Bacteria have inhabited our planet for over 3 billion years and during much of that time have been subjected to infection by viruses (‘phage’). This pressure has driven bacteria to develop a wide range of anti-phage defense systems. Phage in turn have evolved mechanisms to evade those defenses, leading bacteria to develop additional anti-phage mechanisms. This back-and-forth process has been termed an “evolutionary arms race”. The Kaiser lab is interested in studying both sides of this equation; we want to understand the mechanisms of anti-phage systems as well as strategies phage use to evade those defense systems.

We recently discovered and characterized a novel phage protein that counteracts a bacterial defense system called CRISPR-Cas. CRISPR-Cas has received much attention in the last decade because of its potential biotechnology applications, but it is important to know that it evolved as an antiphage system. The phage protein that we discovered—called AcrIIA22—works by a novel and unexpected mechanism to block CRISPR-Cas function. This study was a collaboration with labs at the Fred Hutchinson Cancer Research Center in Seattle. You can read about it here:

The novel anti-CRISPR AcrIIA22 relieves DNA torsion in target plasmids and impairs SpyCas9 activity

Numerous Seattle University students have contributed to this project, both in the format of independent research projects and in class-based labs. The Kaiser lab is currently focusing on a novel bacterial defense system called “BREX”, and SU students will continue to contribute to these studies.