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Epigenetic memory at malaria virulence genes

Thanat Chookajorn1, Ron Dzikowski, Matthias Frank

  • 1Department of Organismic and Evolutionary Biology, Harvard University, Cambridge, MA 02138, USA. chookaj@fas.harvard.edu

Proceedings of the National Academy of Sciences of the United States of America
|January 9, 2007
PubMed

Insights

Malaria parasites like Plasmodium falciparum use epigenetic memory, specifically histone methylation, to control switching of their variant surface proteins (P. falciparum erythrocyte membrane protein 1) for immune evasion.

Area of Science:

  • Parasitology
  • Immunology
  • Epigenetics

Background:

  • The malaria parasite *Plasmodium falciparum* exhibits antigenic variation by switching variant surface proteins (P. falciparum erythrocyte membrane protein 1) to evade host immunity.
  • The *var* gene family encodes these proteins, with each parasite expressing a single *var* gene exclusively, contributing to a vast and diverse gene pool.

Purpose of the Study:

  • To investigate the epigenetic mechanisms underlying the control of *var* gene transcription and antigenic variation in *Plasmodium falciparum*.
  • To explore the role of chromatin memory in the pathogenesis and immune evasion strategies of malaria parasites.

Main Methods:

  • Analysis of epigenetic marks associated with *var* gene expression.
  • Investigation of histone modifications, including methylation of histone H3 at lysine K9 (H3K9me).

Main Results:

  • Control of *var* gene transcription and antigenic variation is linked to a chromatin memory.
  • Methylation of histone H3 at lysine K9 serves as a key epigenetic mark in this memory system.

Conclusions:

  • Epigenetic mechanisms, particularly H3K9me, play a crucial role in regulating antigenic variation in *Plasmodium falciparum*.
  • Understanding this gene transcription memory is vital for comprehending malaria pathogenesis and developing effective immune evasion strategies.

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