Investigating the Relationship between CRISPR-Cas Content and Growth Rate in Bacteria

ABSTRACT CRISPR-Cas systems provide adaptive immunity for prokaryotic cells by recognizing and eliminating the recurrent genetic invaders whose sequences had been captured in a prior infection and stored in the CRISPR arrays as spacers. However, the biological/environmental factors determining the efficiency of this immune system have yet to be fully characterized. Recent studies in cultured bacteria showed that slowing the growth rate of bacterial cells could promote their acquisition of novel spacers. This study examined the relationship between the CRISPR-Cas content and the minimal doubling time across the bacteria and the archaea domains. Every completely sequenced genome could be used to predict a minimal doubling time. With a large data set of 4,142 bacterial samples, we found that the predicted minimal doubling times are positively correlated with spacer number and other parameters of the CRISPR-Cas systems, like array number, Cas gene cluster number, and Cas gene number. Different data sets gave different results. Weak results were obtained in analyzing bacterial empirical minimal doubling times and the archaea domain. Still, the conclusion of more spacers in slowly grown prokaryotes was supported. In addition, we found that the minimal doubling times are negatively correlated with the occurrence of prophages, and the spacer numbers per array are negatively associated with the number of prophages. These observations support the existence of an evolutionary trade-off between bacterial growth and adaptive defense against virulent phages. IMPORTANCE Accumulating evidence indicates that slowing the growth of cultured bacteria could stimulate their CRISPR spacer acquisition. We observed a positive correlation between CRISPR-Cas content and cell cycle duration across the bacteria domain. This observation extends the physiological conclusion to an evolutionary one. In addition, the correlation provides evidence supporting the existence of a trade-off between bacterial growth/reproduction and antiviral resistance.