Pore-forming proteins (PFPs) are a large family of proteins capable of punching holes in their target cell membranes. Cholesterol-dependent cytolysins (CDCs) are a prominent class of bacterial PFPs. Although these proteins have been studied for the past four decades, we still don’t clearly understand the pore formation mechanism of these proteins, especially how these proteins are inserted into their target membranes (1).
The recent identification of cholesterol-dependent cytolysin-like proteins (CDCLs), a novel, diverse family of over 300 uncharacterised proteins, led to a further understanding of the pore-forming mechanism of CDCs. CDCLs and CDCs share a common motif (F/Y-F/Y-Xn-YGR) and show high structural similarity, particularly in the D1, D2 and D3 domains (2). Interestingly, the D4 domain of the CDCLs is very different from that of CDCs, and in some CDCLs, the entire C-terminal D4 domain is absent. Those containing domains 1-4 are referred to as long CDCLs, while those that don’t have a D4 domain are referred to as short CDCLs.
Bacteroides fragilis are gram-negative anaerobic bacteria found in the human colon (3). We are currently investigating the structure and pore-forming activity of a pair of long and short CDCLs from B. fragilis. Previous studies of Elizabethkingia anopheles CDCLs showed that both short and long forms are required for active pore formation, making it a two-component pore system (2).
We aim to study the stoichiometry of B. fragilis CDCLs in their pore state and determine the distinct steps involved in pore formation using X-ray crystallography for individual monomeric states, cryo-electron microscopy for the pore complex and small-angle X-ray scattering for solution structures. Progress towards these aims will be presented. This study will help discover the similarities and differences in how different CDCLs punch holes in their target cell membranes and reveal how different D4 domains influence pore formation.