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Separate transcription and splicing gene networks are linked and coordinated by the pRb-E2F pathway

Simon M Carr1, Geng Liu1, Wojciech Barczak1

  • 1Laboratory of Cancer Biology, Department of Oncology, University of Oxford Old Road Campus Research Building, Oxford OX3 7DQ, United Kingdom.

Nucleic Acids Research
|January 30, 2026
PubMed

Insights

The pRb-E2F pathway regulates gene expression and RNA splicing, impacting cell fate and cancer. This study reveals distinct gene networks controlled by this pathway, influencing biological diversity.

Area of Science:

  • Molecular Biology
  • Genomics
  • Cancer Biology

Background:

  • The Retinoblastoma-E2F (pRb-E2F) pathway is crucial for cell cycle control and is frequently dysregulated in cancer.
  • Recent research indicates the pRb-E2F axis governs extensive gene networks, including those involved in RNA transcription and splicing.

Purpose of the Study:

  • To conduct a comprehensive genome-wide analysis of differentially expressed genes (DEGs) and alternatively spliced (AS) RNA targets regulated by the pRb-E2F pathway.
  • To elucidate the independent regulation of gene expression and splicing networks by the pRb-E2F pathway.

Main Methods:

  • Genome-wide analysis of DEGs and AS RNA targets.
  • Functional analysis of pathway components (E2F1, pRb, PRMT5) using knockout models.
  • E2F1 interactome analysis.

Main Results:

  • Identified broadly non-overlapping DEG and AS networks independently regulated by the pRb-E2F pathway.
  • Demonstrated that E2F1, pRb, and PRMT5 influence DEG and AS networks to varying degrees.
  • Revealed SRSF2 and HNRNPC as potential E2F1 interactors assisting in AS.
  • Observed E2F1's alternative splicing activity during cell cycle progression, DNA damage response, and in tumor models.

Conclusions:

  • The pRb-E2F pathway links and coordinates gene transcription and RNA splicing.
  • pRb, E2F1, and PRMT5 significantly influence biological diversity through RNA splicing regulation.
  • This pathway's disruption is a key factor in cancer development.

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