Same here. I'm 12 on the waitlist position.
I've never experienced that before. Any chance they might increase the accepted number of attendees?

Thanks Aude!
Didn't you say you have a book about Mesopotamian deities? In case we (or others) need more names 😉

Again, this is the results of massive experimental work by @ludopoire.bsky.social and wonderful collaboration with
@francoisrousset.bsky.social
within
@ciri-lyon.bsky.social
.

In all, we unambiguously demonstrate that bacteria have evolved immune systems to specifically defend against conjugative plasmids.
Multiple systems remain to be discovered, with fundamental implications on antimicrobial resistance and plasmid ecology and evolution.

Adding to our results, another immune system was recently shown to also trigger cell death in E. coli upon plasmid conjugation, but it's targeting VirB4 rather than VirB2 or VirB8.
www.biorxiv.org/content/10.6...

Triggering cell death upon conjugation is unexpected. This extreme response confers population-level plasmid protection like defense systems do against virulent phages. Plasmid spread is likely a greater threat to bacterial populations than currently believed.

You can see this happening here, with the bacteria receiving the plasmid (circled in red) stopping growth while everyone else is happily dividing.

We could see this happening under the microscope in the TacC lab. Cells expressing Namtar stop growing as soon as they receive the plasmid, that is visualized as bright green ParB-mChartreuse foci.

E. coli has a Namtar homolog and Julie Baltenneck in @francoisrousset.bsky.social lab showed that does the same thing. It kills cell that receive the R388 plasmid.

The two other genes encode the new Namtar and Attar immune systems, also widespread in bacteria.
They are membrane-associated proteins defending against R388. Namtar depends on sensing VirB8, while Attar senses VirB2. Both trigger a non-growing, ATP-depleted state.
Let's call this death.

Two of them are part of the same family encoding the new Ishtar immune system that is widespread in Bacteria, and also found in Archaea.
Ishtar carries a HEPN domain and specifically promotes loss of RP4 plasmid.

Which genes/function could limit conjugation?
Tn mutagenesis revealed the culprits in 12 strains.
Capsule is one of the barriers. Interestingly, H-NS expression can sometimes lift the barriers.
Most importantly 4 genes of patchy distribution specifically block R388 or RP4 conjugation.

Is conjugation really so efficient? Are there barriers? Do bacteria defend against it?
Ludovic tested 364 A. baumannii strains as recipients of the R388 and RP4 plasmids.
This revealed that resistance to conjugation is the norm and is a fast-evolving phenotype.