12:00noon Monday 9th December
Room 208, 2nd floor,
Microbiology building,
720 Cumberland Street
Prokaryotes are continually threatened by viruses and other selfish genetic elements. This constant challenge has prompted the evolution of numerous defence strategies. Clustered regularly interspaced short palindromic repeats (CRISPR) and CRISPR-associated (Cas) proteins constitute the only known prokaryotic adaptive and heritable immune system. In recent years, considerable progress has been achieved in understanding the function and practical applications of these systems. However, much less is known about the regulatory circuits employed by the cell for the control of CRISPR-Cas immunity. Therefore, to reveal the full potential of the CRISPR-Cas systems, it is crucial to understand the mechanisms of their regulation.
The principal aim of my project was to identify regulators of CRISPR-Cas immune systems in Serratia sp. ATCC39006 (Serratia) and unravel their mode of operation. I demonstrate that a LysR-type transcriptional regulator, PigU, and a cold-shock protein, CspE, regulate the activity of the three Serratia CRISPR-Cas systems (type I-E, I-F and III-A). Specifically, overexpression of PigU inhibits the interference response by all three CRISPR-Cas systems. Conversely, CspE promotes type I CRISPR-Cas activity, presumably on the post-transcriptional/translational level.
Overall, this study increases our understanding of the regulatory mechanisms employed by bacteria for the regulation of the CRISPR-Cas adaptive immunity.
