EMBL-EBI Industry Partnerships: Work with us to solve your data challenges

Partnering with industry has been a core part of EMBL-EBI’s mission right from the very beginning and a significant number of our users come from this sector. As we celebrate an incredible 25 years of industry collaboration next year, let’s hear from Andrew Leach, the new Head of Industry Partnerships at EMBL-EBI to find out a bit more.

Image: Dr Andrew Leach, joined EMBL-EBI in August 2016 following a 20 year career at GSK Research and Development. He took on the role as Head of Industry Partnerships in the summer this year, and will also continue as Head of Chemical Biology.

Industry Partnerships: What does this mean at EMBL-EBI?

Industry Partnerships at EMBL-EBI is about helping to connect public and industry science. We aim to foster and facilitate collaboration, knowledge exchange and networking between scientists and technologists at EMBL-EBI and their counterparts working in industry. We work across multiple sectors and with organisations from very large multinationals to very small start-ups.

Tell us more about the opportunities for scientists in industry to interact with EMBL-EBI.

EMBL-EBI’s Industry Programme is a subscription-based programme for global companies who are using EMBL-EBI’s data and resources as part of their research and development. Representatives from the member companies meet regularly in a forum where we share details of the latest innovations in EMBL-EBI’s services and research. The programme also organises a series of knowledge exchange workshops that explore new emerging areas for R&D. These events are open to any employee of the member companies. The programme also provides a great opportunity for scientists to meet their peers in a pre-competitive, science-oriented environment to discuss the latest developments.

We are always keen to hear of opportunities to explore new strategic partnerships with industry. Open Targets is an excellent example; this ground-breaking public-private consortium was established in 2014 with the overall goal of improving how we identify and prioritise drug targets. Open Targets currently involves six partners: EMBL-EBI, the Wellcome Sanger Institute, GlaxoSmithKline, Bristol Myers Squibb, Takeda and Sanofi.

We also have a proud history of research collaborations that bring together expertise from academia and industry to work on a common research problem or to address a particular data or technology challenge. One particular advantage of collaborating with EMBL-EBI is that we have tremendous flexibility in the way that collaborations can be set up, from small projects lasting a few months, to much larger projects. Key to success is active participation and commitment from everyone involved.

What about smaller companies? 

Every company has to start somewhere and we are committed to engage with small and medium-sized enterprises (SMEs) and start-up enterprises. These are very often the drivers of innovation, and we find that such organisations make extensive use of the resources available at EMBL-EBI. We actively work with organisations such as OneNucleus, the UK Trade and Investment agency (UKTI), the InnovateUK Bioinformatics knowledge-transfer network and the ELIXIR SME and Innovation Forum to showcase the opportunities at EMBL-EBI. Of course, we are also very keen to hear from any smaller company interested in collaborating more directly with us on a particular problem.

What can be achieved by connecting with industry?

Having worked in industry myself (for many years at GSK), I know that industry science is often just as cutting-edge as in traditional academic circles – but historically it has been much less visible due in part to commercial sensitivities together with the fact that publication was not seen as a key goal in industry. These attitudes are changing now; there is a real drive within industry to collaborate externally and especially with leading academic groups and institutions. Industry can bring “real world” applications of the resources and research that we do at the EMBL-EBI; it can be very rewarding to see how the work we do can translate into practical applications. Plus, it can be a way for students and post-docs to get some insights into what a career in industry looks like, and potentially for industry to identify potential recruits for the future!

What would you like to see in the future for Industry Partnerships at EMBL-EBI?

I would like to see our connections with industry continue to grow and strengthen. We have historically had very strong connections with the Pharma and biotech sectors and it would be good to see us strengthen our relationships in other areas of bioscience and also with relevant data science and technology sectors. Of course, we are always keen to create new large-scale strategic partnerships such as Open Targets but we also recognise that a smaller-scale, one-on-one collaboration for example between an SME and an EMBL-EBI Principle Investigator can be equally fruitful. We also want to make further steps to encourage entrepreneurs; this includes working with Jo Mills (Entrepreneurship and Innovation Centre Manager) who with her team is creating a new Startup School for genomics and biodata. This will support early-stage ideas and provide knowledge and confidence to develop them into future products or services.

We always welcome opportunities to explore new partnerships and ventures.

