A single nucleotide polymorphism in a Plasmodium berghei ApiAP2 transcription factor alters the development of host immunity

Malaria causing parasites belonging to genus Plasmodium have a complex life cycle involving two hosts. Within these hosts parasites continuously shift between multiple morphologically distinct stages each of which has unique abilities to invade and survive in different host cell types. As repeatedly shown by independent studies, transcriptional profile of the parasite alters dramatically between stages which highlights the requirement for rapid and precise control of gene expression in these protozoans. However, genome wide studies revealed that plasmodium lacks orthologues of transcription factors found in other eukaryotes, has undefined promotor regions lacking conserved regulatory elements, has a lot smaller predicted specific TF to total proteome ratio compared to other eukaryotes. Instead, these parasites have been shown to contain a sophisticated histone modification machinery, stage specific control of mRNA decay rates, abundance of anti-sense RNA transcription and multiple epigenetic regulatory mechanisms . All these supporting evidences led to the general conception that plasmodium gene expression is primarily regulated by mechanisms other than TFs. Overall design: Plasmodium berghei wild type vs. AP2