Will Smith

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

The problem is this: if one population is antagonising another, how do you STOP that antagonism happening when you plate cells on selective media? After all, biology doesn’t stop for our convenience!

4/n

Survival is then a read-out of competitive interactions: the lower the survival when populations are mixed c.f. control, the stronger the antagonism between them. Survival is often measured using c.f.u. counts on selective media.

3/n

Some background: competition assays are common in microbiology. You mix different populations of microbes (normally 2 types for simplicity), allow them to compete, and then measure how many cells survive from each population, compared with some control where the populations don’t interact.

2/n

Type VI secretion system activity at lethal antibiotic concentrations leads to overestimation of weapon potency Competition assays are a mainstay of modern microbiology, offering a simple and cost-effective means to quantify microbe–microbe interactions in vitro. Here, we demonstrate a key weakness of this meth...

Does your lab perform killing assays?
TL;DR: we’ve identified a problem that can bias the outcome of killing assays, making antagonism look stronger than it really is.
Adding a simple extra step can mitigate this bias!

Out now at #MicrobioJ www.microbiologyresearch.org/content/jour...

1/n

The Royal Society David Attenborough Award and Lecture 2025 is awarded to Dr Roger Highfield for a vast contribution to public engagement, reaching audiences of millions through journalism, broadcast, books and museum-led initiatives. https://royalsociety.org/medals-and-prizes/attenborough-prize/

Check out our latest preprint! We show that the same antibacterial toxin requires different immunity proteins depending whether it’s intra or extracellular

‪Well done @magdalenakurteu.bsky.social,
@matthewjshepherd.bsky.social,
@bexlowrypalms.bsky.social,
@flanagella.bsky.social‬,
Eric Chapman, Joy Hawley, Hannah Jones, Jeremy DeJardin and Logan Sauers!

Go Team! Deeply honoured that the MERMan lab reps won an @manchester.ac.uk‬ "FMBH heroes" award - thanks ‪@fbmh-uom.bsky.social‬ and @mermanchester.bsky.social for nominating us ❤️❤️❤️

Only one week to go until the abstract submission deadline for Understanding and predicting microbial evolutionary dynamics 2025! Make sure to submit by 23:59 BST on 7 July 2025. microb.io/Abstracts #MicroEvo25

Modeling predicts that metabolic diversity increases the ecological impacts of weapon gene transfer. Modeling scenarios for each column are shown across the top row. Bottom row: Example dynamics of the strains (attacker, target, transconjugant) during a contest using parameters that correspond to the cross (X) shown in the parameter sweeps directly below.

#Bacteria use weapons to outcompete rivals, but what happens if they're transferred? @prokaryota.bsky.social @jdpal.bsky.social &co show that HGT of toxin #plasmids is rare but recipients can thrive under relaxed nutrient competition, reshaping bacterial warfare @plosbiology.org 🧪 plos.io/43vC3X7

R-pyocins as targeted antimicrobials against Pseudomonas aeruginosa - npj Antimicrobials and Resistance npj Antimicrobials and Resistance - R-pyocins as targeted antimicrobials against Pseudomonas aeruginosa

Delighted to be able to share our new review on R-pyocins produced by Pseudomonas aeruginosa. It covers genetics, regulation, killing mechanisms and therapeutic potential amongst other things. #MicroSky www.nature.com/articles/s44...

Had a fantastic time at @pintofscience.uk last night! Here I am wobbling on a chair trying to turn a #Phage into a #T6SS. Thanks @magdalenakurteu.bsky.social‬ for the pic!

Had the absolute best time at @pintofscience.uk talking about microbial evolution and some of the work I’ve been doing at @mermanchester.bsky.social with @flanagella.bsky.social and @dannagifford.bsky.social 🧫💊🧬