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Best Poster Awards – EMBO|EMBL Symposium: Organoids 2020

The recent virtual EMBO|EMBL Symposium on Organ Development and Disease in 3D Culture saw the highest number of registrations we have had since we launched the format. A total of 880 researchers from around the world got together online to discuss recent developments in the formation and maintenance of organoids and their use in disease studies and regenerative medicine.

Out of the 200 digital posters that were presented at the three poster sessions, four were distinguished with a poster prize by a committee appointed by the scientific organisers. Here are the winners:

Organoids model transcriptional hallmarks of oncogenic KRAS activation in lung epithelial progenitor cells

PHOTO: Antonella Dost

Authors: Aaron Moye (1), Antonella Dost (1), Marall Vedaie (2), Linh Tran (5), Eileen Fung (5), Dar Heinze (2), Carlos Villacorta-Martin (2), Jessie Huang (2), Ryan Hekman (2), Julian Kwan Kwan (2), Benjamin Blum (2), Sharon Louie (1), Sam Rowbotham (1), Julio Sainz de Aja (1), Mary Piper (4), Preetida Bhetariya (4), Roderick Bronson (3), Andrew Emili (2), Gustavo Mostoslavsky (2), Gregory Fishbein (5), William Wallace (5), Kostyantyn Krysan (5), Steven Dubinett (5), Jane Yanagawa (5), Darrell Kotton (2), Carla Kim (1)

Presenter: Antonella Dost (1)

Mutant KRAS is the most common oncogenic driver of epithelial cancers. Nevertheless, the molecular changes induced by KRAS activation in primary epithelial cells beyond activation of proliferation remain elusive. Here, we determined transcriptional changes at single-cell resolution after KRAS activation in distal lung epithelial cell populations. We developed a new in vitro organoid system to define the early oncogenic KRAS transcriptional program and model early-stage lung adenocarcinoma (LUAD) using primary murine lung cells. Alveolar epithelial progenitor (AT2) cells expressing oncogenic KRAS lost their mature identity and acquired a transcriptional program similar to lung development and progenitor cells. Similar changes were observed in an early-stage LUAD mouse model, in human induced pluripotent stem cell derived AT2 cells, and in stage I lung cancer patient samples, validating our organoid model. While these events have been observed in advanced lung cancers in mice and humans, we show that KRAS induced dedifferentiation occurs in early-stage lung cancer. This work provides a new organoid tool to rapidly recapitulate lung cancer progression in vitro and a window into the transcriptional changes that immediately follow oncogenic KRAS expression in epithelial cells, revealing candidate targets for early intervention of KRAS-driven lung cancer.

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(1) Boston Children’s Hospital, United States of America
(2) Boston University, United States of America
(3) Harvard Medical School, United States of America
(4) Harvard T. C. Chan School of Public Health, United States of America
(5) University of California Los Angeles, United States of America


Using human pluripotent stem cell-derived organoids to investigate regional-specific features of the small intestine

PHOTO: Guillermo Sanchez

Authors: J Guillermo Sanchez, Heather McCauley, Jacob Enriquez, James Wells, Cincinnati Children’s Hospital, United States of America

Presenter: J Guillermo Sanchez

The gastrointestinal tract is the largest endocrine organ in the body. Specialised nutrient sensing cells, called enteroendocrine cells, are embedded in the intestinal epithelium and secrete over 20 hormones that regulate processes such as satiety, gut motility and gastric emptying. Directed differentiation of human pluripotent stem cells into human intestinal organoids has been used to study and mimic intestinal development; however, most of these models generate intestinal tissue which resembles duodenum and proximal jejunum (Spence, et al 2011). The intestine displays distinct regional functions along the proximal-distal axis, with the ileum being important for unique enteroendocrine hormone secretion, bile acid resorption and interactions with the microbiome. It is known that major signaling pathways such as Wnt, FGF and BMP can affect the regional identity of the developing GI tract. Consistent with previous studies (Munera, Tsai) we found that manipulation of the exposure time of intestinal spheroids to these signaling pathways generated distal intestinal tissue by expression of epithelial markers, nutrient transporters, and hormone expression. These distally-patterned human intestinal organoids retain their regional identity after transplantation in vivo, and can be used to generate epithelial-only enteroid cultures. It remains unknown how diverse cellular types and functions are established along the proximal-distal axis of the small intestine. This model enables us to compare the early transcriptional changes involved in conferring regional-specific features, including enteroendocrine cell allocation, to the GI tract.

