RT @phagedirectory: A 75-year-old female patient w/ recurrent Pseudomonas septicaemia & arterial stents was treated using a #phage–meropene….

RT @PrecisionPhage: ✨Phage therapy news!. We are happy to share that phages from PrecisionPhage were successfully used to treat recurrent s….

Forgot to mention that we also made a website for type III enthusiasts! Here you can browse through the analysed loci, filter them by properties and view annotations graphically

See Malcolm's thread for more details

RT @PrecisionPhage: PrecisionPhage took part in the Tahko Ski Lift Pitch - an energising 2-day pitching event with an outstanding startup l….

RT @PrecisionPhage: PrecisionPhage is excited to soon announce the launch of our Software-as-a-Service platform – Phagenomics - designed to….

RT @sundberglr: Four PhD positions available in ⁦@uniofjyvaskyla⁩ Finland, one of these in my research group! The topic is phage-bacterium….

Check out our work on a new antivirus signaling molecule found in type III CRISPR-Cas systems. Thank you @Skr_fi for supporting the project 🎉.

This tale of a hardworking microbe is no longer a preprint 🙌 @sundberglr @Gabriel_MFA.

RT @rafapinilla92: Very excited to see our story online in @NAR_Open!🎉. We found plasmids in nature carry a fascinating diversity of CRISPR….

Since mucosal surfaces are a hotspot for many other bacterial species and their phages to interact, it is likely that this balancing act of defense strategies is widespread. It will be interesting to see follow-up research across species and defense systems 👋.

Phage genome sequencing on the population scale revealed very few mutations and surprisingly, none in the protospacer regions 🤷‍♂️.

Bacterial genome sequencing showed genetic modifications mostly in gliding motility genes. This occurred also in isolates with spacer acquisition, indicating that both defenses are active and are perhaps deployed sequentially.

Most isolates were resistant to the ancestral phage. Also, isolates without SM benefitted from new spacers, while those with SM and new spacers had reduced growth. Adding a competing bacterium to the mix also increased spacer acquisition, similar to Alseth et al. 2019.

In mucin-containing cultures, CRISPR spacer acquisition skyrocketed, especially when using lake water. While generally we get very little or no colonies with expanded CRISPR arrays, in lake water with mucin ~60% of colonies had spacers in either array (types II-C and VI-B) 🚀🚀🚀.

So, we added a component of mucus called mucin to cultures with phage and bacteria. Through a 16-week experiment we followed CRISPR spacer acquisition and morphology change indicative of SM.

However, triggering native F. columnare CRISPR spacer acquisition in the lab is difficult. We wondered if we could accelerate spacer acquisition in a setting that discourages SM (by hinting there’s a fish nearby) but also exerts phage predation.

This bacterium, Flavobacterium columnare, commonly prevents phage entry through surface modification (SM). However, SM also reduces or abolishes the bacterium’s own virulence. Another defense strategy is to use CRISPR-Cas, which degrades incoming phage genomes inside the cell.

We studied a fish pathogen that invades its host through a mucus layer. Invasion is made possible by surface receptors encoded by gliding motility genes. The bacterium is also preyed upon by phages, which utilise these same receptors to gain entry to the cell.