How can conference exhibitors and sponsors help your research?

Matthias with several participants from the EMBL Conference: Transcription and Chromatin 2018. From left to right: Adam Whisnant (University of Würzburg), Melvin Jesus Noe Gonzalez (Francis Crick Institute), Matthias Spiller-Becker (Active Motif Europe), Gabriel Villamil (Max Planck Institute for Biophysical Chemistry). PHOTO: EMBL Events

Meet Matthias Spiller-Becker, Key Account Manager at Active Motif Europe. Matthias acquired his PhD degree in Biology at the Centre for Molecular Biology Heidelberg (ZMBH) where he focused on chromatin and the regulation of the centromere in Drosophila. Now in his 7th year at the company, Matthias is one of the most familiar faces at our conferences on transcription, chromatin and epigenetics – always friendly and welcoming. The popularity of the Active Motif booth at these events has not gone unnoticed, so we asked him what the secret to this success is and what tips he can give to conference attendees when approaching exhibitors.

How many events does your company exhibit at annually? 

In general we participate in about 50+ conferences and meetings/workshops each year, globally. But it’s not only the big and medium-sized conferences that are important to us. We often try to be present at more intimate, local events. Sometimes we sponsor chromatin clubs where only a couple of students and postdocs come together to share their latest research. And we also do a lot of tech talks where we discuss cutting-edge techniques to study gene regulation.

In the era of digital advertising, why do you still choose to be physically present at conferences?

Talking to people face to face changes EVERYTHING!

I think that’s a statement of holistic truth in life! You don’t trust companies in the first place – you trust people. You don’t buy your antibodies or reagents from companies. You buy from people!

And even more: you don’t give away your scientific baby (aka outsourcing your project) to strangers – you give it to people you know and trust. Sure, it happens a lot that folks in the lab search an assay on the web and inform themselves about alternatives on the market before making their “informed” decision, but that is often not the end of the story. It turns out that students and postdocs mostly need to get in touch with us at some point during the experimental process to further discuss their project. And surprisingly often, this first interaction happens at conferences as in “hey, are you working for Active Motif…I think we used your antibody. Can I ask you something?…”. Moreover, being physically present at the conferences is the only way to stay current with cutting-edge research. We discuss with people at their posters and also join the conference sessions in order to see the latest and future trends in chromatin and gene regulation research.

Apart from presenting their newest technology and developments, what else can exhibitors offer participants?

Networking, distraction, fun, and a “Staun-Anlass” (hard to translate that word but probably a reason to positively wonder nails it). Basically, you want to be the red bean in a jar full of green beans. You want to be distinct and recognised among others, leaving a positive impression that lasts.

During my PhD, I always liked companies that didn’t come around too stiff at conferences, but were more approachable”. As a student it takes courage to cross the invisible boarder at a company booth – you don’t want to end up in the web of the sales spider. You are afraid that the company representative might talk you into buying something you never really wanted.

I know this feeling personally – so I try to avoid that when talking to people. My daily goal (whether at a conference or elsewhere) is to be able to help people a bit further. Having a chat at the conference booth can do many things. For example, you may learn that the problem you are discussing with the exhibiting company is indeed a bigger one that’s not to be solved easily. That’s great information! You may also hear that your problem is actually easy to address and solve – even better! You may get info about peers in the same boat as you => networking!

And last but not least, you may simply want to use the chance of talking to people in industry to get an idea about their journey in life & science => career chat!

I try to offer all the above to the people that get in touch with me during a conference!

The Active Motif booth at the EMBO|EMBL Symposium: Metabolism Meets Epigenetics (2019). PHOTO: EMBL Events
What tips can you give participants on how to approach exhibitors?

DON’T BE SHY! Just go and talk to them.

Of course, you need to choose your battles. Often it helps to orient yourself first. Do you already know the company? Is there an overlap between your research and them? If not, just read their banners and roll-ups. Sounds trivial but many people don’t do that. A company would hopefully try to have the most prominent and distinct features of their capabilities written or otherwise sketched out on their banners. If you don’t find any overlap there, I would not necessarily approach them.

But beware: company roll-ups can be like lab websites. Some truths are stated, and some are hidden, so even if your fancy new technique is not mentioned there, as long as the company topic seems to fit your science, go check them out.

If you just want a pen or some chocolate but otherwise, they don’t interest you – simply tell them upfront. You will still get your sweets but honestly, how many pens does a single person need?! 🙂

Can you give an example of a mutually beneficial collaboration that has arisen at your booth through your presence at a conference as an exhibitor?

