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

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.