Location & dates Virtual 7 - 9 Oct 2020
Deadlines Registration closed Abstract submission closed
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EMBL Courses and Conferences during the Coronavirus pandemic

With the onsite programme paused, many of our events are now being offered in virtual formats.


Registration is open as usual for many events, with back-up plans in place to move further courses and conferences online as necessary. Registration fees for any events affected by the COVID-19 disruption are fully refundable.


More information for participants of events at EMBL Heidelberg can be found here.

The following optional webinar will be hosted by the sponsor Eclipse Bioinnovations a day prior to the virtual EMBO I EMBL Symposium: The Complex Life of RNA. Participation in this webinar is free of charge for registered symposium attendees but the number of available places is limited (first come, first served). All symposium participants will receive an email with a registration link.

Industry Webinar by Eclipse Bioinnovations

 

The eCLIP platform: A powerful technology to study RNA binding protein interactions, microRNA targets and RNA modifications

 

6 October 2020, 16:00 - 17:00 (CEST, e.g. Berlin).
To find out the equivalent time zone in your location, enter Berlin, the CEST programme time and your city into the Time Zone Converter.

 

Dr. Sergei Manakov, Eclipse Bioinnovations

 

Eclipse Bio has quickly become a leader in the new frontier of RNA genomics. Our eCLIP technology platform enables all scientists to understand post-transcriptional regulation by mapping targets for RNA binding proteins (RBPs), RNA modifications, and non-coding RNAs such as miRNAs and lncRNAs.

 

eCLIP technology was used to profile targets of 150 RBPs for the ENCODE project (Encyclopedia of DNA Elements), an international collaboration that aims to build a comprehensive parts list to understand how genes are controlled. The recently released paper entitled, “A large-scale binding and functional map of human RNA-binding proteins,” is available open access on Nature as part of a special package of 10 studies from ENCODE Consortium.

 

Sergei Manakov, Principal Scientist Bioinformatics at Eclipse Bioinnovations, will present a detailed overview of the eCLIP technology and its applications for robust and precise mapping of RNA binding proteins, m6A modifications and miRNA-mRNA targets. Eclipse Bio enables researchers in all research fields (including cancer, CNS, genetic disease and virology), to understand RNA regulation in diseases, cells and model organisms.

 

 

Talk Title: m6A regulates lncRNA HOTAIR in breast cancer

 

Dr. Allison Swain, University of Colorado Denver

 

N6-methyladenosine (m6A) is one of the most abundant RNA modifications that has important roles in normal and cancer biology, but knowledge of its function on long noncoding RNAs (lncRNAs) remains limited. To investigate a potential role for m6A on the lncRNA HOTAIR, we mapped m6A at single nucleotide sites in HOTAIR-expressing breast cancer cells using m6A enhanced cross-linking immunoprecipitation (meCLIP) (Van Nostrand et. al. Nature Methods, 2016). We identify at least 11 m6A modified adenosine residues within HOTAIR and show that modification of HOTAIR is mediated by the m6A transferase METTL3/14 complex. A single m6A site in domain 2 of HOTAIR was consistently identified in m6A mapping experiments. When compared to cells overexpressing wild-type HOTAIR, overexpression of a mutated form of HOTAIR with a single A-to-U mutation is unable to enhance breast cancer cell proliferation or soft agar colony formation. We observe interaction between the nuclear m6A reader YTHDC1 and HOTAIR in breast cancer cells, and a single A-to-U mutation resulted in a decreased interaction of in vitro m6A-modified domain 2 of HOTAIR with YTHDC1. Proliferation of cells overexpressing mutant HOTAIR is enhanced by overexpression of YTHDC1 and decreased by knock-down of YTHDC1. We also show that overexpression of YTHDC1 results in increased soft agar colony formation which is enhanced when cells express wild-type HOTAIR. Knockdown of YTHDC1 or mutating multiple m6A sites within HOTAIR results in decreased overall expression levels of HOTAIR. At the molecular level, a single A-to-U mutation decreases chromatin retention of HOTAIR, which is recovered by overexpression of YTHDC1. Finally, in a reporter cell line where HOTAIR is tethered upstream of luciferase to mimic repression by HOTAIR, knockdown of YTHDC1 leads to an increase in luciferase expression. Altogether, these data suggest a mechanism whereby m6A is important in regulating the function of HOTAIR via mediating interaction of YTHDC1 with specific m6A sites. This interaction in turn regulates the stability and chromatin retention of HOTAIR as well as the repression of its target genes. We propose a mechanism whereby YTHDC1 mediates transcriptional interference by HOTAIR to initiate repression and heterochromatin formation at its targets.