All tags Epigenetics Scientist of the month: Robert Schneider

Scientist of the month: Robert Schneider

During the last year the Schneider lab has demonstrated the causality of histone modifications (Tropberger et al., 2013; Tropberger and Schneider, 2013; di Cerbo et al., 2014), integrated for the first time linker histone H1 variants into epigenomic maps (Izzo et al., 2013) and gained new insights into the pathways of pericentromeric heterochromatin formation (Lange et al., 2013). We spoke with him to find out more about his latest research and what we can expect from the upcoming Chromatin and Epigenetics: From Omics to Single Cells conference in Strasbourg. 

Brief biography

​​​​Rob Schneider PhD

Robert Schneider did his PhD at the University of Munich in close collaboration with the LMB in Cambridge, UK. He then moved to Cambridge to join the group of Tony Kouzarides at the Gurdon Institute as a postdoc, where he focused on lysine methylation in the histone H3 tail. From there he went to the Max Planck Institute for Immunobiology and Epigenetics in Freiburg, Germany to start his own group, and extended his research towards novel sites and types of histone modifications.

Since 2012 he has been the senior group leader at the Institute of Genetics and Molecular and Cellular Biology (IGMBC) in Strasbourg, France. Apart from continuing his work on new histone modifications, he has also become excited about single cell epigenetics.

Rob is holder of an ERC starting grant and the Chaire Gutenburg. Amongst other awards he has received an HFSP Career Development Award and is member of EpiGeneSys. He has authored more than 70 publications. Furthermore, Rob is founder of the TriRhena Chromatin Club and organizer of the Abcam Chromatin and Epigenetics meetings in 2012 and 2014.

Q. What sparked your passion for science?

I have always been curious about discovering how things really work. That's the fun part about science and my daily motivation.

Q. What exciting research projects are occurring in your lab?

One major question we are interested in in my lab is: are histone modifications really causative (e.g. for transcription) or just "boring" by-products (of e.g. transcribing polymerase passing by)? We are now able to show that specific histone modifications can directly stimulate transcription and hence can be indeed causative in the regulation of chromatin function.

Of special interest for us is also the often forgotten fifth histone, the linker histone H1, and its puzzling complexity of histone variants (up to eleven in mammalian cells!). We have now managed to dissect the function of histone H1 variants in vivo with surprising roles of these variants in e.g. epigenetic reprogramming.

More recently we got excited about the inheritance of epigenetic information. But since it's difficult to define the heritability of epigenetic states in a population of cells because of cell heterogeneity and varying levels of stability of these states, we developed novel single-cell approaches to address these questions. We are now observing these processes in live cells and are using high-throughput screening to understand how chromatin states and epigenetic modulators mediate "epigenetic" inheritance. So far, we have already got some fascinating results about the inheritance of transcriptional states in individual cells and the mechanisms mediating inheritance of these states to progeny... stay tuned for this. If you are interested and want to join the team, feel free to contact me.

Q. What made you focus on epigenetics research?

During my PhD I studied the organization of DNA in E. coli in the so-called nucleoid. But without a nucleus and histones somehow something was missing there.


Q. You are chairing the upcoming Chromatin and Epigenetics: From Omics to Single Cells conference in Strasbourg. How did you first connect with Abcam and come to chair this conference?

As I started my postdoc in Cambridge, Abcam was in an annex building of the university next door (I still remember the parties there!), with at the time a staff of three or four people. Since then we have kept in contact and even collaborated on some projects. Four years ago during a discussion with Abcam we came up with the idea of organizing a European epigenetics and chromatin meeting in a compact format in the heart of Europe with high-profile speakers.


Q. What makes this meeting different from other epigenetics meetings?

Our meeting has a well-defined novel topic and thereby is already different to most "standard" chromatin meetings. The format (two full days) is very compact, however, with enough time for interactions and talks selected from the abstracts. At the last meeting these selected talks were a real highlight and our list of invited speakers has been outstanding for both meetings. Of course Strasbourg is centrally located, a UNESCO world cultural heritage site with excellent French food and wine.


Q. The meeting is about bridging single cell concepts with epigenomics. What has changed in the field over the last 5-10 years?

Yes, we want indeed to bridge the "omics" with the single-cell field. In the last years the limitations of studying cell populations have become obvious. Of course there is now the emerging topic of single-cell omics, however, all these omics methods are based on cell lysis so cannot be used to follow cells over multiple generations, which is important for studying truly epigenetic processes. On the other hand the live cell imaging approaches aren't able to look at interactions and modifications on a genome-wide level. So that's why we want to bring these two seemingly separate fields together - there is a lot to do. We also want to provoke a thorough brainstorming on this, by bringing together leaders in both fields and researchers wanting to push the limits of epigenetics.

Q. Where do you see things going? What do you think will be the next big breakthrough in epigenetics research?

I am a strong supporter of the "single-cell revolution", however, this still requires a lot of new technology development. Microfluidics can be a big step forward in this direction, but very few biologists are actually using it to its full potential since it requires a lot of engineering. Of course a future big breakthrough would be single-cell epigenetics in multicellular organisms to unravel not only the dynamic nature of epigenetic changes in normal and diseased state but also the mechanisms behind them.

Q. What new and exciting developments may we hear more of at the meeting?

Single-cell and epigenomic approaches are currently at the frontier of epigenetics research and push the limits of resolution for every type of analysis - we will hear a lot about this at the meeting. We can also expect to hear fascinating new insights about the role of chromatin modifications, chromatin-modifying enzymes, binding proteins and ncRNAs genome-wide and in single cells, but also about variability in transcriptional responses and nuclear organization. We hope that the studies presented at this meeting will reach towards identifying carriers of epigenetic information and the actual heritability of epigenetic processes. And, as I mentioned above, we are expecting a brainstorming meeting with discussions that will inspire new challenges to address over the next couple of years.

Q. We have a great line up of international speakers for the conference. Is there a particular topic or speaker you are looking forward to hearing?

Of course I am particularly looking forward to the two keynote lectures by John Gurdon and Tony Kouzarides, but also to the presentations of all our colleagues who immediately responded and accepted our invitation to come in spite of their busy schedules. We selected all the invited speakers carefully to get this great line up and are looking forward to hearing lots of exciting unpublished data. I am also sure that the talks selected from the abstracts will be highlights.

Q. What are the highlights of your career so far?

As I became interested in histone modifications I did lots of studies on histone methylation and e.g. showed that in mammals H3K4me3 is a mark for active transcription. The obvious next challenge was to move to the question of histone modification functionality. Luckily we were able to decipher mechanisms and demonstrate direct functions of histone modifications rather than observe mere correlations. So I can say that one of my highlights is that we have proven the significance of adding small chemical groups to histones!


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