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Functional Evaluation of Olfactory Pathways in Living Xenopus Tadpoles
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PTENα regulates endocytosis and modulates olfactory function.

Yuyao Yuan1,2, Xuyang Zhao2, Pan Wang1,2

  • 1Institute of Systems Biomedicine, Peking University Health Science Center, Beijing, China.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|July 11, 2019
PubMed
Summary
This summary is machine-generated.

Phosphatase and tensin homolog deleted on chromosome 10 alpha (PTENα) maintains olfactory bulb mitral cells and regulates neuronal endocytosis. Mutations in PTENα are linked to neurodegenerative diseases with early olfactory loss.

Keywords:
Ap2b1amphiphysinneurodegenerative diseaseolfaction

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Phosphatase and tensin homolog deleted on chromosome 10 alpha (PTENα) is an isoform of the PTEN tumor suppressor.
  • PTENα has known roles in learning, memory, cardiac homeostasis, and immunity.
  • Its specific functions in the olfactory system are largely unexplored.

Purpose of the Study:

  • To investigate the role of PTENα in olfactory bulb (OB) function and olfactory behaviors.
  • To elucidate the molecular mechanisms by which PTENα influences neuronal endocytosis.
  • To explore the potential link between PTENα mutations and olfactory dysfunction in neurodegenerative diseases.

Main Methods:

  • Investigated PTENα's role in maintaining mitral cells and regulating endocytosis in OB neurons using mouse models.
  • Examined PTENα's direct dephosphorylation of amphiphysin and its interaction with Ap2b1.
  • Analyzed N-terminal PTENα mutations in patients with Parkinson disease and Lewy-body dementia.
  • Assessed the effect of PTENα mutant H169N overexpression on odor sensitivity in mice.

Main Results:

  • PTENα maintains mitral cells in the olfactory bulb and regulates endocytosis in OB neurons.
  • PTENα directly dephosphorylates amphiphysin, promoting its binding to Ap2b1.
  • Identified PTENα N-terminal mutations in patients with Parkinson disease and Lewy-body dementia.
  • Overexpression of PTENα mutant H169N in mice OB reduced odor sensitivity.

Conclusions:

  • PTENα plays a crucial role in maintaining olfactory function by regulating neuronal endocytosis.
  • Dysfunction of PTENα may contribute to olfactory deficits observed in neurodegenerative disorders.
  • PTENα's interaction with amphiphysin and Ap2b1 provides a molecular mechanism for its role in olfaction.