The Canonical Histone H2A, of the Malaria Parasite Plasmodium falciparum is Phosphorylated and Recruited to Foci of Damaged DNA

Plasmodium falciparum parasites proliferate within the circulating red blood cells and is responsible for the deadliest form of human malaria. These parasites are exposed to numerous intrinsic and external sources that could cause DNA damage, therefore, they have evolved efficient mechanisms to protect their genome integrity and allow them to proliferate in such conditions. In yeast and mammals, double strand breaks rapidly lead to phosphorylation of the core histone variant H2A.X which marks the site of damaged DNA. Here we show that in Plasmodium falciparum parasites, that lack the H2A.X variant, the canonical PfH2A is phosphorylated on serine 121(SQ motif) upon exposure to DNA damage. We further demonstrate that phosphorylated PfH2A is recruited to foci of damaged chromatin shortly after exposure to source of damage and that the phosphorylation is decreased over time as the parasite repairs its DNA. Altogether these findings present novel marker for DNA damage in Plasmodium that could be used as a useful tool to study DNA damage response in these deadly pathogens.