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Nucleocytoplasmic Shuttling of FTO Does Not Affect Starvation-Induced Autophagy

Aleksander Aas1, Pauline Isakson1, Christian Bindesbøll1

  • 1Department of Molecular Medicine, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.

Plos One
|March 14, 2017
PubMed

Insights

The fat mass and obesity (FTO) gene

Area of Science:

  • Genetics and molecular biology
  • Obesity research
  • Cellular biology

Background:

  • Polymorphic variants of the FTO gene are associated with body mass index (BMI) in humans.
  • FTO's role in energy homeostasis involves amino acid sensing and potential regulation of autophagy via mTORC1.
  • FTO is known to localize in both the nucleus and cytoplasm.

Purpose of the Study:

  • To investigate the molecular mechanisms underlying FTO's association with BMI.
  • To identify functional regions of FTO involved in nuclear localization.
  • To determine FTO's role in regulating autophagy.

Main Methods:

  • Identification of a functional nuclear localization signal (NLS) in FTO's N-terminus.
  • Analysis of nuclear localization information in FTO's C-terminus.
  • Assessment of autophagy in cells with inhibited FTO nuclear transport and FTO-depleted cells.

Main Results:

  • A functional NLS was identified in the N-terminus of FTO.
  • Nuclear transport inhibition did not affect autophagy.
  • No difference in starvation-induced autophagy was observed in FTO-depleted cells compared to controls.

Conclusions:

  • FTO's nuclear transport is not essential for autophagy regulation.
  • The proposed role of FTO in autophagy is not supported by these findings.
  • Further research into FTO's cellular functions is needed to understand its link to body weight regulation.

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