PfAP2Tel, harbouring a non-canonical DNA-binding AP2 domain, binds to Plasmodium falciparum telomeres.

The telomeres of the malaria parasite Plasmodium falciparum are essential not only for chromosome end maintenance during blood stage development in humans but also to generate genetic diversity by facilitating homologous recombination of subtelomeric, multigene virulence families such as var and rifin. However, other than the telomerase PfTERT, proteins that act at P. falciparum telomeres are poorly characterised.

Impact of chromosome ends on the biology and virulence of Plasmodium falciparum.

In recent years, many studies have focused on heterochromatin located at chromosome ends, which plays an important role in regulating gene expression in many organisms ranging from yeast to humans. Similarly, in the protozoan Plasmodium falciparum, which is the most virulent human malaria parasite, the heterochromatin present in telomeres and subtelomeric regions exerts a silencing effect on the virulence gene families located therein. Studies addressing P.

Two long non-coding RNAs generated from subtelomeric regions accumulate in a novel perinuclear compartment in Plasmodium falciparum.

Chromosome ends have been implicated in the default silencing of clonally variant gene families in the human malaria parasite Plasmodium falciparum. These chromosome regions are organized into heterochromatin, as defined by the presence of a repressive histone H3 lysine 9 trimethylated marker and heterochromatin protein 1. Here, we show that the non-coding subtelomeric region adjacent to virulence genes forms facultative heterochromatin in a cell cycle-dependent manner.