There are so many examples. It frequently happens that conference participants approach me and tell me that they have an issue with a given technique, mostly Chromatin IP. It turns out that talking them through the experiment step by step often yields at least one weak spot in the setup.

A classic is that people often use the same amount of antibody for ChIP, independent of the varying targets and the respective antibody clones they may use. This is (like many protocol-related “facts” in the life sciences) a dogmatic – or nearly a religious – topic. People can be determined to use “always 2 µg of antibody”. Then you ask them “but did it work when using 2 µg?” and they may need to admit that “no, it didn’t”.

This is a good example that talking with a person outside your own lab can help you to critically re-consider an established protocol, and see things from a new angle.

Another example is that some projects can truly benefit from outsourcing parts of it. Everybody does it in academia but they mostly call it a “collaboration”.

You can take it a step further and outsource parts of your work to a company that offers paid scientific services. This “commercial relationship” can truly boost creativity and assay development. A company that does ChIP-Seq as a paid research service for years will always see more model organisms, more common and uncommon obstacles and more antibody targets than any other lab working only on their own project.

What approach do you use to get into contact with participants?

“It’s just me, myself and I” LOL…

No, it’s not 100 % like that but mostly…you need to simply engage the people!

I try to see every interaction with a person as the most important one in my life at that specific moment. I tend to call that my “Dalai Lama approach”.

How else can you do it!? At Active Motif, we often use our chromatin-related T-shirts to break the invisible barrier between conference audience and the booth. People usually like nerdy science shirts and ours are no exception to that rule. I mostly play a game where people can win the shirts or at least have some distraction from the packed conference program. Often, I implement a little quiz session: people need to give me one or two lines about their research and I create a question around it. If they can answer it, they can play the game to win a shirt. This shows them that we belong to the chromatin community and they often feel more encouraged to talk about a given experiment or planned project.

Is there anything you always wanted to try out at a conference but didn’t do yet?

YES! In a perfect world, I would want to sit in a tweed jacket in my very British armchair, a boiling tea kettle next to me…people can sit down in my little chromatin tea room called “The Nucleosome” and have a relaxed chat around gene regulation and epigenetics with me, or do some networking with others.


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Best Poster Awards – Target Validation Using Genomics and Informatics

Meet Giovanni Spirito and Borja Gomez Ramos – the two poster prize winners at the recent EMBL – Wellcome Genome Campus Conference: Target Validation Using Genomics and Informatics (8 – 10 Dec 2019).

Identification and prioritization of candidate causal genomic variations from individuals affected by ASD

PHOTO: Giovanni Spirito

Authors: Giovanni Spirito (1), Diego Vozzi (2), Martina Servetti (3), Margherita Lerone (3), Maria Teresa Divizia (3), Giulia Rosti (3), Livia Pisciotta (4), Lino Nobili (4), Irene Serio (4), Stefano Gustincich (2), Remo Sanges (1)

Next generation sequencing (NGS) technologies enabled the extensive study of the genomics underlying human diseases. Namely whole exome sequencing (WES) represents a cost-efficient method which can lead to the detection of multiple classes of genomic variants and the discovery of novel disease-associated genes. One of the drawbacks of this approach however, is the large number of genomic variants detected in each analysis. Automated variant prioritization strategies are therefore required. This is particularly important in the case of complex disease such as ASD, whose genetic etiology is still poorly understood. To this aim we built a custom computational framework capable, from raw WES data, to automatically detect four classes of genomic variants (SNPs, indels, copy number variants and short tandem repeat variants) and prioritize them in regards to their relevance to a specific phenotype. We tested this framework on a selection of 29 trios including probands affected by severe and undiagnosed rare phenotypes and a small cohort of 10 trios all featuring healthy parents and one offspring affected by autism spectrum disorder (ASD). We were able to successfully detect rare and de novo high penetrance variants which have been validated and confirmed as causative among the undiagnosed probands. In the specific case of the ASD cohort we could highlight several genes which are not implicated in autism susceptibility, but nevertheless whose connections to genes relevant for ASD could suggest a possible involvement in the phenotype. Furthermore, our approach enabled us to detect several instances characterized by the presence of multiple candidate variants within genes belonging to the same canonical pathway in one proband. Our workflow allows to detect and prioritize multiple classes of genomic variants in order to both highlight rare high penetrance disease-causative mutation, and possibly reconstruct the genomics at the basis of complex ASD phenotypes.

