Will Smith

Fantastic talk about the impact of inflammation on Pseudomonas aeruginosa evolution by @taoranfu.bsky.social #MicroEvo25

Find out more about DNA repair protein single-molecule tracking from @bexlowrypalms.bsky.social at poster 18🔬 #MicroEvo25

Come chat to Dan at poster 22 to learn about endosymbiosis evolution #MicroEvo25

Had the best day at #MicroEvo25 yesterday! Excited for day two and to be chatting more about hot spring microbial community coalescence 🌋 find me at poster 62 (likely with a coffee in hand)

EDIT: I was wrong, I was poster 070! 🤦‍♂️

Come and see @willpjsmith.bsky.social at poster 71 to find out more about microbial warfare! #MicroEvo25

The type VI secretion system and associated effector proteins - Nature Reviews Microbiology In this Review, Basler and colleagues examine the type VI secretion system (T6SS), focusing on the diversity of antibacterial T6SS effectors and the evolutionary forces that shape them. They explain h...

Happy to share our latest T6SS review:
nature.com/articles/s41...

Thank you, Jan, Danny (@dannyjamesward.bsky.social), Joana (@joanampereira.bsky.social), as well as reviewers and editors @natrevmicro.nature.com!

Strain displacement in microbiomes via ecological competition - Nature Microbiology Mathematical modelling and experimental tests reveal principles that govern displacement of a resident strain by an invader in microbial communities.

Can we leverage bacterial competition for targeted replacement of harmful strains? Maybe! Our recent piece in @natmicrobiol.nature.com provides a theoretical framework and a set of experiments to show what it might take: www.nature.com/articles/s41...

Had a fabulous time at the @wellcometrust.bsky.social ECR meeting today! Thanks for sharing some inspiring science and innovations to improve research culture 🧑‍🔬 and sustainability 🌱

Bacterial warfare is associated with virulence and antimicrobial resistance - Nature Communications Bacteria employ a range of competition systems that deliver toxins to inhibit competing strains. This study shows that these systems are particularly important for the ecology of virulent and antibiot...

So happy to share this! Bacteriocins were first discovered over 100 years ago, but what do they actually do? We look at >1000 bacteriocin plasmids and find links to virulence and antimicrobial resistance, and frequent bacteriocin sharing in Enterobacteriaceae.
www.nature.com/articles/s41...

Hello everyone, take a look at my cool bugs from the Microbial Dark Matter phylum Saccharibacteria! These ultrasmall bacteria (in green) track down Actinobacteria hosts (not in green) and grow on the host cell envelope.

Open position to work on Type IX secretion (#T9SS) in our lab, in collaboration withe the group of Eric Reynolds at the Dental School of the University of Melbourne. Please spread the word, and forward to anyone potentially interested ! Apply here:
emploi.cnrs.fr/Offres/Docto...

🧐Checkout our preprint revealing the stepwise firing💥 mechanism of a Contractile Injection System @xujwet.bsky.social&@chipericson.bsky.social trapped the complex by structure-guided engineering🧪 in multiple intermediate states and imaged them by multimodal #cryoEM❄️🔬
www.biorxiv.org/content/10.1...

Metabolic interplay drives population cycles in a cross-feeding microbial community - Nature Communications Here the authors leverage a crossfeeding, engineered microbial community to demonstrate that strain abundance cycles are robust across environmental conditions. They pair this with a nonlinear dynamic model to elucidate population cycles.

Metabolic interplay drives population cycles in a cross-feeding microbial community www.nature.com/articles/s41... #jcampubs

LOL wet! I don't think it's stopped raining for the last 24h ^^

YES! Amazing news, big congrats Rachel! 🎉

Phage "satellites" that produce capsids but have no genes to produce tails have puzzled scientists for a long time. These are abundant as prophages in bacteria, but it was unclear how they can infect without tails

Now, Penadés & co show that they hijack tails from other phages. Incredible!

FIG. 3: Time lapse visualizations of a two player coordination game with payo matrix A = [10 5; 510]. The images show the spatial con guration (lattice size L = 256) at t = 0246810 with dt = 005. White corresponds to player 1 and black is player 2. Starting from well mixed initial condition, initial fraction of player 1 is 05, the two players separate into domains whose characteristic length scales (patch size) grow over time.

New preprint bubbling up in our group for a while:

"Phase separation and coexistence in spatial coordination games between microbes"

www.biorxiv.org/content/10.1...

Generalizes findings of phase separation in microbes using T6SSs to a broad range of interaction mechanisms.

Li + Steinbach et al.

Thanks for reading this thread! We hope the paper is interesting and useful Huge thanks to my coauthor @prokaryota.bsky.social for a really cool and enjoyable collab, Elisa is the best :-)

16/16

If your lab does competition assays where microbial antagonism is (or may be!) involved, it might be worth doing a ground-truth check for biases like these. Also, some assays won't be affected e.g. if you use colorimetric killing assays that don't rely on a selection step or c.f.u. counting.

15/n

Bacterial species rarely work together Competition is prevalent and could be harnessed as an alternative to antibiotics

What's our take-away? Competitive interactions are very common (see e.g. www.science.org/doi/10.1126/...) and we've shown they can be hard to quench in a killing assay. This can lead to over-estimation of strong competitive interactions.

14/n

Conversely, when Susceptible cells are rare (e.g. if they *didn't* do well in the competition assay), few dilutions are required to count Susceptible c.f.u.s. and there will be proportionally more contact with T6SS-armed Attackers. More T6SS contact, more residual killing, fewer c.f.u.s.

13/n

When Susceptible cells are abundant (e.g. if they did pretty well in the competition assay), large dilutions are necessary to count c.f.u.s. These dilutions will tend to separate Attackers and Susceptibles and minimise residual killing on the selective media.

12/n

Why does this bias results most where the Attacker : Susceptible ratio is high?

Here's a little cartoon explainer:

11/n

We also found that, if cell mixtures are pre-incubated in a liquid antibiotic that selects against T6SS attackers, this reduces the bias, especially for longer pre-incubation times.

10/n

We found that there was a strong, T6SS-dependent reduction in the number of E. coli c.f.u.s recovered, compared with the “”ground truth” densities we knew we should be getting (plotted here as a pink zone). The deviation tended to increase with increasing Attacker / Susceptible ratio.

9/n

We wondered how this would bias the results of a killing assay. We devised a "ground-truth" experiment where we mixed E. coli and A. baylyi in known ratios, before diluting and plating on selective media as per a regular killing assay, to see what c.f.u. counts we'd get back.

8/n

In other words, Kanamycin really isn’t quenching T6SS antagonism effectively in the aftermath of a killing assay, and so you’d predict that you’d get fewer E. coli CFUs as a result.

7/n

We found that T6SS-armed A. baylyi ADP1 bacteria (often used to study T6SSs), will transiently still fire their T6SS harpoons under lethal selective conditions. Here we see ADP1 killing some green E. coli when ADP1 is supposed to be dead!

6/n

Thinking about this in our own studies, we did some tests. Turns out that some antagonistic interactions, like those via harpoon-like Type 6 Secretion Systems (T6SSs), DON’T STOP just because cells are being selected against by lethal concentrations of antibiotic.

5/n