Poster currently not available


Recapitulating the somitogenesis in vitro to identify novel causative genes for congenital bone diseases

PHOTO: Marina Matsumiya

Authors: Marina Matsumiya (1), Mitsuhiro Matsuda (1), Nao Otomo (2), Yoshiro Yonezawa (2), Shiro Ikegawa (2), Miki Ebisuya (1)

Presenter: Marina Matsumiya

Somites are periodically formed though the segmentation of anterior parts of presomitic mesoderm (PSM) in embryos. This periodicity is controlled by the segmentation clock gene Hes7, which exhibits a wave-like oscillatory expression in the PSM. The periodical somite formation is a crucial event for body segment formation and abnormal somitogenesis leads to congenital bone diseases.

Spondylocostal dysostosis (SCD) is a bone malformation disease which is characterised by morphological abnormalities of vertebrae and ribs. Mutations in several somitogenesis-related genes, including HES7, are already known as the cause of SCD. As for 75% of SCD patients, however, the causative gene and at what stage of bone development the abnormality occurs are still unclear.

Thus, the aim of this study is to establish a method to recapitulate the somitogenesis in vitro and to identify novel a causative gene of SCD.

To recapitulate the somitogenesis in vitro, we previously reported a simple and efficient method to generate mouse embryonic stem (ES) cell-derived PSM-like tissues (Matsumiya et al., Development, 2018). In these tissues, Hes7 oscillation was synchronized among neighboring cells, the anterior-posterior axis was self-organised, and somite-like structures were observed. We are currently developing a similar method to recapitulate the human somitogenesis by using human induced pluripotent stem (iPS) cells instead mouse ES cells. Furthermore, by using human iPS cell lines that lack the candidate gene of SCD for the in vitro somitogenesis, we are trying to identify a novel causative gene of SCD.

Poster currently not available

(1) EMBL Barcelona, Spain
(2) RIKEN Center for Integrative Medical Sciences, Japan


Heme oxygenase 1 upregulation is induced by stress via alpha-synuclein aggregation in transgenic mice and in Parkinson’s disease derived brain organoids

PHOTO: Silke Frahm-Barske

Authors: Silke Frahm-Barske (2), Sebastian Diecke (2), Franz Theuring (1)

Presenter: Silke Frahm-Barske

Excessive accumulation of alpha-synuclein (a-syn) predisposes to the development of Parkinson’s disease (PD), a disorder characterised by neurodegeneration in the substantia nigra and concomitant motor impairments. It was previously shown that stress-induced release of glucocorticoids accelerates the progression of PD and that the glucocorticoid receptor (GR) is downregulated in several neurodegenerative as well as in stress-related diseases. The impact of altered a-syn protein levels on GR dysfunction and stress-related protein expression is largely unexplored, but may have severe implications for PD manifestation and disease progression. Therefore, we examined the effect of chronic stress in two models overexpressing human a-syn: a transgenic mouse model (h-a-synL62) and brain organoids derived from iPSCs of a PD patient. Wildtype mice that underwent daily restraint for 6 weeks presented typical chronic stress induced features, such as GR-deficiency and increased a-syn protein levels in prefrontal cortex and hippocampus. Importantly, these molecular alterations were reproduced in forebrain organoids generated from healthy donors after treatment with the synthetic glucocorticoid Dexamethasone for 2 weeks. In contrast, glucocorticoid exposure had no effect on GR expression and normalised the level of a-syn in h-a-synL62 mice and PD brain organoids. Accordingly, heme oxygenase 1 (HO-1), an antioxidant protein that can be induced by soluble oligomers and protofibrils and that triggers proteosomal degradation of a-syn, was upregulated. Together, our work provides a new link between a-syn overexpression, GR-deficiency and oxidative stress and their contribution to the development and progression of PD. Further, we established and validated a human 3D tissue culture model that can be used to study stress related diseases, offering replacement of research animals exposed to disturbing procedures.

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(1) Charité – University Medicine Berlin, Germany
(2) Max-Delbrück-Center, Germany


Working on your own conference poster? Then check out these 8 tips for preparing a digital poster that stands out from the crowd.

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