UCL @ the Crick


Crick Attachments

One important way to help fulfil the Crick's Discovery Without Boundaries strategy is to bring together researchers from the Crick laboratory and its partners to undertake new interdisciplinary collaborations.

To help achieve this, university staff from 32 research groups have already been selected through two recruitment rounds and are moving into the Crick as secondments, satellite groups or sabbaticals. These arrangements are known as attachments to reflect their highly flexible nature.

Types of Attachments

Secondments: A group leader (often in the early stages of their career) and all or part of their laboratory transfer to the Crick for three to six years

Satellites: Groups of one to three researchers from a university group transfer to the Crick for an agreed period (usually between one to three years) and embed within a research group or STP to undertake specific collaborative projects. The PI will remain in their home institution

Sabbbaticals: A University group leader spends up to a year working in a Crick research group, typically learning new techniques or undertaking hands-on research


 Applications will be assessed on the quality of the proposed research and its multi-disciplinary nature, especially in the physical, mathematical and computational sciences, and in clinical translation. 

Consistent with the Crick's aim to create future science leaders, applications involving early career researchers are particularly encouraged. 

It is expected that projects will be externally funded. Applications where funding is not yet in place can be considered but selection will be contingent upon a successful grant application.

Current Attachments


Dr Paola Bonfanti
Photograph of Paola Bonfanti

Group size: 7

Start date: January 2017

Duration: 6 years

Research to be undertaken at the Crick: 

The main goal of our research is to understand and manipulate the function of human thymus, which is the primary lymphoid organ essential for the establishment of immune T cell competence and induction of self-tolerance.  

Our work brings a multidisciplinary approach by combining epithelial cell biology, novel tissue engineering technologies, and molecular analysis of T cell development. The outcome of this work will set the basis for novel clinical protocols for organ transplantation and immunodeficiency disorders.

Because of a broader interest in epithelial stem cell biology our group is also studying self-renewal and differentiation potency of human epithelial oesophageal cells with the aim of providing a functional and growing epithelium for a tissue engineering approach for neonatal atresia.

Finally, we are studying human pancreas development and building in vitro model systems to dissect fate and potency of pancreatic progenitors. 

Dr Paola Bonfanti's UCL profile 

Professor Sonia Gandhi

Photograph of Sonia Gandhi

Group size: 7

Start date: September 2017

Duration: 6 years

Research to be undertaken at the Crick:

The Gandhi laboratory for Neurodegeneration Biology is based at the Francis Crick Institute. Parkinson’s disease is a common devastating neurodegenerative disorder, that remains incurable due to our lack of understanding about its cause. Our research group studies the pathways that lead to the neuronal death in the human brain, so that we can finally understand when and how to intervene in this process.

Powerful genetic clues highlight protein aggregation, mitochondrial homeostasis, and inflammation to be causal in Parkinson’s disease. Harnessing the power of induced pluripotent stem cell technology to model human disease, we generate region specific human neurons and astrocytes to investigate these mechanisms. Our research focuses on how and why protein misfolding occurs in neurons, how impaired mitochondria leads to the development of disease and whether, and how, these processes are interdependent. In addition, we investigate the role of glia, and how interactions between neurons and glia may drive progression of neurodegeneration. 

Research in our group is highly collaborative and cross-disciplinary, integrating (i) single molecule and super resolution biophysical tools to complex human systems to resolve aggregation at nanoscale, (ii) single cell imaging of human induced pluripotent stem cells (iii) computational modelling and bioinformatic approaches to imaging, and transcriptomic and proteomic data in brain and cells.

Translation of scientific discovery to patient benefit is integral to our research vision. Our aim is that reverse translation from patient cells to disease mechanism, and forward translation from disease mechanism to drug discovery will ultimately lead to improved care.
Eukaryotic cells possess myriad strategies to mitigate diverse stressful stimuli. Upon stress, ribonucleoprotein (RNP) granules assemble into stress granules due to prion-like polymerization of RNA binding proteins (RBPs) together with RNAs.