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(1) SISSA, Italy, (2) IIT, Italy, (3) Gaslini Institute, Italy, (4) University of Genova, Italy


Omics data integration for the identification of cell-type-specific gene regulatory networks and regulatory variants in Parkinson’s disease

PHOTO: Borja Gomez Ramos

Authors: Borja Gomez Ramos (1,2), Jochen Ohnmacht (1,2), Nikola de Lange (2), Aurélien Ginolhac (1), Aleksandar Rakovic (5), Christine Klein (5), Roland Krause (2) , Marcel H. Schulz (6), Thomas Sauter (1), Rejko Krüger (2,3,4) and Lasse Sinkkonen (1)

Genome-Wide Association Studies (GWAS) have identified many variants associated with different diseases. However, it is still a challenge to make sense of this data as the majority of genetic variants are located in non-coding regions, complicating the understanding of their functionality. In the last few years, it has been found that non-coding genetic variants concentrate in regulatory regions in the genome, which are cell type and cell-stage specific. In this project, we seek to identify functional Parkinson’s disease GWAS non-coding genetic variants that could make carriers more prone to developing PD. To do so, we are using induced pluripotent stem cell (iPSC) technology to differentiate somatic cells into midbrain dopaminergic (mDA) neurons, astrocytes and microglia. Assessing their chromatin accessibility, active chromatin regions and transcriptome, we can identify crucial regulatory regions in the genome, key transcription factors and derive the gene regulatory networks for the three different cell types. Then, we will map the non-coding genetic variants to the different regulatory regions and predict their effect in silico for the subsequent validation in vitro. This innovative approach will also identify novel factors controlling cell fate and cell identity.

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(1) Life Sciences Research Unit, University of Luxembourg, Luxembourg, (2) Luxembourg Centre for Systems Biomedicine (LCSB), University of Luxembourg, Luxembourg, (3) Centre Hospitalier de Luxembourg (CHL), Luxembourg, (4) Luxembourg Institute of Health (LIH), Luxembourg, (5) Institute of Neurogenetics, University of Lübeck, Germany, (6) Institute for Cardiovascular Regeneration, Uniklinikum and Goethe University Frankfurt, Germany


Working on your own conference poster? Then check out 10 tips to create a scientific poster people want to stop by.

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Best Poster Awards – Metabolism Meets Epigenetics

In its first edition, the EMBO|EMBL Symposium: Metabolism Meets Epigenetics brought together 289 world-leading researchers who examined how metabolites and metabolic networks impact gene regulation, what their roles are in disease and how this opens novel therapeutic avenues.

In addition to the 21 invited speakers and 22 selected short talks, 142 posters were presented during the two poster sessions. Today we present three of the five award-winning posters decided by popular vote.

Citrate carrier links intermediate metabolism to histone acetylation upon ageing of mouse mesenchymal stem cells (MSCs)

PHOTO: Andromachi Pouikli

Authors: Andromachi Pouikli (1), Monika Maleszewska (2), Swati Parekh (1), Chrysa Nikopoulou (1), Maarouf Baghdadi (1), Linda Partridge (1), Peter Tessarz (1)

Chromatin and metabolism interact in a reciprocal manner; on one hand metabolism-related genes are subjected to epigenetic modifications, which regulate gene expression. On the other hand, intracellular metabolism provides metabolites which can serve as essential co-factors and substrates for chromatin-modifying enzymes, affecting their activity. Although, it is well established that the process of ageing is accompanied by changes in metabolism and by chromatin alterations, their interplay in this context remains still poorly understood. In this study we sought to determine how ageing impinges on the relationship between cellular metabolism and the epigenome, using mouse mesenchymal stem cells from the bone marrow (BM-MSCs). In brief, our data suggest that there is a strong and direct link between the metabolic and the epigenetic states of the cell, with ageing-driven changes in metabolism regulating gene transcription and BM-MSC’s stemness, via alterations of the chromatin structure. We conclude that physiological ageing elicits changes in metabolism, resulting in suppressed glycolysis and impaired lipid biogenesis. Moreover, we demonstrate that during ageing there are lower levels of histone acetylation, despite the higher acetyl-CoA levels. We provide a solid explanation for this apparent discrepancy, pointing to the impaired export of acetyl-CoA from mitochondria to the cytosol. Indeed, the protein levels of the citrate carrier Slc25a1 decrease dramatically upon ageing. Using inhibition and supplementation experiments we provide a causal relationship between Slc25a1 function and the levels of histone acetylation, which directly influence chromatin accessibility and plasticity. Collectively, our data establish a tight, age-dependent connection between metabolism, epigenome and stemness and identify citrate carrier as the responsible protein for the mitochondrial-nuclear communication.

