New rotation student doing his first Gibson!

Look out world - @baym.lol is stepping back into the lab and is already breaking things!

Provirus induction diversifies adaptive variation in Pseudomonas aeruginosa lysogen populations Pseudomonas aeruginosa is a Gram-negative opportunistic pathogen that forms chronic infections in people with cystic fibrosis. Often P. aeruginosa strains are lysogens, infected with proviruses, that ...

Happy new year! The second big project of my PhD in Rachel Whitaker's lab is now up! 🎉 We look at how provirus infection affects the evolution of the bacterial chromosome with different types of viral induction – with CRISPRs or antibiotics. Take a peek 🦠 www.biorxiv.org/content/10.6...

Arya (my best friend) does not have social media, he asked me to tweet this for him. But if you want to chat about science (or offer him a job) you can contact him at arya.casa/contact. He’ll (probably) be defending soon!

GitHub - baymlab/deletion-born-fusion-manuscript Contribute to baymlab/deletion-born-fusion-manuscript development by creating an account on GitHub.

💻 github.com/baymlab/deletion-born-fusion-manuscript
🔧 github.com/aryakaul/prefixsuffix-kmer
Many thanks to co-authors @fernpizza.bsky.social , @brinda.eu & @baym.lol + GenScale/Baym lab! Funded by NIH, Packard, Pew, Sloan & a Chateaubriand Fellowship!

Some ~caveats~
🔹 We haven't proven any deletion was beneficial
🔹 No functional deletion-born fusion yet - selection analyses show mainly diversifying selection
🔹 Our method misses fusions with terminal mutations (requires exact 54bp matches)

The "deletional bias" in bacterial genomes has long been framed as destructive - the pruning away of genetic material.

Our findings suggest it might also be creative: deletions don't just remove genes, they can also build new ones!

GitHub - aryakaul/prefixsuffix-kmer: ✂️🧬🧩 - rapidly identify structural variation across the bacterial ToL ✂️🧬🧩 - rapidly identify structural variation across the bacterial ToL - aryakaul/prefixsuffix-kmer

You can try the prefix-suffix approach yourself! Find the Snakemake pipeline here github.com/aryakaul/pre...

The prefix-suffix approach isn't just for fusions. We also found:
🔹 Internal deletions
🔹 Repeat prophage insertions
🔹 Variable gene cargo in mobile elements

It's a general tool for surveying structural variation at scale!

But here's the CATCH: detection depends on sampling depth.

When we queried well-sampled protein families we found significantly more fusions than from uniformly sampled families.

We're only seeing the tip of the iceberg. As databases grow, we expect to find more.

Applying the prefix-suffix approach to type strains from 5 commonly studied bacteria (E. coli, N. gonorr., M. tubercul., Strep. pneumo., C. jejuni) we find deletion-born fusions across the bacterial Tree of Life:

How common is this across the bacterial tree of life?

We developed a new method to query 2.4M+ genomes (thanks to @zaminiqbal.bsky.social AllTheBacteria!): look for the “prefix” and “suffix” k-mer of an input gene at variable distances.

If the distance changes → structural variation.

It's not just in the lab. During the M. tuberculosis–M. bovis split, we found 2 deletion-born fusions:
🔹 acrR-glcD
🔹 mlaE-htpX

These arose during speciation and persist in natural populations today.

We found one in the @relenski.bsky.social LTEE: a 57.5 kb deletion in E. coli in the Ara+1 lineage fused yjcO (unknown function) to lysU (lysyl-tRNA synthetase).

Sequencing shows it's transcribed, translated, and swept to fixation in ~500 generations.

Most new genes die before they do anything useful, lost to genome streamlining and drift.

But deletion-born fusions are different! They hitchhike on beneficial deletions, getting a "free ride" to high frequency.

This buys them TIME to evolve function.

Here's the idea: when a deletion is beneficial (reducing genome size, removing costly genes), it can bring two distant gene fragments together.

The result? A brand new fusion gene - created entirely by accident

Duplication is constrained by existing templates. Overprinting produces disordered proteins & must preserve the original gene. HGT just imports genes born elsewhere.

What if deletions - usually viewed as destructive - could also create?

Pangenome studies find tens of thousands of protein families per species. Metagenomics reveals millions of genes of unknown function.

So where does all this novelty come from?

🎉 New year, NEW PREPRINT!

Bacteria exhibit astonishing genetic diversity, but where do new genes come from?

My best friend Arya Kaul (/labmate in the @baym lab) investigates how advantageous deletions can spawn new genes - "deletion-born fusions." 🧵:

Happy to share that I’m opening my lab at the Weizmann Institute of Science!
We’ll study systems-level regulation of bacterial defense, driven by RNA-protein interactions shaping cell fate.
Now recruiting PhD students & postdocs
tinyurl.com/4yfa55vd
Please reach out and share!

I know you are but what am I

“It is a damn poor mind that can think of only one way to spell a word”

-Andrew Jackson

Awe shucks

I almost forgot

Thanks to @baym.lol for giving me a home and the opportunity, @fernpizza.bsky.social who taught me the ropes of evolutionary biology, @wheezenfeld.bsky.social @theshreyaspai.bsky.social @nquinoneso.bsky.social, @celiasouque.bsky.social for the help along the way and the rest of the Baym lab crew!

This work highlights how interactions between MGEs can produce unique effects where both benefit from their nested existence. Furthermore, we have extended TnpB’s mechanism that sheds light on why TnpB is so successful.

So we did a similar experiment with conjugative plasmids and found that IS605 provides offensive and defensive benefits to conjugative plasmids, acting like a primitive anti-self defense mechanism to spread plasmids between cells.

Moreover we also noticed that IS605 tended to cluster in conserved plasmid regions of conjugative plasmids.

And specifically it is the RNA-guided nuclease activity that is responsible for this benefit - confirming our hypothesis!

Which we were able to show experimentally by competing plasmids in a displacement assay. We see plasmids that contain an IS605 have an enormous advantage over those that don’t, despite the IS itself being detrimental to plasmid replication