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Human DHX29 detects nonoptimal codon usage to regulate mRNA stability.

Fabian Hia1, Yitong Wu1, Masanori Yoshinaga1

  • 1Department of Medical Chemistry, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

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Summary
This summary is machine-generated.

Researchers found that the RNA-binding protein DHX29 regulates gene expression by interacting with ribosomes. DHX29 suppresses nonoptimal messenger RNA (mRNA) translation, linking codon usage to gene expression control.

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Area of Science:

  • Molecular Biology
  • Genetics
  • Biochemistry

Background:

  • Synonymous codon usage influences global gene expression in prokaryotes and eukaryotes.
  • Nonoptimal codons are known to trigger mRNA decay, but the mechanism in human cells is unclear.

Purpose of the Study:

  • To identify the molecular mechanism regulating codon-dependent gene expression in human cells.
  • To elucidate the role of RNA-binding proteins in this process.

Main Methods:

  • Genome-wide CRISPR screening to identify key regulators.
  • Cryogenic electron microscopy and selective ribosome profiling to study protein-ribosome interactions.
  • Proteomic analysis to identify interacting protein complexes.

Main Results:

  • The RNA-binding protein DHX29 was identified as a critical regulator of codon-dependent gene expression.
  • DHX29 directly interacts with the 80S ribosome's A-site, suggesting a role in monitoring aminoacyl-tRNA sampling.
  • DHX29 recruits the GIGYF2•4EHP complex to suppress nonoptimal mRNAs globally.

Conclusions:

  • DHX29 acts as a key mediator linking synonymous codon usage to gene expression regulation.
  • This study establishes a mechanistic link between codon bias and mRNA regulation in human cells.