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(1) Max Planck Institute for Biology of Ageing, Germany, (2) Personalis Inc, Germany


Epigenetics meets metabolism through histone acetyltransferase NAA40

PHOTO: Christina Demetriadou

Authors: Christina Demetriadou (1), Anastasia Raoukka (1), Agathi Elpidoforou  (1), Constantine Mylonas (2), Swati Parekh (2), Peter Tessarz (2), Antonis Kirmizis (1)

N-alpha-acetyltransferase 40 (NAA40) is distinct among other histone acetyltransferases (HATs) because it deposits an acetyl moiety on the alpha-amino group at the very N-terminal tip of histones H4 and H2A, instead on the lysine side chain. The biological function of this evolutionarily conserved enzyme remained unexplored for several decades because it was thought to mediate an inert modification. However, we previously showed that NAA40-mediated N-terminal acetylation of histone H4 (N-acH4) crosstalks with an adjacent arginine methylation mark to regulate yeast cellular aging in response to caloric restriction through transcriptional control of several metabolic genes. Therefore, we are currently interested in deciphering the function of human NAA40 in carcinogenesis. We recently showed that NAA40 is frequently upregulated in primary human colorectal cancer (CRC) samples. Remarkably, depletion of NAA40 and its accompanied reduction in N-acH4 blocked colon cancer cell proliferation and reduced cell survival in vitro and in xenograft models. We also found that loss of NAA40 expression or of its HAT activity markedly induce global histone methylation. Additionally, whole transcriptome analysis showed that NAA40 knockdown leads to upregulation of key enzymes involved in one-carbon metabolism. Intriguingly, silencing of methylenetetrahydrofolate reductase (MTHFR), which links the folate to methionine cycle, rescues the induction of global histone methylation and loss of cell viability triggered by NAA40 depletion. Hence, this recent work implies that NAA40 may transcriptionally regulate vital metabolic enzymes to control the flux of carbon units into the methionine cycle influencing S-adenosylmethionine (SAM) levels and triggering epigenome reprogramming of cancer cells. Overall, our findings thus far propose that NAA40 and its associated N-acH4 are crucial epigenetic modulators in tumourigenesis and implicate these factors in rewiring cancer cell metabolism.

Poster currently not available.

(1) University of Cyprus, Cyprus
(2) Max Planck Institute for Biology of Ageing, Germany


Role of MOF acetyl transferase in mitochondrial homeostasis

PHOTO: Sukanya Guhathakurta

Authors: Sukanya Guhathakurta (1), Christoph Martensson (2), Alexander Schendzielorz (3), Bettina Warsheid (3), Thomas Becker (2), Asifa Akhtar (1)

Mitochondria lies at the centre of cellular and organismal energy homeostasis, housing a large repertoire of enzymes that are required for the synergy of various metabolic pathways. Mitochondrial gene expression and protein acetylation are two important fundamental processes situated at the crossroad between mitochondrial function and metabolic status of a cell. Gene transcription in the mitochondria has been studied over several decades, but enzymatic acetylation of mitochondria proteins has stayed so far enigmatic. MOF acetyl transferase and its KANSL complex members dually localize to the nucleus and the mitochondria in mouse and human cells. The MOF-KANSL complex regulates metabolic gene transcription in the nucleus and expression of Electron Transport Chain (mtETC) components from the mtDNA, in a cell type dependent fashion. Regulation of nuclear gene transcription by MOF is well understood, however, its control of mitochondrial function remains elusive. Here, we report that loss of MOF leads to severe mitochondrial dysfunction in Mouse Embryonic Fibroblasts (MEFs), sprouting from a stalled oxidative phosphorylation. We address the mechanisms by which the enzyme maintains mitochondrial function in these cells by using a multi-omics approach. We discovered that the role of MOF-KANSL complex in the mitochondria of aerobically respiring cells could be decoupled from its regulation of steady state RNA levels, and could further be attributed to the acetylation of mitochondrial proteins. We characterize the role of acetylation on these proteins through generation of acetylated and non-acetylated mimics. Collectively our data, along with previously published works, suggests that MOF has emerged as a moderator to strike a harmony in the context of communication between the nucleus and the mitochondria. Recent progress on the project will be discussed.

(1) Max Planck Institute for Immunobiology and Epigenetics, Germany
(2) Institute of Biochemistry and Molecular Biology, Germany
(3) Institute for Biology II, Germany

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Meet the Trainer – María del Mar Vivanco

PHOTO: María del Mar Vivanco

Meet María del Mar Vivanco, Team Leader at CIC bioGUNE in Bilbao, Spain. Maria is one of the organisers of the EMBO Practical Course: Techniques for Mammary Gland Research (1 – 6 March 2020).

What is your research focus?

I am interested in cancer heterogeneity, why some cells respond to therapy while others do not, thus contributing to development of resistance and metastasis. In particular, I am intrigued about the complex effects of transcription factors, which are required for normal physiology of the mammary gland and are also implicated in tumorigenesis and development of resistance to therapy in breast cancer.

