Overall, we conclude that while CRISPR-immunity prevents bacteria from dying at high phage doses, a subpopulation undergoes SOS-response mediated growth defects and elongation. Conversely, surface-based resistant bacteria do not, thus favouring this type of resistance at high phage dose.

Finally, we used flux cytometry to confirm that the elongated phenotype was linked with SOS response induction.

However, we noticed some heterogeneity in the population, with some CRISPR-immune bacteria stalling and suffering from elongation, particularly at high phage doses, which is consistent with this second hypothesis

We then tested our second hypothesis, that CRISPR-immune bacteria were displayed growth defects compared to surface-based resistant bacteria at high phage doses. We did not observe a significant difference in growth rate at the whole population level.

Our first hypothesis was that at high phage dose, surface-based resistance offered more protection than CRISPR-immunity. However, we showed that both types of defences offer a similar, almost perfect protection against phages regardless of the phage dose.

While CRISPR-Cas system inability to fully prevent phage gene expression seemed to play a role, it was still unclear what was causing the apparent CRISPR-Cas fitness cost at high phage doses. Here we investigated two hypotheses by using a microfluidics set-up to follow single bacteria in microscopy.

Pseudomonas aeruginosa can choose between CRISPR-Cas immunity and resistance through surface receptor mutation to evade their phages foes. Previous work from the lab had shown that the choice depends on the strength of phage selection pressure, with CRISPR-immunity being favoured at low phage dose.

Thanks a lot for your insightful presentation! That was great to have you here in Toulouse! You're most welcome to visit us again anytime 😀