RNA meeting 2019 – Part 1

The RNA society meeting is big. With over 150 talks and almost 700 posters, there’s a lot of new stuff to learn. This was my first RNA society meeting and I decided from the beginning to take it easy. That is why I did not live tweet like I usually do.

Instead, I thought of writing a summery blog post.

I arrived late to Krakow, so I missed the first keynote talk by Phil Sharp. At least, I came in time to listen to a wonderful piano concert. It was music by Chopin, and it was beautiful. I think every meeting should start with a piano concert, Chopin being a top choice, of course.

Following my “take it easy” decision, I slept late the next day skipped the first session on splicing. Instead I started the meeting at the excellent keynote lecture by Tom Cech. He told us about the polycomb complex PRC2. It has an interesting RNA binding region that binds G-rich RNAs. RNA binding is related to its chromatin regulatory roles, in particular for developmental genes, such as heart development.

Next was the RNA localization session, chaired by Jeff Chao, which is always fun. It started with Orna Amster-Choder, discussing RNA localization in bacteria.  This wasn’t news to me, she published it already in 2011, and continue to work on that since. But now she expanded to whole transcriptome, including both mRNAs and small RNAs. Surprisingly, many of the small RNAs are at the poles.

Igor Ulitsky talked about SIRLOIN  – the cis element that mediates RNA retention in the nucleus, through its association with hnRNP K, and possibly splicing factors.

Susanne Kramer showed something that looked like co-transcriptional export of mRNA in trypanosomes. When inhibited RNA granules are formed attached to the nucleus, which she can isolate and dissect its contents.

Marie-Louise Hammarskjold told us about a cis element called CTE in viral RNAs that allows export of intron containing mRNA, with the export factor NXF1, which has its own CTE. Very interesting regulation of NXF1 activity.

Eneko Villanueva used a method to create integrated maps of protein, RNA and RNA-binding protein localizations in the cell, based on analysis of cell fractionation to different organelles. This seems like a very useful method.

The last one I want to mention for this session is that of my friend Evelina Tutucci, who just accepted a PI position in Amsterdam. She showed a very peculiar finding: the CLB2 mRNA localizes to the bud in yeast, using the same She2/3 mechanism as the canonical ASH1 mRNA. But, unlike Ash1 protein that also localize to the bud, Clb2 protein localizes to the nucleus, in the mother! Why? It is still not clear, but could be a form of cell-cycle timer that measures the readiness of the bud.

There were a few takes in other sessions that also qualify for RNA localization. Mark Ashe discussed his recent publication on “translation” granules: RNA granules, in yeast, that harbor mRNAs encoding translation factor regulators, and – separately – mRNA encoding glycolytic enzymes. These mRNAs are translated in the granules, and are inherited to the bud.

A less convincing talk was that of David Rueda, who is trying to use the RNA-Mango aptamer to visualize single-molecule mRNAs. There is big promise there but I was not convinced by the data. Also, right at the beginning he claimed the Mango array is 3-4 fold shorter than MS2x24 array. But the figure showed its 8x135nt. That’s 1.1 kb, compared to 1.5kb of MS2 – shorter, but not 3-fold. (Maybe he meant that the molecular weight is 3-4 smaller. That makes more sense).


Many translation talks were very interesting. Maria Barna, who won the RNA society early career award, gave a great talk (most of it I heard already at her visit to Weizmann) on ribosome heterogeneity and ribosomal RNA extensions that mediated HOX translation via an IRES. Frankly, I’m more excited about her work on nanotubes which she told me is almost ready. Can’t wait to read that!

There was another talk on differential expression of ribosomal protein paralogs in fly gonads, by Julie Aspden. It’s great to see how the field grows. A paper by another lab on a similar subject was published just a few days earlier.

There were several talks about elements in the UTRs that affect translation. Fatima Alghoul from Franck Martin lab in Paris talked about the TIE element (discovered by Barna) in the 5’UTR. This is a type of uORF found in HOX genes, for instance, but each TIE works by a different mechanism to inhibit translation. Kamili Singh from Wendel lab found a cis element that is affected by Myc and SRSF1.

Other talks discussed translation in the UTRs and how this affects the protein product. Joanna Kufel showed, in yeast, that many mRNAs can have multiple translation start sites, but from downstream non-annotated AUG (producing an N-terminal truncated protein), or non-canonical start codon (mostly CUG) upstream of the canonical AUG, producing a protein with extended N-terminal. Over 1500 genes show this variability. As a physiological example, she showed how these can add or remove a mitochondria transport signal, which affects the protein localization. Xuebing Wu sent a video lecture (or was it live video? I’m not sure) telling us that translation that goes into the 3’UTR (or fusing a short peptide to the C-terminal) can produce in many cases a peptide that codes to the C-end rule and rapid degradation of the protein.

Ribosome foot-printing is advancing to the next level, with two interesting talks. Susan Wagner from Thomas Preiss’ lab showed the foot-prints of the 40S ribosomal subunit prior to translation elongation (as expected – at the 5’UTR and 1st AUG), but also the foot-print of the eIF2 and eIF3 complexes (with the 40S, 80S). David Gatfield showed foot-prints of disomes – a pair of very close ribosomes. He analyzed the occurrence of these, relative to different codons or elements, under the assumption that disomes occur due to stacking or pausing. Some were stochastic events, but others seemed to be more or less based on which amino acid is at the P or A sites and which codon is used. The combination DI (aspartate at P site and isoleucine at A site) results in the highest occurrence of disomes.


To be continued….

(when I find more time to write it all up)

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