1:00 pm, Monday, 4 September
Room BIG13, Ground Floor
Biochemistry Building
710 Cumberland St
David Mayo Muñoz
Microbiology & Immunology
The CRISPR conflict: strategies for defence and anti-defence
Mobile genetic elements (MGEs), such as bacteriophages and plasmids, can provide beneficial traits to their bacterial hosts but also come with a fitness cost, leading to the evolution of defence systems against them. In turn, MGEs have developed strategies to evade host immunity, resulting in an ongoing arms race between MGE-host.
During my PhD studies, I explored the molecular mechanisms underlying immune function and regulation of CRISPR–Cas systems, one of the most widespread bacterial defences. We unveiled post-transcriptional control of CRISPR–Cas in Serratia ruled by the RNA chaperone Hfq and associated small RNAs, as well as the induction of CRISPR-mediated abortive infection to protect the bacterial population against nucleus-forming jumbo phages. On the other side of the coin, we investigated how CRISPR–Cas systems and components thereof are recruited by phages and plasmids for non-canonical functions, e.g. mediating inter-plasmid warfare or, paradoxically, acting as anti-CRISPRs to block host immunity.
The research presented broadens our understanding of the complex interactions that arise in this evolutionary arms race and lays the foundation for promising biotechnologies.
