A Plasmodium falciparum histone deacetylase regulates antigenic variation and gametocyte conversion.

ABSTRACT: The asexual forms of the malaria parasite Plasmodium falciparum are adapted for chronic persistence in human red blood cells, continuously evading host immunity using epigenetically regulated antigenic variation of virulence-associated genes. Parasite survival on a population level also requires differentiation into sexual forms, an obligatory step for further human transmission. We reveal that the essential nuclear gene, P. falciparum histone deacetylase 2 (PfHda2), is a global silencer of virulence gene expression and controls the frequency of switching from the asexual cycle to sexual development. PfHda2 depletion leads to dysregulated expression of both virulence-associated var genes and PfAP2-g, a transcription factor controlling sexual conversion, and is accompanied by increases in g

SUBMITTER: Coleman BI 

PROVIDER: S-EPMC4188636 | biostudies-literature | 2014 Aug

REPOSITORIES: biostudies-literature