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Lin28 mediates the terminal uridylation of let-7 precursor MicroRNA

Inha Heo1, Chirlmin Joo, Jun Cho

  • 1National Creative Research Center and School of Biological Sciences, Seoul National University, Seoul 151-742, Korea.

Molecular Cell
|October 28, 2008
PubMed

Insights

Lin28 proteins repress microRNA (miRNA) let-7 biogenesis by adding uracil to precursor let-7, causing its degradation. This posttranscriptional regulation is crucial for development and cancer.

Area of Science:

  • Molecular Biology
  • Developmental Biology
  • RNA Biology

Background:

  • MicroRNA (miRNA) biogenesis is essential for cellular functions and embryonic development.
  • Dysregulation of miRNA pathways is linked to various human diseases.
  • The mechanisms governing miRNA degradation and regulation remain largely uncharacterized.

Purpose of the Study:

  • To identify regulators of microRNA (miRNA) let-7 biogenesis.
  • To elucidate the posttranscriptional mechanisms controlling miRNA maturation and turnover.
  • To investigate the role of Lin28 proteins in miRNA regulation.

Main Methods:

  • Investigated the interaction between Lin28 proteins and precursor let-7 (pre-let-7).
  • Analyzed the effect of Lin28 on pre-let-7 uridylation in the cytoplasm.
  • Assessed the impact of uridylation on Dicer processing and pre-let-7 stability.

Main Results:

  • Identified Lin28a and Lin28b as posttranscriptional repressors of let-7 miRNA biogenesis.
  • Demonstrated that Lin28 proteins induce uridylation of pre-let-7 at its 3' end.
  • Showed that uridylated pre-let-7 (up-let-7) is resistant to Dicer processing and is degraded.

Conclusions:

  • Lin28 proteins provide a mechanism for posttranscriptional repression of miRNA biogenesis.
  • Lin28-mediated downregulation of let-7 may be critical in embryonic development, stem cell programming, and tumorigenesis.
  • Lin28's role in regulating let-7 highlights its significance in undifferentiated and cancer cells.

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