Professor Gandhi's UCL profile

Professor Rickie Patani
Photograph of Rickie Patani

Group size: 10

Start date: September 2017

Duration: 6 years

Research to be undertaken at the Crick:

We study diseases of the nervous system, focusing on motor neuron disease (ALS) and dementia. In ALS, patients lose the ability to move, eat, speak and ultimately breathe. ALS is untreatable because we do not understand the underlying cause(s) of disease. In order to understand disease mechanisms, we use human stem cells generated from real patients. With over a decade of experience using this technology, we can now transform stem cells from patients into human nerve cells and, separately, their support cells (called glia). This approach allows us to determine the sequence of disease-related events within particular cell types. Our overarching goal is to identify precisely what goes wrong, when this begins and in which cell type. We specifically focus on how the following three factors contribute to nerve cell death in ALS:

  1. Messages called RNAs, which are made from our DNA blueprint
  2. Astrocytes, which are star-shaped cells that normally support nerve cells
  3. Ageing, which is the biggest risk factor for many neurodegenerative diseases including ALS

The more we understand about human neurological diseases using this approach, the more we will be able to therapeutically target underlying disease mechanisms. We ultimately wish to use this new information to benefit patients with untreatable neurological diseases.

Professor Patani's UCL profile

Professor Jernej Ule
Photograph of Jernej Ule

Group size: 10

Start date: August 2016

Duration: 6 years

Research to be undertaken at the Crick:

During our time at the Crick, we will study the structure of protein-RNA using new methods, crossing the boundaries of genomics, biophysics and computational biology to ask the following questions:

  1. What is the structure of regulatory protein-RNA complexes in neurons, and how does the structure instruct their function?
  2. How do the non-coding regulatory elements contribute to the processing and regulation of neuronal RNAs? Can mutations in these elements cause disease?
  3. Mutations that change the sequence of RNA-binding proteins can cause motor neuron disease. Do these mutations disrupt the dynamics of protein-RNA complexes, and what treatments could ameliorate this?
  4. How do protein-RNA complexes respond to cellular signals? In particular, how do they coordinate local translation in neuronal dendrites to regulate synaptic plasticity?

Professor Ule's UCL profile

Professor Saverio Tedesco
Picture of Saverio Tedesco

Group size: 6

Start date: January 2020

Duration: 6 years

Research to be undertaken at the Crick:

We are interested in understanding how skeletal muscle stem cells sustain tissue regeneration and how this process could be improved to develop therapies for incurable neuromuscular diseases such as muscular dystrophies.

We pioneered the use of human artificial chromosomes and induced pluripotent stem (iPS) cells for muscle gene and cell therapy, as well as human iPS cell-based platforms for complex neuromuscular disease modelling and tissue engineering. More recently, we have identified signalling pathways governing muscle cell fate plasticity and migration. Our overall goal is the clinical translation of these novel regenerative strategies into therapies for severe muscle diseases.

Our research programme at the Crick will focus on: 1) elucidating the cellular and molecular mechanisms underpinning muscle diseases; 2) generating high-fidelity in vitro models of neuromuscular diseases; 3) developing next-generation therapeutics for neuromuscular disorders. We are also teaming up with other Crick labs with common interests and complementary expertise to setup an innovative hub to develop human neuromuscular models.

Professor Tedesco's UCL profile

Professor Mariya Moosajee
Picture of Mariya Moosajee

 Group size: 5

Start date: January 2020

Duration: 3 years

Research to be undertaken at the Crick

Our research is focused on dissecting the molecular basis of genetic eye disease using multi-omic approaches such as whole genome sequencing, RNA-Seq, methylomics and metabolomics. In addition to undertaking detailed clinical studies to understand the natural history of these conditions in patients, in the lab we generate zebrafish disease models using CRISPR/Cas9 gene editing and human induced pluripotent stem cell derived retinal cells to further advance our knowledge of disease mechanisms. This permits the identification of potential therapeutic targets for development of treatment strategies and trial outcome measures for a wide range of inherited eye disorders.

At the Crick, we will be developing non-viral gene therapy, an alternative to conventional adeno-associated virus (AAV) delivery systems. Non-viral gene therapy has several advantages in that it can accommodate large genes of any size, it lacks viral components and therefore has less chance of evoking an immune response, and it remains episomal, thus reducing the risk of insertional mutagenesis. Together with Crick group leaders, we will use scaffold/matrix attachment region DNA vectors to optimise delivery into photoreceptors and retinal pigment epithelium, whilst exploring the innate intracellular immune response to the introduction of this foreign DNA to assess the safety and efficacy of this approach. 

