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The evolutionarily conserved PRP4K-CHMP4B/vps32 splicing circuit regulates autophagy.

Sabateeshan Mathavarajah1, Sandhya Chipurupalli1, Elias B Habib1

  • 1Department of Pathology, Faculty of Medicine, Dalhousie University, Halifax, NS B3H 4R2, Canada.

Cell Reports
|June 18, 2025
PubMed
Summary

The pre-mRNA processing factor 4 kinase (PRP4K) regulates autophagy by controlling splicing of key genes. PRP4K knockout impairs autophagosome-lysosome fusion, revealing a conserved splicing circuit essential for cellular function.

Keywords:
CHMP4BCP: Cell biologyCP: Developmental biologyDictyosteliumESCRT IIIPRP4KPRPF4Bautophagysplicing kinase

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Genetics

Background:

  • The pre-mRNA processing factor 4 kinase (PRP4K) is crucial in animal cells, but its functions are difficult to study.
  • Investigating PRP4K's role requires models that allow for functional genetic interrogation.

Purpose of the Study:

  • To characterize a viable knockout model of PRP4K in Dictyostelium discoideum.
  • To elucidate the function of PRP4K in splicing events controlling autophagy and multicellular development.

Main Methods:

  • Generation and analysis of a prp4k knockout Dictyostelium discoideum model.
  • Assessment of autophagy, differentiation, and secretion pathways in knockout and wild-type cells.
  • Investigation of autophagosome-lysosome fusion in both Dictyostelium and human cell lines.
  • Analysis of ESCRT-III gene (CHMP4B/vps32) splicing and expression.

Main Results:

  • PRP4K knockout in Dictyostelium leads to developmental defects, abnormal autophagy, and aberrant c-di-GMP secretion.
  • Autophagosome-lysosome fusion is impaired in both PRP4K-deficient human cells and Dictyostelium.
  • PRP4K loss causes mis-splicing and reduced expression of CHMP4B (human) and vps32 (Dictyostelium).
  • Restoring CHMP4B or Vps32 expression rescues autophagosome-lysosome fusion defects.

Conclusions:

  • A conserved splicing circuit involving PRP4K and CHMP4B/vps32 regulates autophagy.
  • This PRP4K-CHMP4B/vps32 pathway is essential for autophagosome-lysosome fusion and is conserved across evolution.
  • The study provides insights into the fundamental mechanisms of autophagy regulation.