Not knowing exactly what to expect from this brand new symposium, we were excited to see what the Cambridge Epigenetics Symposium had in store. University of Cambridge’s Daisy Hessenberger was on hand to capture the event, and fill us in on all the juicy details. Check out her report below:
The first of it’s kind; the Inaugural Cambridge Epigenetics Symposium brought together the epigenetic community in Cambridge for a half day of talks at the Babraham Institute. It was organized by the Cambridge Epigenetics Club, which is known for its termly meetings which bring in high quality international researchers (Find Talk Archives here). The club, only 4 years old, is the brainchild of Prof. Wolf Reik, Prof. Anne Ferguson-Smith and Prof. David Baulcombe. The main aim of the symposium was to increase networking between different groups that commonly attend the termly meetings and to open up the Cambridge Epigenetics club to other people including groups from Sheffield and Norwich.
Despite the attraction of the beautiful green grounds of Babraham on a sunny day, the first session, Epigenetic sensing: genome and environment, held the audiences attention. The session ended with a short presentation by sponsor CEGX introducing their new technology that allows users to differentiate between methyl-cytosine and hyroxy-methyl-cytosine in bisulfite sequencing. The following sessions, Mechanisms of epigenetic genome regulation and Functional genomics, covered various epigenetic mechanisms from DNA methylation to histone modifications to the mRNA-tRNA expression regulation using a variety of model organisms including mammalian and plant systems.
The day ended with a bbq out on the grass where attendees could network in the sun. The lack of tables and the beautiful day meant that group boundaries were forgotten as people spilled onto the grass to enjoy the social component of the afternoon. Overall the symposium, comprised of ten talks, was a nice way to wrap up the 2013-2014 calendar for the Cambridge Epigenetics club and hopefully it is the start of a new annual event.
Single-cell RNA-seq and Allelic Expression in Mammalian Cells
Rickard Sandberg, Ludwig Institute for cancer Research
Prof. Sandberg opened the symposium with a keynote talk that set a high standard for the rest of the day. His emphasis on the new single-cell RNA-seq technology was fitting with the theme of new uses of cutting edge technologies that pervaded the symposium. Instead of just explaining single cell gene expression methods, Sandberg immersed the audience in these techniques using a story about an old biological problem: how can the same genetic background manifest in different phenotypes? Throughout the talk Sandberg impressed upon the audience that gene expression is stochastic and noisy making it more important to have highly sensitive methods for global single cell gene expression to comparison between cells with identical genetic backgrounds.
The Sandberg lab used Smart-seq2 (a single-cell RNA-seq method with 40% sensitivity) to study single cell allelic expression across cells of mouse pre-implantation embryos. They used embryos of a cross where the parent mice had known SNPs to allow differentiation between different alleles of genes. The results showed a higher than previously recorded level of bi-allelic expression from genes: approximately 50% of the genes are bi-allelic and 50% are mono-allelic with 25% of mono-allelic genes from one parental allele and the other 25% from the other parental allele. The higher sensitivity afforded by Smart-seq2 exposed false positives in previous data sets; low sensitivity of previous techniques meant that genes with lower coverage had a high chance of being incorrectly labelled as mono-allelic. Allelic expression was also found to be extremely dynamic as genes in the mouse embryo data set fluctuated between states of mono-allelic and bi-allelic expression in single cells in a manner consistent with models of transcriptional bursting.
PRDE-1, Novel piRNA biogenesis Factor Reveals Two Classes of piRNA
Eva-Maria Weick, Miska lab, The Gurdon Institute
The idea of this symposium was conceived with the aim of giving young researchers, PhD students and post doctorates, a new platform to present their research. Eva-Maria Weick gave an excellent talk on her PhD work identifying a novel component of the piRNA pathway in C. elegans. Although the work of Eric Miska’s lab is well known in the Cambridge epigenetics scene (many attendees have seen Prof. Miska give a talk at some point) it was a refreshing change to hear about a section of their work in more detail.
Taking advantage of the piRNA pathway sensor developed by the Miska lab, a forward genetic screen identified PRDE-1 (piRNA defective 1), which acts to stabilize PRG-1, a piwi-related Argonaute essential for the accumulation of piRNAs. Eva-Maria also showed how PRDE-1 was exclusively required for biogenesis of motif dependent piRNAs and their secondary sRNAs. During question time, she suggested that motif independent and dependent piRNAs have biologically distinct functions as they target different types of genes (pathogen response genes and classical gene targets respectively).
Exploring the mRNA–tRNA interface using next-generation sequencing
Konrad Rudolph, Marioni lab, EMBL-EBI
Another graduate student, Konrad Rudolph, introduced the less familiar world of the mRNA-tRNA interface. Using ChIP-seq of DNA Pol III (the polymerase responsible for tRNA transcription) in conjunction with RNA-seq, they were able to quantify tRNA gene expression. When tRNA gene expression was compared between six stages of mouse development in the liver and brain, both mRNA and tRNA expression data distinguishes beautifully between the tissues, clustering in a similar fashion in principal component analyses.
Despite the dramatic change in tRNA expression however, the codon usage is completely stable across development (although Rudolph did point out that this is not true for other metazoans). It seems there is a great level of change of protein coding and tRNA genes but at the level of codons and anticodons this is being compensated for. This compensation could be controlled through the activity of transcription factors or via the epigenetic marks enriched near tRNA genes.
**EpiGenie would like to give a huge “Thanks!” to Daisy Hessenberger, who is a PhD student in the Baulcombe lab at the University of Cambridge for graciously providing coverage of this symposium**