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Transcriptome profiling in preadipocytes identifies long noncoding RNAs as Sam68 targets.

Naomi Li1,2,3, Steven Hébert1,4, Jingwen Song1,2,3

  • 1Segal Cancer Center, Sir Mortimer B Davis Jewish General Hospital, Lady Davis Institute for Medical Research, Montréal, Québec H3T 1E2, Canada.

Oncotarget
|November 16, 2017
PubMed
Summary
This summary is machine-generated.

The RNA binding protein Sam68 regulates adipogenesis by controlling long non-coding RNAs (lncRNAs). Loss of Sam68 impacts lncRNA stability and adipocyte differentiation, revealing a novel regulatory role.

Keywords:
RNA binding proteinsSam68adipogenesislncRNAspreadipocytes

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Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • Sam68 (a KH-type RNA binding protein) is crucial for adipogenesis.
  • Sam68-deficient mice exhibit a lean phenotype and protection against obesity.
  • Previous work linked Sam68 deficiency to defects in mTOR and S6K1 alternative splicing.

Purpose of the Study:

  • To investigate the role of Sam68 in regulating the transcriptome during adipogenesis.
  • To identify specific long non-coding RNAs (lncRNAs) modulated by Sam68.
  • To elucidate the functional impact of Sam68-regulated lncRNAs on adipocyte differentiation.

Main Methods:

  • Transcriptome profiling of Sam68 wild type and deficient 3T3-L1 preadipocytes.
  • Identification and characterization of differentially expressed protein-coding genes and lncRNAs.
  • RNA stability assays to determine the effect of Sam68 deficiency on lncRNA half-lives.
  • Functional studies involving lncRNA depletion in wild type and Sam68-deficient cells.

Main Results:

  • Loss of Sam68 significantly altered 652 protein-coding genes and 9 ncRNAs.
  • Downregulated genes were associated with cell migration and fat cell differentiation; upregulated genes with neurogenesis.
  • Sam68 regulates the stability of specific lncRNAs, including Hotair, Mir155hg, SR-lncRNA-1, and SR-lncRNA-2.
  • Depletion of Hotair and SR-lncRNA-1 impaired adipogenesis, while SR-lncRNA-2 partially rescued adipogenesis defects in Sam68-deficient cells.

Conclusions:

  • Sam68 plays a critical role in regulating lncRNA expression and stability during adipogenic differentiation.
  • Sam68's function extends beyond protein-coding gene splicing to include lncRNA-mediated regulation of adipogenesis.
  • These findings establish a novel mechanism by which Sam68 controls fat cell development through lncRNA modulation.