3D7 PfHda2 Knockdown vs. Wildtype

The asexual forms of the malaria parasite Plasmodium falciparum are uniquely adapted for chronic persistence in human red blood cells, continuously evading the immune system using an epigenetically regulated process. However, parasite survival on a population level also requires transmission of sexual parasite forms to subsequent human hosts. Here, we reveal that the essential nuclear gene, P. falciparum histone deacetylase 2 (PfHda2), silences specific subsets of genes involved in antigenic variation or conversion to sexual stages. Two parallel timecourses resulting in a total of 22 samples (11 wildtype, 11 PfHda2 knockdown) were hybridized against a Cy3-labeled reference pool of 3D7 mixed stage parasites on a two-color array.