Infectious diseases from protozoan parasites and Mycobacterium tuberculosis cause millions of deaths per year worldwide. The emergence of resistant strains is a further problem, necessitating the need to discover new drug targets. One strategy to eliminate these deadly organisms is to compromise their essential pathways. For this, we turn our attention to the AAA+ ATPase enzyme, p97. A highly conserved and essential protein, p97 is a homohexameric unfoldase involved in various cellular activities such as endoplasmic reticulum-associated degradation (ERAD), autophagy, membrane fusion and more. Our approach is to inhibit this enzyme to cause proteotoxic stress, resulting in death of the pathogen. Here, we present the bioinfomatics analysis of the p97 homologues from five pathogenic organisms and virtual screening results for potential novel and specific inhibitors.
Sequences of the homologues were obtained with sequence identities ranging 36-75%. Multiple sequence alignment showed that nucleotide-binding sites were highly conserved between species, but the interface between D1 and D2 domains showed higher sequence variability. 3D models of the homologues were generated using homology modelling. These models were used for protein-ligand docking of known p97 inhibitors. Docking showed consistency in binding to the nucleotide-binding site but more variation for a potential allosteric site at the D1-D2 interface. Virtual screening of a lead-like compound library (5921 ligands) predicted several compounds that bind to the latter site in each of the p97 homologues.
The research aims to provide insight into the structure and function of p97 homologues in protozoan parasites and M. tuberculosis. The selective targeting of the p97 protein in these pathogens is a novel concept with potential for future studies in drug design. In the near future, in vitro assays will be developed to confirm the binding affinity of these compounds. This study will also be accompanied by experiments for structural determination and biochemical characterisation.