Some impressions from the rather fabulous #EMBOmobilegenome Mobile Genome meeting in Heidelberg
Morning walk through the woods, exciting panel discussion, flash talks, lab community, drosophila friends, …
@events.embl.org

The transposon community is going very strong. see you all again in 2027!!

Julia is a VBC PhD student (@vbcscitraining.bsky.social), co-mentored by Clemens Plaschka (@impvienna.bsky.social) and me (@imbavienna.bsky.social).

The collaboration with the Plaschka lab has been simply fantastic! A big Thank You to both labs, especially the co-authors.

To our surprise, the Piwi* logic isn’t restricted to nuclear Piwi. Immunofluorescence, IP-MS and AlphaFold predictions confirmed that cytoplasmic PIWI proteins also form PIWI* assemblies.
But in this case, the RNA helicase Spindle-E/TDRD9 is being recruited instead of the heterochromatin machinery.

My favorite experiment:
targeted mutations in Piwi in flies that prevent it from binding Gtsf1/Asterix generate a Piwi protein that is loaded with piRNAs, translocates into the nucleus, but is unable to silence transposons, causing full sterility. A mutation we have been dreaming of for years.

Focusing on the nuclear Piwi protein in Drosophila, Julia used AlphaFold to predict a complex, termed Piwi*, consisting of target-engaged Piwi, Gtsf1/Asterix, and Maelstrom.

Showcasing the power of AlphaFold, every predicted interface that Julia tested in functional assays confirmed the model.

PIWI clade Argonautes are essential for transposon silencing. Without them, animals are sterile due to massive transposon activity.

But how does piRNA-guided target interaction translate into silencing?

PhD student Júlia Portell Montserrat has an intriguing answer

www.cell.com/molecular-ce...