Identification of a sequence element regulating H3K9 methylation at the ap2-g locus in Plasmodium falciparum.

Authors

Mai Nakashima, Shiroh Iwanaga, Toshiyuki Mori

Published in

Scientific reports. Jul 13, 2026. Epub Jul 13, 2026.

Abstract

Plasmodium falciparum, the causative agent of malaria, undergoes a critical cell fate switch during the erythrocytic stage, when a subset of parasites exits asexual replication and differentiates into gametocytes-the forms required for transmission. This conversion is controlled by the transcription factor AP2-G, whose expression is normally repressed by H3K9me3 marked heterochromatin. The mechanism by which this silenced state is abolished has remained unknown. Here we identify a cis-regulatory element, URE-G, that is required for high levels of H3K9 methylation at the ap2-g locus. Deletion of URE-G decreases this modification, resulting in AP2-G activation and increased gametocyte formation, without altering global heterochromatin structure. These findings suggest a sequence-dependent mechanism for regulating heterochromatinized genes and provide insights into cell fate determination in malaria parasites.

PMID:
42443261
Bibliographic data and abstract were imported from PubMed on 14 Jul 2026.

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