BSB PhD Exit Seminar: Characterising aspects of the CoA biosynthesis pathway in P. falciparum and T. gondii

Vanessa Howieson, Saliba Group, BSB, RSB

Malaria is an ancient disease leading to the death of more than half a million people every year. Malaria is caused by a parasite of the genus Plasmodium, with P. falciparum being the deadliest Plasmodium species.  P. falciparum has started to show signs of resistance to the current best class of antimalarial drugs –  artemisinin-based combination therapies. As such it is vital that new classes of compounds are discovered to add to our arsenal against the parasite. Our lab and has been studying pantothenate (vitamin B5) metabolism and utilisation by P. falciparum as a potential drug target. Pantothenate is the key precursor for the coenzyme A (CoA) biosynthesis pathway and CoA is essential to an estimated 9% of cellular metabolic processes. The malaria parasite cannot survive its disease-causing red blood cell stage without access to an exogenous supply of pantothenate as it cannot synthesise it de novo. During my PhD I have investigated aspects of pantothenate kinase, the first enzyme in the CoA biosynthesis pathway, in P. falciparum and another apicomplexan parasite T. gondii, an organism that is often used as a model organism for P. falciparum. Interestingly, unlike P. falciparum, T. gondii has been reported to be capable of pantothenate biosynthesis. I have therefore also investigated pantothenate synthetase, a key enzyme in pantothenate biosynthesis, in T. gondii.  In addition, I have explored a variety of compounds as potential anti-Plasmodium or anti-Toxoplasma drugs targeting CoA or pantothenate biosynthesis in these organisms. The key findings from my thesis will be presented at the seminar.  

 

Aditya Yadav will present her talk after Vanessa, please find more details here.