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A Biogenesis Step Upstream of Microprocessor Controls miR-17∼92 Expression.

Peng Du1, Longfei Wang2, Piotr Sliz3

  • 1Stem Cell Program, Boston Children's Hospital, Boston, MA 02115, USA; Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA.

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Embryonic stem cell differentiation dynamically regulates miR-17∼92 microRNA (miRNA) expression. A key intermediate, progenitor-miRNA (pro-miRNA), controls the processing and expression of specific miRNAs from this cluster.

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Area of Science:

  • Molecular Biology
  • Developmental Biology
  • RNA Biology

Background:

  • The miR-17∼92 microRNA (miRNA) cluster is crucial for development, with its dysregulation linked to oncogenesis.
  • Precise control over miRNA expression is vital during embryonic development.

Purpose of the Study:

  • To investigate the dynamic regulation of the miR-17∼92 miRNA cluster during embryonic stem cell (ESC) differentiation.
  • To elucidate the mechanisms controlling the processing and expression of individual miRNAs within the miR-17∼92 cluster.

Main Methods:

  • Analysis of primary miR-17∼92 (pri-miR-17∼92) transcript processing during ESC differentiation.
  • Identification of intermediate RNA structures and processing factors involved in miRNA biogenesis.
  • Investigating the role of cis-regulatory elements and protein factors (CPSF3, ISY1) in miRNA production.

Main Results:

  • Relative expression of six miRNAs from the miR-17∼92 cluster is dynamically regulated during ESC differentiation.
  • Pri-miR-17∼92 is processed into a progenitor-miRNA (pro-miRNA) intermediate, essential for licensing the production of specific pre-miRNAs.
  • Autoinhibitory RNA conformations within pri-miR-17∼92 regulate miRNA processing, with CPSF3 and ISY1 mediating pro-miRNA biogenesis for most cluster miRNAs.

Conclusions:

  • Developmentally regulated pro-miRNA processing is a critical control point for miR-17∼92 miRNA expression.
  • This study reveals a novel posttranscriptional regulatory mechanism governing miR-17∼92 cluster expression during development.