Cip1 and Cip2 are novel RNA-recognition-motif proteins that counteract Csx1 function during oxidative stress

Victoria Martín1, Miguel A Rodríguez-Gabriel, W Hayes McDonald

  • 1Department of Molecular Biology, The Scripps Research Institute, La Jolla, CA 92037, USA.

Insights

Two RNA-binding proteins, Cip1 and Cip2, regulate gene expression during oxidative stress in yeast. They counteract Csx1

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • Eukaryotic cells alter gene expression in response to stress.
  • The RNA-binding protein Csx1 is crucial for oxidative stress response in Schizosaccharomyces pombe.
  • Csx1 stabilizes atf1(+) mRNA, essential for oxidative stress gene expression.

Purpose of the Study:

  • Identify novel proteins interacting with Csx1.
  • Investigate the function of Cip1 and Cip2 in oxidative stress response.
  • Elucidate the interplay between Csx1, Cip1, and Cip2 in posttranscriptional regulation.

Main Methods:

  • Multidimensional protein identification technology (MudPIT) for protein identification.
  • Genetic epistasis studies to determine genetic interactions.
  • Whole genome expression profiling to analyze gene expression changes.
  • Analysis of cellular morphology and growth rates.

Main Results:

  • Cip1 and Cip2 were identified as Csx1-interacting proteins.
  • Cip1 and Cip2 are cytoplasmic proteins with RNA recognition motifs (RRMs).
  • Loss of Cip1 and Cip2 leads to poor growth and altered morphology.
  • Cip1 and Cip2 negatively regulate gene expression, counteracted by Csx1.
  • Mutations in cip1 and cip2 partially rescue the oxidative stress sensitivity of csx1Δ cells.

Conclusions:

  • Cip1 and Cip2 play a significant role in posttranscriptional control of gene expression during oxidative stress.
  • The balance between Csx1 and Cip1/Cip2 activity is critical for modulating mRNA stability and cellular response to stress.
  • This study highlights the complex regulatory network involving RNA-binding proteins in eukaryotic stress response pathways.

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