNA- miRNA hybrids. We are using recently developed techniques to investigate the Wt1 RNA interactome and the functional significance of these interactions.

Highlighted research outputs

  1. Wilms' tumour 1 (WT1) in development, homeostasis and disease

    Research output: Contribution to journalReview articlepeer-review

  2. Wilms Tumor 1b defines a wound-specific sheath cell subpopulation associated with notochord repair

    Research output: Contribution to journalArticlepeer-review

  3. Transcription factor, Wilms’ Tumour 1 regulates developmental RNAs through 3’ UTR interaction.

    Research output: Contribution to journalArticlepeer-review

  4. Visceral and subcutaneous fat have different origins and evidence supports a mesothelial source

    Research output: Contribution to journalArticlepeer-review

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