Why did you choose to become a scientist?

When I was young I had a variety of interests – psychology, physics, art, biology… However, I was intrigued by science and anything related to DNA and its regulation. Then I did my PhD at EMBL Heidelberg (Gene Expression Programme) and discovered the opportunities in research for identifying problems, looking for solutions and the thrill of finding some of the answers…and I was hooked!

Where do you see this field heading in the future?

Despite significant progress in cancer research and clinical advances, breast cancer still is the most commonly diagnosed cancer – one in eight women will develop this disease during their lifetime – and it claims the lives of more women than any other cancer, plus men can also get breast cancer. This highlights the unmet clinical need for improved strategies for prevention, early detection and more efficient and specific treatments in order to accelerate progress and help more patients survive the disease.

One of the features that characterises breast cancer is its heterogeneity, both among patients and within each patient tumor. This heterogeneity is found at molecular, phenotypic and functional levels, complicating diagnosis and challenging approaches to therapy. Currently, huge efforts are dedicated to understanding this heterogeneity at all levels, including at single-cell resolution, which is anticipated to open new possibilities for more efficient and specific anti-cancer therapies.

How has training influenced your career? 

Doing my PhD at EMBL marked the way I envision science, and this vision was reinforced and developed further at UCSF. Science can – and SHOULD – be fun. Later on, funding struggles and the current publishing madness have somehow taken a toll on the fun element, so I just have to remind myself sometimes that science is still exciting!

If you weren’t a scientist, what would you be?

An artist.

You are one of the organisers of the EMBO Practical Course: Techniques for Mammary Gland Research (1 – 6 March 2020). What is the greatest benefit of the course for the scientific community and what could the techniques in this course be used for in the bigger picture?

Some of the techniques practiced at this course are specific for the mammary gland and thus it provides a solid base for researchers starting in this field. In addition, there is a significant emphasis on imaging and comparison of mouse and human studies, the two major systems for looking at normal physiology and cancer research that, when combined, offer great insights into this heterogeneous disease. In addition, having the opportunity to work alongside other trainees contributes to the establishment of a network that may be helpful in the future. Cancer is a very complex problem, and having collaborators with different views and expertise will be very useful in your career.

Interested in this course? Submit your application by 8 December!

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Best Poster Awards – Cancer Genomics

The 4th EMBL Conference: Cancer Genomics (4 – 6 November 2019) brought together over 240 scientists in the field of cancer research to present the latest findings in cancer functional genomics, systems biology, cancer immunogenomics and epigenomics, as well as their translation and clinical impact.

123 posters were presented at the two poster sessions, out of which two were selected as the winners by popular vote. 

Infinite sites violations during tumour evolution reveal local mutational determinants

Jonas Demeulemeester is a postdoctoral researcher at the Francis Crick Insitute in UK. PHOTO: Jonas Demeulemeester

Authors: Jonas Demeulemeester (1), Stefan C. Dentro (2), Moritz Gerstung (2), Peter Van Loo (1)

The infinite sites model of molecular evolution requires that every base in the genome is mutated at most once. It is a cornerstone of (tumour) phylogenetic analysis, and is often implied when calling, phasing and interpreting variants or studying the mutational landscape as a whole. It is unclear however, whether this assumption holds in practice for bulk tumour samples. Here we provide frameworks to model and detect infinite sites violations, identifying 24,459 in total, including 6 candidate biallelic driver events, in 700 bulk tumour samples (26.3%) from the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes project. Violations generally occur at mutational hotspots and their frequency and type can accurately be predicted from the overall mutation spectrum. In melanoma, their local sequence context evidences how not only ETS, but also NFAT-family transcription factor binding creates hotspots for UV-induced cyclobutane pyrimidine dimer formation. In colorectal adenocarcinoma, violations reveal hypermutable special cases of the trinucleotide mutational contexts identified in POLE-mutant tumours. Taken together, we reveal the infinite sites model breaks down at the bulk level for a considerable fraction of tumours. These results warrant a careful evaluation of current pipelines relying on the validity of the infinite sites assumption, especially when scaling up to larger sets of mutations and lineages in the future.

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(1) The Francis Crick Institute, United Kingdom, (2) EMBL-EBI, United Kingdom


The other award-winning poster was:

Understanding the early impact of activating PIK3CA mutation on cellular and genetic heterogeneity presented by Evelyn Lau, UCL Cancer Institute, United Kingdom


Working on your own conference poster? Then check out 10 tips to create a scientific poster people want to stop by .

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