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Updated: Jun 24, 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 axonemal intron splicing program sustains Plasmodium male development

Jiepeng Guan1, Peijia Wu1, Xiaoli Mo1

  • 1State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Faculty of Medicine and Life Sciences, Xiamen University, Xiamen, China.

Nature Communications
|June 1, 2024
PubMed

Insights

A newly discovered male-specific RNA-binding protein, RBPm1, is crucial for malaria parasite development in mosquitoes. It ensures proper axoneme assembly for male gamete formation, enabling transmission.

Area of Science:

  • Malaria parasite biology
  • Molecular parasitology
  • Post-transcriptional gene regulation

Background:

  • Male gametogenesis in Plasmodium is essential for mosquito transmission.
  • RNA-binding proteins (RBPs) regulate gene expression post-transcriptionally.
  • The specific role of RBPs in male Plasmodium development is not fully understood.

Purpose of the Study:

  • To identify male-specific RBPs in Plasmodium.
  • To investigate the function of a novel RBP, RBPm1, in male gametogenesis.
  • To elucidate the mechanism of RBPm1 in regulating axoneme assembly.

Main Methods:

  • Genome-wide screening for gender-specific RBPs.
  • Generation and analysis of RBPm1-deficient Plasmodium parasites.
  • Interaction studies with the spliceosome complex.
  • Splicing assays using reporter and endogenous genes.
  • Analysis of axonemal gene expression and protein production.

Main Results:

  • Identified a novel male-specific RBP, RBPm1, essential for Plasmodium male gametogenesis.
  • RBPm1 deficiency leads to failed axoneme assembly and impaired mosquito transmission.
  • RBPm1 interacts with the spliceosome and regulates splicing initiation of 26 axonemal genes.
  • RBPm1 deficiency causes intron retention and loss of axonemal proteins.
  • Intron deletion partially rescues axonemal defects.

Conclusions:

  • RBPm1 is a critical splicing activator for axonemal genes.
  • An axonemal intron splicing program regulated by RBPm1 is essential for male gametogenesis.
  • RBPm1 plays a vital role in the post-transcriptional regulation required for malaria parasite transmission.

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