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A novel factor Iss10 regulates Mmi1-mediated selective elimination of meiotic transcripts

Akira Yamashita1, Tomomi Takayama, Ryo Iwata

  • 1Laboratory of Gene Function, Kazusa DNA Research Institute, 2-6-7 Kazusa-kamatari, Kisarazu, Chiba, 292-0818, Japan and Department of Biophysics and Biochemistry, Graduate School of Science, University of Tokyo, Hongo, Tokyo, 113-0033, Japan.

Nucleic Acids Research
|August 28, 2013
PubMed

Insights

Iss10 regulates the Mmi1/DSR elimination system by controlling the Mmi1-Red1 interaction. Loss of Iss10 impairs this interaction, leading to ectopic expression of meiotic transcripts during mitosis.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • Meiosis-specific transcripts are eliminated during mitosis in fission yeast via the Mmi1/DSR system.
  • Mmi1 (RNA-binding protein) targets transcripts with the DSR region for nuclear exosome-mediated elimination.
  • Red1 (zinc-finger protein) is implicated in this system, but its function is unclear.

Purpose of the Study:

  • To elucidate the molecular mechanisms of the Mmi1/DSR elimination system.
  • To identify genetic factors interacting with Mmi1.
  • To determine the role of Iss10 in regulating Mmi1-mediated transcript elimination.

Main Methods:

  • Genetic interaction studies to identify factors affecting Mmi1 function.
  • Analysis of Mmi1-Red1 protein interactions.
  • Assessment of meiotic transcript levels during mitotic and meiotic cycles.

Main Results:

  • Iss10 was identified as a key regulator of the Mmi1/DSR system.
  • Iss10 controls the interaction between Mmi1 and Red1.
  • Loss of Iss10 disrupts Mmi1-Red1 association, causing ectopic mitotic expression of Mmi1 targets.
  • Iss10 downregulation during meiosis dissociates Red1 from Mmi1, suppressing Mmi1 activity.

Conclusions:

  • Iss10 is essential for proper Mmi1/DSR-mediated transcript elimination.
  • Iss10 acts by modulating the Mmi1-Red1 interaction, ensuring accurate regulation of meiotic transcripts during the cell cycle.

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