Professor Moosajee's UCL profile

Professor Veronica Kinsler
Picture of Veronica Kinsler

Group size: 8

Start date: December 2019

Duration: 6 years

Research to be undertaken at the Crick

Somatic mosaicism is the result of single cell pathogenic variants and subsequent developmental expansion of the clone in the embryo and fetus. Solving the causes of these diseases has only really been possible over the last decade due to improvements in sequencing, and to better understanding of the patterns of mosaic disease.  The variants are frequently in key oncogenes, and the individuals only survive the dramatic developmental effects by being mosaic.  All our work is therefore not only applicable to childhood disease, but also to common cancers in the general population, from understanding the pathogenesis, to targeting treatments.

Our work at the Crick will exploit the knowledge we have gleaned in recent years to address three fundamental challenges:

1)    To understand the biology of why certain somatic variants occur more commonly in certain individuals;
2)    To analyse and model embryological patterns of cell development which have persisted due to the variants;
3)    To continue to develop highly targeted therapies for mosaic disorders.

Collaboration with key Crick group leaders Dr Julian Downward (Oncology Signaling Laboratory) and Dr Simon Boulton (DSB Repair Metabolism Laboratory) will bring expertise from different perspectives, leading ultimately to more profound biological insight, and to much needed translational advance. 

Professor Kinsler's UCL profile


Professor Joerg Albert
Photograph of Joerg Albert

Group size: 3

Start date: September 2019

Duration: 2 years

Research to be undertaken at the Crick:

Mosquitoes mate within swarms, where they use their complex ears to recognize the wing beats of mating partners. Despite the importance of this behaviour and its implications for mosquito control, the molecular and mechanical processes involved in mosquito partner recognition are poorly understood. 

At the Crick, we would like to shed some light on this significant topic by using the antennal ears of disease transmitting mosquitoes (primary focus on Anopheles, with Culex and Aedes as additional controls) to study mosquito hearing and acoustic communication. 

The work will focus on three key aspects: 

(i) the physiological roles (and mechanistic origins) of distortion products (DPs); 

(ii) the sensory ecology and neurobiology of biogenic amine (BA) signalling in the mosquito ear and 

(iii) the interrelation between mosquito auditory sensitivity and the circadian clock.

Professor Albert's UCL profile

Professor John Christodoulou
Picture of John Christodoulou

Group size: 2

Start date: June 2019

Duration: 3 years

Research to be undertaken at the Crick:

Proteins begin to fold co-translationally during biosynthesis on the ribosome. Our group use an integrated structural biology approach merging the unique advantages of NMR, cryoEM and computational approaches to report upon the dynamic process of protein folding processes where they begin – on the ribosome – and from in vitro to in vivo to develop a high-resolution comprehensive description of the co-translational protein folding landscape.

In particular, we have pioneered the use of NMR spectroscopy to study the co-translational folding process using ribosome–nascent chain complexes (e.g. Anaïs Cassaignau et al, NSMB 2016 and Chris Waudby et al, PNAS, 2018) and seek to advance this capability to study the protein dynamics of co-translational events in the cell at the Crick together with Dr Tom Frenkiel. Membrane proteins can insert into the lipid bilayer during biosynthesis and fold concurrently. Through a collaboration with Prof Paula Booth’s Crick satellite, the mechanistic details of these events and their interplay with the translocon machinery and the SRP protein will be probed using our technologies. Such structural measurements will be complemented with biophysical methods such as single molecule force-clamp spectroscopy with Prof Sergi Manyes.  

Professor Christodoulou's UCL profile

Dr Edina Rosta
Picture of Edina Rosta

Group size: 3

Start date: August 2020

Duration: 2 years

Research to be undertaken at the Crick:

The Rosta group focuses on how to enable computational design by understanding the catalytic power of enzymes using atomistic molecular modelling tools, including hybrid quantum mechanics/molecular mechanics (QM/MM) simulations. To quantitatively and accurately assess how enzymes achieve their extraordinary efficiency and specificity in performing chemical reactions, we develop and use modern enhanced sampling methods. Biased simulations are usually required to reach the relevant timescales of important biological processes using current simulation resources. We develop novel algorithms to calculate molecular kinetics in addition to free energies from biased molecular simulations using Markov chains defined on molecular conformational networks. Applications aim at understanding and molecular design concerning the most prominent chemical reactions of living organisms: phosphate transfer and cleavage. 

Dr Rosta's UCL Profile