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Updated: May 23, 2025

Author Spotlight: Identifying Compensatory Pathways in Malaria Parasites Containing Hypomorphic Allele of Essential Protein Kinases
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Author Spotlight: Identifying Compensatory Pathways in Malaria Parasites Containing Hypomorphic Allele of Essential Protein Kinases

Published on: November 22, 2024

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An Essential Adaptor for Apicoplast Fission and Inheritance in Malaria Parasites

James Blauwkamp1, Krithika Rajaram2,3, Sophia R Staggers4

  • 1Indiana University School of Medicine, Department of Pharmacology and Toxicology, Indianapolis.

Research Square
|May 19, 2025
PubMed

Insights

A newly identified protein, PfAnchor, is essential for apicoplast fission and inheritance in malaria parasites. Its disruption prevents organelle division, leading to parasite death, offering a potential new antimalarial drug target.

Area of Science:

  • Cell Biology
  • Parasitology
  • Molecular Biology

Background:

  • The malaria parasite *Plasmodium falciparum* depends on its apicoplast, a non-photosynthetic plastid, for survival.
  • Apicoplast inheritance requires precise positioning and fission during parasite division, but the underlying molecular mechanisms are unclear.
  • Targeting the apicoplast is a promising strategy for antimalarial drug development.

Purpose of the Study:

  • To identify key regulators of apicoplast fission and inheritance in *P. falciparum* blood-stage parasites.
  • To elucidate the molecular function of a novel protein, PfAnchor, in apicoplast division.
  • To explore the therapeutic potential of targeting apicoplast fission.

Main Methods:

  • Ultrastructure Expansion Microscopy (U-ExM) to visualize PfAnchor localization.
  • Conditional gene depletion to assess the function of PfAnchor.
  • Immunoprecipitation to identify interacting proteins, including PfDyn2.

Main Results:

  • PfAnchor localizes to the apicoplast throughout asexual blood-stage development.
  • Conditional depletion of PfAnchor inhibits apicoplast fission, causing incomplete cytokinesis and parasite death.
  • PfAnchor interacts with PfDyn2, a dynamin-like GTPase, acting as an apicoplast-specific adaptor.

Conclusions:

  • PfAnchor is an essential regulator of apicoplast fission and inheritance in *P. falciparum*.
  • The findings highlight parasite-specific organelle division as a potential vulnerability for antimalarial interventions.
  • PfAnchor represents a novel target for developing new antimalarial therapies.

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